free ebooks ==> www.el CHAPTER { 4 Periodontics Historical Background Anatomical Considerations — Gingiva = Periodontal Ligament — Alveolar Procass = Cementum Gingival Crevicular Fiuid (GCF) Periodontal Etiology, Immunology and Microbiology Periodontal Diseases Bone Destruction Patterns MHISTORICAL BACKGROUND + Hippocrates: + Father of modern medicine + Plorre Fauchard + Father of dantiety ‘© John W Riggs + ‘Riggs disease’ Father of periedonties I ANATOMICAL CONSIDERATIONS Gingiva ‘+ Isa masticatory mucosa and covers the alveolar process of the jaw and surrounds the neck ofthe teeth. Extends from the dentogingival junction to the alveolar mucosa, where itis limited by mucogingival junction, It is subject to friction and pressure of mastication, ‘The alveolar mucosa is red and contains numerous ‘small vessels coursing close tothe surface. Advances in Periodontal Diagnosis Prognosis Periodontal Treatment Periodontal Dressings Healing Periodontic Endodontic Continuum Halitosis, Laser Periodontal Microsurgery Miscellaneous Ling mucosa +p, chooks for of mouth soft palate ental part of tongue ‘Species mucosa + Dersum of tongue Fig. 14.1-Pats of oral mucosa www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 535 ~The gingiva is normally pink but sometimes have ‘grayish tnt. ~ The stratified squamous epithelium may be Keratinized or non-keratinized but most often it is parakeratinized, * Types of gingiva: The gingival is divided into two types: ere “+ Terminal edge of the «Its the continuation of the ‘gingival wich is usualy ee gingval and extends up bout imm wide and to the alveolar mucosa, ‘surrounds the teeth. + Extonde from tro gingival ‘+ Forms one of the walls ‘groove to mucogingival ine. ‘ofthe gingival sulcus (PGI 2007, 2009) fandis separated fom ©. Normally stippled and the attached gingival jeratiobed bya groove called froo (a1PG 2011,2008) ‘gingival groove. Width of Attached Gingiva:(AIPG 2007) Greatest in incisor region ©. Maxilla: .5-4.5mm_ > Mandible: 33 3.9 mm ~ Least in first premolar region (AIPG 2010, 2011, AP 2010, AIMS May 2010) ©. Maxilla: 9mm © Mandible: 18mm ~ Increases with age and in supraerupted teeth (MAHE 2008) ics of attached gingiva in children are: © Unique characte ~The imterdental clefts: Normal anatomic features found in the interradicular zones underlying the saddle areas = Retrocuspid papilla: found approximately Imm below the free gingival groove on the attached gingiva lingual to the mandibular canine. Occurs in 85% of shileren and apparently decreases with age. ‘Interdental papilla: ~ Fills the space between two adjacent teeth. — From oral or vestibular aspect, the surface of the interdental papilla is triangular. ~The depressed part of interdental papilla is called COL. © Stippling: — Stippling is seen in attached gingiva and central core of nterdental papilla (KAR 2010, Man 2002, AIPG 1995) = Absent in marginal gingiva — Form of adaptive specialization or reinforcement for function. = Produced by alternate rounded protuberance and depressions in gingival snleus ~ Feature of healthy gingiva = Loss of stippling is reversible and isa common sign of gingival disease Itis absent in infants and old age. (AIPG 1997) Appears in children about the age of 5 years Interdental Col: ~ Non keratinized (AIIMS Nov 2013, AIPG 2009, 2011, KAR 1999) = Lining is composed of non keratinized reduced ‘enamel epithelium, so more prone to attack by injurious agents and less resistant to inflammatory changes. (PGI 2002) ~ Oral hygiene accessibility islimited (AIPG 2011) ~ Area for food entrapment Gingival sulcus: ~ _V shaped shallow crevice ot space that encircles the tooth and presents between root and gingiva (KAR 2002) ~ Bounded by the surface of the tooth on one side and the epithelium lining on the other side. (Mar 2011) = Inideal conditions, depth is Omm = Probing depth of clinically normal gingiva is 2-3 mm (AIPG 2005, 2009,2004, PGI 2003, 2002, AIMS Nov 2010) ‘The gingival epithelium: 3 types: = Outer or oral epithelium ~ Suleular epithelium = _Junctional epithelium. Gingival epthtiur| ‘or oral] Suleuar spiel) Junctional Spitheum) | + stratum basale 1+ stratum com Ly stratum spinosum Outer or oral epithelium:-The epithelium consists of the following layers: — Stratum basal: Stratum spinosum: = Stratum corneum: Cuboidal ells large polyhedral cells superficial most. layer, Large, wide, flat and lacking nucleus.536 free ebooks ==> www.ebook777.com Review of All Dental Subjects Stratum sranulosum Stratum spinosum Stratum basale Sulcular epithelium: = Extends from the coronal area of the junctional epithelium to the free margin of the gingival. = Extends from gingival margin to base of histological sulcus. = Epithelium is nonkeratinized. = Epithelium lacks heavy ridges and papillae = Acts as semipermeable membrane through which injurious bacterial products pass into the gingiva and tissue fluid from the gingiva seeps into the sulcus (AIPG 2011, AIIMS 2008) = Sulcular epithelium has the potential to keratinize if it is reflected and exposed to the oral cavity or the bacterial flora ofthe sulcus is totally eliminated Lipid droplet Keratohyaline Lamelatee granules Tonoforie Golgi complex dntercollr space Desmosome Mitochondte Granuar endoplasmic reticulum Basement membrane Attached to tooth by means of an internal basal lamina and to the gingival connective tissue by means of external basal lamina, “The internal basal lamina contains lamina densa and lamina lucida to which hemtidesmosomes are attached. Attachment to tooth is by hemidesmosomes (AIPG 1997) Basal lamina of junctional epithelium is devoid of type IV collagen, instead type VIILis present. ‘Has a high turnover rate (AIPG 1996) “The length of JE ranges from 0.25-1.35 mm (PGI 1999) “The distance between JE and alveolar bone remains (KAR 1998) constant-1.07-1.97 mm. Junctional epitheli Cells become cuboidal after ameloblasts have finished formation of enamel. Forms a collar around the tooth, Gingiva is attached to tooth by junctional epithelium (AIPG 93) Wider at the floor of gingival sulcus and tapers apically to final thickness of 3-4 cells. It consist of stratified squamous nonkeratinizing epithelium. Divided into internal and external basal lamina Dentogingival unit: JE + Gingival fibres-reinforces the attachment to tooth-so together known as dentogingival unit. (AP 1999, 2003) Keratinization: Depends on functional stimulation and is age related Adaptive mechanism for masticatory forces, Maximum on hard palate, followed by gingiva, tongue, cheek (least keratinized) www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics. 537 «In which the supercal cols form In whith the super calls elan Inwith he srtae col are nucleated a show Sealesefkeran swicee heir” pyknoic nucle arc Sow come signs no sors of eraser + Asvetumayanutsur is resert cfoeira eraineed. (IPG 2002) + Hoveves te satin gubsum is generally sort. © Blood supply: Blood supply of gingiva is by ALVEOLAR ARTERY © Three sources of Blood supply of the gingiva are as follows: SSE PSE ‘Alorg the facial sn lingual suifaces of Which exter into te gincWval 21d Which errerce fom the crest of the irterdental the aheola” bone. from whicn cepilaies anastovose with capillaries of fe sulcus sects end extend caval to the cest of te bone exten alerg the stlculst epit-elum ard area to ansstorose wit vessels cf te pericdontal between the ‘ete peos of the exteral licarert. win cepilzres ir te gingival CevicLler cingwal surface, Gocasioxel ranches of ress ar vessels tat un over the aheclr crest the atercle cess tvo.en te alveclar bore to the pericgcntal igement cr run over the crest of ie ahecler bone © Nerve supply: Nerve supply ——_Mofitary Mandibular Nasopalaine nerve > (suppes focal aspect of | lorie aiveota nerve ‘anterior tooth) > Posterior superior sveolar nerve _y Greater palatine nerve (Supplies lingual aspect of Antero palatine neve “> (lope ing pest ‘© Cells in gingival Epithelium: = Keratinocytes: comprises about 90% of the total cell production = Non Keratinocytes: a Keratinosomes or Calan bodies Modified lysosomes cresent in. Destruction cf crcarelle rembr=1e statur soirosum Mefanccytes _(AIPG 2008) Dendritic colls lccates in the basal Trey syatesize melanin in relanoscrses ‘and spinous layers of iraival epithelia (Almis May 2010, AIPG 2007) Langernans cells (COMEDK 2063) Dendritic cells kocated atthe Phagocytic reictlcowdothelial eystom macccphazes with ‘suprabasal layers ard are aosert in ossiok antigenic orcperty SE ofnorral once Merkel cells Locatec in deap layers of epithelium Se-ve as tate “sceptcrs + Gingival connective tissue: = Collagen fibre bundles 60-65% = Cellular elements (fibroblasts 5%, various levkocytes, mast cells, tissue macrophages, et: 3%) = Vascular elements (blood and lymph vessels) nerves and ground substance about 35%free ebooks ==> www.ebook777.com 538 Review of All Dental Subjects «ing ie CSL oreo PERE Ee SR er ox rarer omen care a renee ee rT ae reer Es aaa 08 irto the attached Ta PES io ey pc cnc ti et nc tt ero 2 Roti Se ee nica 9 Desmodont, (AIPG 2005) ° omen 2 bape 2 eee thickness ranges from 0.5mm to 0.38m1m, average 021mm, = Periodontal ligament is hourglass shaped, being wider at ends and narrower in the middle (fulcrum of tooth) rincipal Fibres = Mainly composed of collagen, Collagen type Is predominant and type Ills also present, ‘Transseptal fibresconsidered part POM ait Gives intersrexinel suoport of both periodontal and gingival ‘This fre group is called as interdental_« They can be regenerated after damage OMS E UR ligament. “+ These mun fer cenertim fh ricsl + They prevent extrusion ofthe oct. ‘ection tthe aheolar crest moverrerts (GE Tlgay * These run fom cemerti to ahecley + These are maximum ir numer, susperc the POR TCP yg cre in ccroral rection cot ad ret vera msictoy tosses in apical rection Exord at ichtancles for ceme-tumtc + They alc resist vertical cisclacement fhe ‘sheoler core feet www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 539 + Trey atise fom reat jendsandare coset + They resist tation roverrert in neo rpletely ermed “scts(AIPG 2608) + Trey far cutoementamte the tothin the furcation 262 of muliootes teeth Good to Know “The largest group of principal fibres is oblique group, extending from the cementum in a coronal direction obliquely to the bone. “The principal fibres of PDL group that prevents extrusion of tooth and resists lateral tooth movements is alveolar crest group Principal fibres embedded in cementum are known as Sharpey’s fibres. Principal connective tissue cells present in periodontal ligament ate fibroblasts. These cells perform the dual function of new collagen synthesis and old collagen phagocytosis. The latter function is done via pseudopodia like processes that phagocytosis old collagen fibres and degrade them via enzyme hydrolysis. Main blood supply is from superior and inferior alveolar arteries. “The PDL supplies nutrients to the bone and gingiva via blood vessels Indifferent fibre plexus: (AIPG 2011, MAHE 2011, MP 2011) = Small collagen fibres associated with large principal collagen fibres. = Measure around 1400 A in diameter in SEM = These course in every direction throughout the area between bone and cementum without particular orientation, They anastomose extensively with the principal fibres to form a continuous fibrous matrix Fibroblasts = Fibroblasts are the predominant cell of connective tissue = Because all tissues of the tooth and its supporting apparatus are connective, fibroblast play an important role in the development, structure and function of the tooth, Fibroblasts function to form the fibers of connective tissue, that is collagen and elastin = They produce and maintain the ground substance in which they and their fibrous products are enmeshed. = They exhibit contractility and motility which are lized in determing the structural organization of connective tissue. Cementoblasts = The cells of the dental follicle differentiate into cementoblasts = Once differentiated they insert cytoplasmic processes into the unmineralised hyaline layer and begin to deposit collagen fibrils within it a right angles to the root surface. = The cementoblasts then migrate away from the hyaline layer but continue to deposit collagen so that the fine fiber bundles not only lengthen to maintain a fibrous fringe on the root surface, but also thicken to form. the fibrous matrix of acellular cementum, Cementoblasts also secrete non-collagenous protein such as gailprotein and osteocalcin. ‘Mast Cells = ‘They increase in chronic inflammatory states and may be prevalent during the first 7 to 10 days of healing after surgery. = They appear markedly granular with a large deeply staining nucleus ~The ces synthesise histamine by the decarboxylation of the aminoacid histidine and may be a connective tissue source of heparin and the sulfate = Injury to the cells elicit degranulation with the release of histamine and the hydrolytic enzymes into the tissues, = This produces immediate hypersensitivity response Other vasoactive kinins associated with issue injury and. healing are of plasma and pancreatic origins and are released at the site of injury by the action of trypsin. Bradykinin is a most important non peptide and is related to the early post surgical inflammatory process. Aprotinin, a protease inhibitor, found to antagonize bradykinin activ \ ag i ty ‘Mononuclear Macrophages = Apphagocytic cell important in tissue repair = Derived by mitosis or differentiation from the blood monocyte it migrates on connective tissue and fibrinoid strands towards and into the wound, = Itis responsible for the phagocytosis and digestion of cellular debris, bacteria, particulate exogenous matter, and so on = Histocyte has various hydrolytic enzymes such as acid phosphatases, collagenases, proteases, lipases, cathepsins, it demonstrates intracytoplasmic inclusions of phagocytized debris.free ebooks ==> www.ebook777.com 540 Review of All Dental Subjects ISTE RISE + \ © Schroeder's Classification of cementum: + Contairs -etrer cals nor extirsic or © Consists of Peay invinsc eolagen fores = An external plate of compact bone (KAR 1998) [DoJ TEs) + Ory mreralesd round stostance = Inner socket wall of thin compact bone called + Productof cerentolests “alveolar bone proper “+ Fournin coronal cementum = Cancellous or spongy trabecular bone, in between these two compact bones It acts as @ supporting bone. + Cancellous bone is found predominantly in the inter- radicular and interdental spaces. (AIPG 2011, 2009, ALIMS 2006) ‘+ Alveolar bone proper is a thin layer of bone lining the roots ofthe teeth and provides attachment to principal fibres of periodontal ligament. + Radiographically this bundle bone appears as thin radio-opaque line surrounding the roots of teeth, then called the lamina dura + “Thealveolarboneis perforated with numerous openings by branches of intra-alveolar nerves and blood vessels. and therefore called cribriform plate. ‘cellular extrin- [ky ces TNS) + Lacks cots IST) Product of fsoblasts and comentodiasts + Foundin the cervical 13” of the roots STGUE ° ts covpossc of extinsi Srapeys Seiteeecas) fres) and predominant mnste Mores rye anc contains cols 1+ Produetofbot foroblasts and Camencbists ‘+ Acpeats primarily in apical ira of roots sri fireation areas Composed almost ertely of cersely packed sharpey’s bres Cellular intnsic fi fibre camentum i (ola) : Contains cols but no collagen fibres Itisforr2e by oemertoolaste In human i fis resorpton lacunae © ‘The distance between the crest ofthe alveolar bone and the cementoenamel junction in young adults vaties from 0.75 and 149mm. Iholated areas in which the root is denuded of bone and. is covered only by periosteum and overlying gingiva, is called fenestration. ‘When the denuded area includes marginal bone, the defect is called dehiscence ‘Cementum overlaps enamel in 60% cases ») Butt joint is seen in 30% cases ‘Cementum does not meet enamel in 10% cases - results in sensitivity Width of cementum (acellular) at the cervical third-20- 50pm. L Width of cementum (cellular) at the apex-150-200.un, Cementum Aceltular cementum forms first and before tooth reaches occlusal plane, TEEN * First formed cementum Most desirable cementum in regeneration-acellular rr Primary cementum (AP 2004) extrinsic fibre cementum, ci - rm) Co not contain cemertooytes Itis he oementur thats forres before ‘he toh reacnes the cod.sal plane It covers the cecvcal hid or half of rt 1+ Thicaress anges fem 30 fo 290 ym + Shaypey' flores make up most of the stucture of acellulee cerertim wich Fas 2 principal cle F supperting tooth ‘+ More caleifid tan cebular coma Formac ater the tooh reaches tre Docusal olane + Secondary cementum (WAHE 2014) + Itis more imegular 7c oortzirs cementooytes n lacinae + Collar cementum is rore fectert o1 cic raf + Thichest around the apex. Incremental lines-rest periods in cementum formation and are more mineralized than adjacent cementum. Fusion of cementum and alveolar bone with obliteration ‘of periodontal ligament is knowns ankylosis. Anomalies of cementum = Enamel projections: Seen in localized areas in the furcation of mandibular molars during development. Enamel pearls: Globules of enamel on the root surface in the cervical area are known as enamel eas. Fppercementoas (emental hyperplasia) Cementicles: Globular masses of cementum arranged in concentric lamella that may be either found lying free in PDL or adhering to the root surface. They may develop from: www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 541 ©) Galeiied epithelial cel resus of Malazsea >, © Small spicules of cementum that may traumatically get displaced in PDL © Calcified sharpey’s fibres © Caleified thrombosed vessels in PDL ‘Age Changes In Periodontium:(AIPG 2010) + Altered cell density and flattening of rete pegs © Decreased number of fibroblasts Apical migration of JE and gingival recession (AIPG 2010, 2012, COMEDK 2007)» Coarser and denser connective tissue Decreased organic matrix production and epithelial cell + Increase in soluble to insoluble collagen, increase in rests strength and increased denaturing Increased amounts of elastic fibres (COMEDK 2007). Increased permeability to bacterial antigens and decreased ‘The width of attached gingiva increases with age resistance to functional trauma (MATTE 2008) , decreased ke a Decreased thickness of cementum. “Thinning and decreased keratinization of epithelium. (PG12008 MAN 2002) ° Accumulation of resorption bays leads to increasing surface irregularity of cementum IEGINGIVAL CREVICULAR FLUID (GCF) ‘An exudate; Can be harvested non-invasively. GCF is a transudate in health and an exudate in inflammation. The total protein content of GCF is much less than that in serum. Contains rich array of cellular/biochemical mediators that reflect the metabolic status of periodontal tissues Enzymes in GCF: - Proteinases (mammalian/bacterial) ~ Acid phosphatase © Cathepsin D = Alkaline phosphatase © Blastase = Pyrophosphatase © Cathepsin G = Beta ghucuronidase © Plasminogen activators = Lysozyme © Collagenase = Hyaluronidase (AIG 2011) ~~ _‘Laetic dehydrogenase ‘he cellular immune components present in the GCF include PMNs (95-97%), monocytes (2-3%), T cells (29%) and Bells (71%) ‘The humoral immune components present in GCF include IgG (IgGl-IgG4), IgA, IgM and complement components ‘There isa gradual increase inthe flow of the GCF from 6 am to 10pm and a decrease afterwards. As GCF traverses the inflammed tissue, it carries molecules involved in the destructive process which is potential to be detected in advance of irreversible bone loss. Its close association with the site of destruction — provide more information than markers in the serum/urine Plasma proteins, enzymes with collagenolytic activity, other microbial and host cell enzymes, inflammatory mediators -> all ‘these mediators present in the crevicular fluid has been used to facilitate the diagnosis of periodontal disease. Methods of collecting GCF: = Placing filter paper into sulcus (intracrevicular) (MP 2006, KAR 1998) = Placing paper atthe entrance of sulcus (extracreviculas) = Placing pre weighed twisted threads or mictopipettes and crevicular washings Periotron ~ used to measure GCE (KAR 2002) ration in GCF is 3-4 times greater than in serum, (COMEDK 2007, AIPG 2005) Protein content is much less than the GCE Amount of GCF secreted per day: 0.5-2.4m1 lucose conetfree ebooks ==> www.ebook777.com 542 Review of AllDental Subjects © Factors that increase GCF production >) = Gireadian rhythm = Sexhormones = Mechanical stimulation = Smoking = Periodontal therapy = Gingivitis (GCE production sno afte by trauma rom ocasion (P1206) GCF products can be grouped into 3 general categories Inflammatory mediators | Host derived enzym Extra cellular Breer + tha, + Abalire shoschatase (ALF) ‘+ May ect as 2 predicionimarko of peserufture + LB, + Predictor of presert sisease actty ona + Lane + TNE Xx © Oxygen coefficient of normal gingiva-1.6 0.37 (AIPG 2005) © Standard probing force recommended: 25g ot 0.25N ot 2.5g wt © Probing force that can be tolerated-75g ot 0.75N ot 7.5g wt lI PERIODONTAL ETIOLOGY, IMMUNOLOGY AND MICROBIOLOGY Plaque ‘Biofilm with regular intercellular matrix consisting predominantly of micro organisms responsible for periodontitis (AIPG 2008) + The most common cause of gingivitis and periodontitis is plague (MP 2011, COMEDK 2006, AIIMS 2000,1995, AIPG 2003, 1990, MAN 2002, MAHE 1998) © Formation of plaque occurs in following stages ~ Formation of pellicle Passive transport of microorganisms to the coated tooth surface by the flow of oral fluids = Reversible bacterial adhesion Irreversible bacterial adhesion = Coadhesion or co aggregation Multiplication of the attached micro organisms = Active detachment ©The first formed layer after tooth brushing is pellicle (PGI 1997, 1999) + Pelicle is of salivary origin and appears on tooth surfaces immediately after cleaning, Itis organic in nature © Paice formation on enamel starts with the edsorption of glycoproteins from saliva, No bacteria are present in pellicle, (PGI 2003, ATIMS 2000, MP 2011, IGNOU 2011) © Itisa prerequisite for plaque formation. Bacteria progressively accumulate to form dental plague, (AIMS 2008, AP 2004) © The average concentration of micro organisms in saliva is approximately 750 million cells per ml (ALIMS 2006, 2009) www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 543 Materia Alba = Yellow or white soft sticky deposit consisting of bacteria but does not contain the regular internal pattern, (AIPG 1995, AIIMS 1992, MAN 2002,APPSC 1999, AP 2009) = Less adherent than dental plaque = Consists of microorganisms, desquamated epithelial cells and salivary proteins - disorganized. © S. mutans readily use sucrose with the help of enzyme glucosyl transferase. (PGI 2000, ATIMS 1995, AIPG 2001) ‘© Following exposure to sucrose, they produce = Acid = Intracellular polysaccharides (ICP), that provide a reserve source of energy for each bacterium. © Extracellular polysaccharides including glucans (dextran) and fructans (levan). ‘These help anchor the bacteria to the pellicle, as well as stabilize the plaque mass. (PGI 2000) © ‘The glucans and fructans ate major contributors to the intercellular plague matrix (extracellular) © ‘The interbacterial matrix accounts for 20-30% of plaque mass © Glucans contribute approximately 20% of plaque dry weight, levans about 10% and bacteria the remaining 70-80%. © Dextrans are sticky insoluble whereas levans are soluble and weakly adherent. (MAN 1995) ‘© Dextrans help in establishment of bacteria in plaque and plague to tooth. (AUMS 1999, APPSC 1999) (AIPG 2010) © Water content of plague is about 80% (PG11997, 1998) © The inorganic component of plague is primarily calcium and phosphorus (KAR 1997) © Maximum accumulation of plaque takes place in approximately 21 days, (AUIMS 2008, AIPG 2009, 2011) Within seconds ‘Acquires pellicle femation adtoscteral adhesion (Alms May 2015, 2008, MAHE 2010) Within 2 hours lral plaque formation tates place, rreversiblecolonizati (lp 2008), Within 6 hours Supreainghal lecue fs well establishes Within 2 cays Plaque covbles ir mass By 57 days Plaque maturation dominated by flamentous bacteria By 21 cays Becteal atively stable By 12 weoks ‘el iforetises subghcival pleque is forred, corrinates by gram reastive © Barly supragingival plaque contains gram positive cocci and rods © Mature supragingival plaque contains spirochaetes and gram negative rods ¢g, Bacteroides, These cause gingivitis (AIPG 2011, AIMS MAY 2013) "© Subgingival tooth associated plaque contains gram positive cocci and rods, e.g. Actinomyces, which results in root surface caries “© Subgingival epithelium associated plaque contains gram negative rods and filaments and causes periodontitis, (MAHE 2008, PGI 2000, 2001) “© During night, the flow of saliva is less, hence the plaque growth is decreased by 50% (AIPG 1992, 1997) “© Plaque preferentially forms on non-self cleaning areas, Plaque accumulates on the gingival third of tooth surface due to lack of movement of food and tissue during mastication and also in cracks, pits and fissures, (ALIMS 1993)free ebooks ==> www.ebook777.com 544 Review of All Dental Subjects Calculus (AIPG 2002) ‘Supragingival calculus ‘Subgingival calculus ‘Supragingival callus i only about 30% mineralized ‘Subpingival calculus i about is about 60% mineralized ‘+ White orwhitish yelow *+ Dense, dark brown or greenish back (AIPG 1990, 2006, 2011, AP 2007) ‘+ Hard clay ike consistency ‘+ Hard fit lke consistency(AIPG 2008) (AIPG 2008) “+ Minera source is salva, so caieg as salivary calculus + Mineral source is GCF and so calee a8 cerumal calculus (AIPG 2011) '+ Hydroxyapatite and octacalcium phosphate are tne major» Hydroxyapatite and magneslum whtlockite are the major crystal forms, (COMEDK 2011, IPG 2011) crystal forms. (APPSC 2008) {Mote conmon in the upper rst molar region Mave cannot ine koe tein regio ‘+ Can be easily detached ‘+ itis harder, thinner, and more closely adapted to tooth surface Imperfections, subgingival calculus can be more dificult to Femove than supragingval calcu. © Modes of attachment: ~ By acquired pellicle or secondary dental cuticle — _ By chemical interlocking of crystals of calculus and tooth structure = By physical penetration of calculus into cementum (mechanical interlocking) = Calculus attached to cementum by means of pelicle can be detached. = Calculus embedded deeply into the cementum appearing morphologically 2s cementum is called “caleulocementum: (AIPG 1994) ‘Theories of Mineralization of calculus: = Booster mechanism: suggests that the precipitation of calculus phosphate salts results from a local rise in the degree of saturation of calcium and phosphate ions. ~ _ Epitactic concept/Heterogeneous Nucleation Concept: calculus formation may be initiated through epitaxis/seeding by organic complexes in the matrix. © Dental calculus, salivary duct calculus, and calcified dental tissues are similar in inorganic composition. Only the crystalline component changes. ‘+ The ratio of calcium to phosphate is higher subgingivally, and the sodium content increases with the depth of periodontal pockets. Micro organisms are not always ess calculus formation because calculus occurs readily in germ free rodents + Plaque hae the ability to concentrate calcium at 2 to 20 times it level in saliva + Calculus does not directly irritate the gingiva but it providesa fixed nidus for continued accumulation of plaque, thus acts asa contributing factor. (KAR 2003) © Subgingivalcalcutusis highest in lower anterior region whereas supragingival calculusis highest on upper molar region. + Calculus has approximately 75% to 85% inorganic content which is close to dentin (65%) as compared to enamel (96%) and cementum (55%). (AP 2010) ‘Filamentous organisms, diphtheroids, Bacterionema and Vellonella species have the ability to form intercellular apatite crystals. Microbiology ‘© Streptococcus sanguis, Smits, S.mutans and Actinomyces viscosus ate present in plaque “© Streptococcus salivarius isthe first organism to appear in the mouth after birth and is the predominant organism in saliva, www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 545 © Itisnot usually found in plaque. It is non-pathogenic bacterium and forms the longest chains ‘© Itismost commonly found on the tongue, Plaque Hypothesis © Both specific and non specific plaque hypothesis were proposed by Loesche (MAN 1998, KAR 1998, PGI 2007, 2008) © Non specific hypothesis: ~ Stats that periodontal discase results from elaboration of noxious products by the entire plaque flora, = Theperiodontal disease can be treated by debridement (surgical or non surgical) and oral hygiene measures, © Specific hypothesis: = _ States that only certain plaque is pathogenic (a1PG 2012) + Even though non-specific hypothesis is discarded, much of clinical treatment is stil based on nonspecific plaque hypothesis only = Robert Koch developed the criteria by which a microorganism can be judged to be the causative agent in human infections ‘These are called as ‘Koch’s postulates’ © Socransky modified the Koch postulates as related to periodontal disease (AIMS May 2013, Nov 2010, 2009) © Sigmond Socransky criteria for judging periodontal pathogens: = Be associated with disease wit = Be eliminated or decreased wit = Demonstrate host response — Demonstrate virulence factors capable of causing disease in experimental animals. increase in number of organisms at diseased sites reatment Evidence supporting a role of A. actinomycetemcomitans and P. gingivalis as Pathogen in Periodontal Disease: Socransky’s Criteria PEN ‘Association Inoases i localizes sagressive periodontitis LA®) lncressea'in percscntits Isic: kesors (AIPG 2014) urd assccietes win crewculer epivelirr Increases in some chronic pericconttslesicn Detectec inte tissues of LAP lesions i svocessfulth Elimination Supressed or eliminated ir Found ir ecurert cveeeultheccy Suporesses or ef ins urd in recurrent esior Py Host response Increase serum anc local antoccy levels in LAP Increased! syste as local antiboay kvels in Peiodortiis ‘Animal Studies Capable cf inducing disease in grctbiotc “ts ach tulence factors. Hest tissLe cell irvasior, le,Kotcxn, cclagenase. “osttissye cell nererce adinvasiorcolecerase, trypsin ‘endotoxin (LPS), epitheitoxn, foroblatinhibtng endotoxin factor bone rescrplionsucing Factor fcters rat affect >WN furction © Corn cob structures: © Coaggregation is the ability of different species and = Secn in supragingival plaque towatds tooth surface genera of plaque bacteria to adhere to one another, It is = Gram-positive cocei and short rods predominate at Predominant among gram negative organisms (AP 2004) the tooth surface, whereas gram negative rods and as * Quorum: Sensing: Mo te capacity or bacteria to well a spirochetes predominate in the outer surface of communicate with each other. This involves regulation the mature plague mass. of expreson of pecic genes through the accumulation of signaling compounds that mediate intercellular ~ Highly specific cell-to-cell interactions are also communications which when reaches a threshold level evident from the comcol} structures. (quorum cell density), gene expression is activated. (KAR 2002, AP 2000, 2001, IGNOU 2011) (KAR 2011, COMEDK 2010, MAHE 2007)free ebooks ==> www.ebook777.com 546 = Many species of bacteria use quorum sensing to coordinate their gene expression according to the local density of their population, Bacteria that use * quorum sensing constantly produce and secrete certain signaling molecules (called autoinducers or pheromones). These bacteria also have @ receptor = Nomenclature: ‘Actinobacitus Bacteroides gingivalis Bacteroides intermedius acters malanagenicus Wolinela recta Gingivosis Periodontosis Periodontal Micro-organisms: (AlIMS MAY 2009) + Early colonizers = Independent of defined complexes ~ Blue complex = Yelow compen Purple complex + Secondary colonizers ~ Green complexes = Orange complaves ~ Red complexes Review of All Dental Subjects that can specifically detect the signaling molecule (inducer). Interactions of secondary colonizers with early colonizers ~ Coaggregation of Enucleatum with Ssanguis = Coaggregation of Prevotellaloeschii with A.viscosus ~ Co aggregation of Capnocytophaga ochracea with Awiscosus ‘Aggregatbacter Porphyromonas gingivalis (back pigmented bacteria) Prevotela intermedius Prevotalla melanogenius (commen in Down's syndrama) Campylobacter recta Desquamative gingivitis iovenile periodontitis “+ Naslund Aviscosus Streplococeus sop + Odontotytioue ‘+ Corrodens, Actinobacilus actinomycetemcomitans serum a ype. ‘and Capnocytophegs species. Fusohacterim, Penvotalla, and Campylohactee spp Aeting- bacilus actnomycetemcomitans (Aggregatbacter) serum 'b’ ‘ype (AlPG 2014) P. gingivalis, B.forsythus, and Tdenticola Blue, yellow, purple and green sites are associated with healthy sites. Green and orange complexes include species recognized as pathogens in periodontal and nonperiodontal sections. ‘Orange and red complex consists of microbes associated with initiation and progression of the periodontal disease. © ‘Thered complex particularly important because itis associated with bleeding on probing, which isan important clinical parameter of destructive periodontal disease. © Actinobacillus actinomycetemcomitans (Aggregatibacter) serum ‘type (green complex) iskind to host and Actinobacillus ‘actinomycetemcomitans (Aggregatibacter) serum 'b type is more aggressive. www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics + Slow progressing . 8 No periodontitis + Prewiella terre + Aacomt + Spice orchyrororas gingivalis Frewotelle hte recs Capnoytepnege . melanogenicus + Rapidly prooressing periodontitis + Frepubertal periodontitis « + Caprocytepreae + Bimelencgenions + Juvenite periodontitis + ANconitens: (MAN 2001, KAR 2002, 2010, AIPG 2006, HP D0) + Generalized Aggressive + Pintermedia perioacntts + Caonooy + Pregnancy gingivitis + Provetella interred (MAE 2009, PGI 2007, 2008) The Bacteria Associated with Periodontal Health are (Protective Species) © Streptococcus sanguis © S.mitis © Actinomycosis viscosus © Capnocytophaga © Neisseria Veillonella Bacterial Enzymes (AIPG 2009, 2011) + Collagenases + Peirgivalis (@iPG 1991, 1992, C ryote 20062011, AIMS. 1997, 12002, AP 2608) ‘+ Typsin like enzyme + Pichoiale + Tedertcols + Aactinomyostemcoritans + Aryisulftase + Crectis + Torys + Pirreleninogerica 547 + Fibronectin degradation + F.chzivalis. ‘enzyme + Pirtemecia + Phospholipidase A . Virulence Factors ofA. Actinomycetemcomitans © Factors that promote colonization and persistence in oral cavity = Adhesins = Invasins = Bacteriocins = Antibiotic resistance © Factors that interfere with the host's defenses: = Leukotoxin = Chemotactic inhibitors = Immunosuppressive proteins Factors that destroy host tissues: = Cytotoxins = Collagenases Bone resorption agents = Stimulators of inflammatory mediators "© Factors that inhibit repair of host tissues Inhibition of fibroblast proliferation = Inhibitors of bone formation Virulence Factors of Pgingival © Fimbriae = Adherence to host proteins = Intracellular signaling = Specific receptors © Proteases ~ Arg-gingipain: Disruption of fibrinogen- integrin interactions in gingival fbroblasts = Sustenins: Gingipain R degrades fibrinogen and activates prekalikrein directly in plasma. 11-6 induction causes bone _resorption/osteoclast. formation. © Hemagglutinins © Lipopolysaccharidesfree ebooks ==> www.ebook777.com 548 Review of All Dental Subjects Pacers een Periodontal Disease re a Cane seeioeny orem nema Dore See eee eaeecen sey eS as arora ed ers aS phagocytosis + lysis) decreased bacterial counts ‘Antibody mediated hypersensitivity ‘Cell mediated immune response ‘Activation of tissue factors ~ Lymphocyte and macrophage produced chemotactic factors for fibroblasts — fibroblast. activating factore Models of Periodontal Disease Activity (Socransky) ‘© The term periodontal disease activity refers specifically to, the stage of the disease, which is characterized by loss of attachment and alveolar bone. ~ Continuous Paradigm: Implies slow, continuous, and progressive destruction of periodontal attachment until tooth loss eventually results = Random burst theory: Periodontal disease progression ‘occurs as short periods of destruction followed by periods of non destruction occurring randomnly with respect to time and site within an individual. ~ Synchronous multiple Burst Theory: Tissue destruction occurs at a definite period of time in ‘one’ life and then pass on toa state of remission, e.g juvenile periodontit © Clinical indicators of disease activity = Bleeding on probing - Exudation = GCF assessment — Increase in gram negative anaerobic species = Increased silcular temperature Good to Know © Predominant immunoglobin in GCF is IgG (COMEDK 2006, KAR 2000) Predominant immunoglobin in saliva is IgA (arms 1993) ‘The predominant cell type in GCF is the PMN. They account for 92% of the total leukocytes while the ‘mononuclear cells account for 8% (AIPG 1991,1999, 2003,200, 2011) Among the mononuclear cells, 58% are B lymphocytes and 249% are T lymphocytes ‘The normal T:B lymphocyte ratio in peripheral blood is 1 and value i reversed to about 1:3in GCF. (AIMS 1998, MP 2010) Orogranulocytes are the PMNs that reach the oral cavity hy migrating thromgh the lining ofthe gingival sulcws (KAR 2000) Immunoglobulins are accreted by plasma clls of humoral immunity and get inactivated or destroyed by bacterial proteases. Lysozyme present in saliva causes cell wall lysis, of bacteria. It is antibacterial to Vellionella and. Actinobacillus (MP 2011) Lactoperoxidase thiocyanate system in saliva is bactericidal to Lactobacillus and Streptococcus (KAR 2011) Lactoferrin acts against Actinobacillus Myeloperoxidase, released by leukocytes and is bactericidal for Actinobacillus and also inhibits the attachment of Actinomyces strain to hydroxyapatite. (PGI 2005. 2006) ‘The earliest sign of gingival inflammation is bleeding con probing. Reason is proliferation of capillaries and increased formation of capillary loops between rete pegs oF ridges. Neutrophils are best suited for rapid response mein defence cells in acute inflammation. They are the only cells. that can survive in the hypoxic environment of gingival sulcus. They are released as a response of epithelial axis of innate immunity to bacteria inthe sulcus, (AIIMS MAY 2013, AIPG 2009, 2011) Monocytes and fixed macrophages belong to connective tissue axis. Remember that lymphocytes and monocytes ‘do not follow the neutrophils into gingival sulcus Monocytes are referred as macrophages when they leave vascular compartment and enter tissue compartment. Increased number of peripheral blood lymphocytes as a response toall bacteria is indicative of severe periodontitis B cells differentiate to form plasma cells in GALT in response to antigen exposure. Plasma cells secrete www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 549 immunoglobulins ~ antibodies that are glycoproteins in a nature. (AlPG 2011) ‘© Antibodies are highly specific and sensitive. Specificity of every antibody with particular antigen is due to ite unique amino acid sequence and tertiary structure of ts antibody ~ combining sites. © Memory B cells give rise to plasma cells upon secondary exposure to antigen and produce high affinity antibodies, 7 Gingivitsisknown asa Tealllesion and periodontitis») isknown asa B cell lesion. © IgM is released first and ite levels are greater in initial slages of infection that generally decrease dusing later stages of infection and become negligible in comparison with those of IgG. © Gell mediated immune delayed hypersensitivity do not involve antibodies. They are based on the interaction of antigens with T lymphocytes (AIMS MAY 2013) © RBC lysis, ie hemolysis due to complement activation after Ag-Ab reaction is the basis for complement fixation assay, Hemolysis is also the basis of colour of subgingival caleulus also known as serumal calculus. Supragingival calculus sealed as salivary calculus. reactions or © A true pocket never forms in ankylosed teeth because apical proliferation of epithelium along root is not possible due to ankylosis, © Osteoclasts, formed by fusion of circulating monocytes, possess elaborately developed ruffled border from which hydrolytic enaymes and acids ~ citric acid and lactic acid are secreted. © Most common cause of physiologic mesial migration is failure to replace extracted Ist permanent molar. Smoking produces an immediate transient but marked increase in GCF flow as result of blood flow changes induced by nicotine. © Molecules for enzyme inhibition: = Cathepsins inhibit cysteine protease = _Antilekoproteases inhibit elastase = TIMP inhibits collagenases Defective Neutrophil Function is Found In: (AIPG 1990) © Diabetes © Chediak Higashi syndrome © Juvenile syndrome © Papillon lefevre syndrome © Neutropenia © Agranulocytosis WBC Disorders That Affect Periodontium Are Classified As: (AIPG 2010) © Quantitative leukocyte disorders = Neutropenia = Agranulocytosis = Leukemia Qualitative leukocyte disorders ‘Multiple myeloma ‘Chediak Higashi syndrome Leukocyte adhesion deficiency Histiocytosis syndrome histiocytosis) (Langerhans cell Erinn Doe ‘Chromosomal abnormality _ | Periodontal manifestations Neutropenia, os ume of retircpris agranulocytosis Chesiak-Higashi ——» Decreased neutroxhil chemotaxis © ‘syncrume Brosevetion s + Netohil urrues fase to form Ccratecteristic Sst ararles calles ‘mega bosies Papillon LeFevre +‘Mulile functional neatroshil + symerome defects. nelcira 7. 3 ciency as well as defective ‘erotans 215 chanooyt ity associated in affected indivdvale win. 2 mutsicn in he cathepsin C a= “Aggressive periodontitis Carermosome “q42o43 The syrcrome is caused oy 2 multtation in te Weoscmel teafficking reguator gene LYST + Asuresshe ce-ocorttis ard oral akttion Crremsore 11 . sive LS fs caused by Tutations ir ition tar the cathepsin C ere. lecstes Wy may inelve on chromoscme 11 the parry 21 perrarert entition550 Review of All Dental Subjects Neutrophil abnormality Chromosomal abnormality _ | Periodontal manifestations Leukocyte adhesion Defects in leukocyte functon due deficiency-type! lack of integrin 32 subunit (CD18), (PGI 2006) Neutrophil defects include impaired ‘migration and phagocytosis. Histologically almost no extravascular eutophis re evident in penedontal lesions. Leukocyte adhesion Neuirophis fl to express the ligand doficiency-type ll (CD15) for P- and E ~selecns, “Chromosome 21 ‘+ Mutations inthe gene encoding the B2-integrin CD12 on | ‘chromosome 21 21¢22.3 resuitng in absent or markedly Teauced expression of LUTIai core ‘+ Chromosome 11, 19p, and 19q Fur aliferent fucasy! + Aggressive peviodonttis, at an early age and affecting primary and permanent entiton in inividuals who ‘are homezygous forthe etectve gene, + Aggressive periodontitis at 3 young age Fesuting in impaired vansendothelal migration in response to infiammaton ~ etectve fucose metabolism Diabetes and Periodontitis (Changes in subgingival environment Altered tissue hemostasis and wound healing [Changes in host immunoinflammatory response transferases would have to be affected (sle X~ sialyl Lewis Xr (CD 160) and E ana P selectin) + Altered microbiota ‘= Change in GCF composition ‘© Decreased colagen production ‘© Increased matrix metalloprotease activity ‘+ Accumulation of advanced glycation end products tumover ‘Decreased polymorphonucear leukocyte chemotaxis, adherence, ‘phagocytosis ‘+ Elevated proinflammatory cytokine response from monacytes! ‘macrophages (1B, PGE2, TNFa) + Wnereased tissue oxidant stress “Tiseve destruction Teen Fnzymase lastaselcolagenase'B-lucuronidase PMNS Impaired chemotaxis ‘oytokines IL1, INF Monocyte/macrophage stimulation Chron Advanced glycation end produc ReuwdSigaion cap ich ee } rae Lape hes sts : Lge lag Role of Sex Hormones on The Periodontium Estrogen = Influences the cyto differentiation of stratified squamous epithelinm and = Synthesis and maintenance of fibrous collagen = Fetrogen receptors in asteablast-like cell © Periosteal fibroblast > Scattered fibroblast of lamina propria and © Periodontal Ligament fibroblast providing the direct action on different periodontal tissues - The inflammatory mediators may be affected by www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 551 estrogen hormone level, which may be attributed to the production of prostaglandins (PGs) by the involvement of estradiol and progesterone = Amount of circulating estradiol Prevalence ofpeiodontl disease = Other Eifects In The Periodontium Are 5 TAmount of plaque with no increase of gingival Inflammation © Inhibit pro-inflammatory cytokines release by human marrow cells © 4 T-cell mediated inflammation © Suppressed leukocyte production from the bone marrow © Inhibit PMN chemotaxi © Stimulate PMN phagocys Progesterone: = Play a role in coupling of bone resorption and bone formation, = Action on bone Ditetlyby engaging Dicey by competing ovtecblatrecepor fora ~ Other effects in the periodontium are: 7 Production of prostaglandins (self limiting process) + PMN and PGEz in PGE J Glucocorticoid ant-inlammatory effect Altered collagen and non collagencous protein synthesis Alter PDI fibroblast Metabolism 7 Vascular permeability eo0oce = In relation to the elevated levels of estrogen and progesterone in pregnancy, the following changes occur: Subgingival plaque composition: © Anaerobic to aerobic ratio increases © Higher concentration of Prevotella intermedia (substitutes sex hormone for Vitamin K asa growth factor) © Higher concentration of Bacteroides melaninogenicus © Higher concentration of Porphyromonas gingivalis ~ Increases cellular proliferation in blood vessels, increases vascular dilation, thus increases permeability (results in ‘edema and accumulation of inflammatory cells) Decreases keratinization = Increased bleeding tendency = Pregnancy gingivitis begins in the 2nd or 3rd month and increases upto 8th month and decreases during 9th month. Effects of androgens on the periodontium > = Stimulates Matrix synthesis by osteoblasts and PL fibroblasts = Stimulates osteoblast proliferation and differentiation, = IL-6 production during inflammation = Inhibit PG secretion = Enhance OPG Concentration ‘This suggests that overall, Androgens may protect the periodontium via a positive anabolic effect on periodontal cells, a negative ‘effect on the production and presence of mediators of inflammation and an inhibitory effet on osteoclastic function, Testosterone had inhibitory effects in the cycloxygenace pathway of arachidonic acid metabolism in the gingiva and speculated that this sex hormone may have antiinflammatory effects on the periodontium.free ebooks ==> www.ebook777.com 552 Review of All Dental Subjects 1 PERIODONTAL DISEASES Gingivitis an — a nn cea co ed Paes — eee re Nae oe Bi eet oonch Gar en Sacer 2000, 2007, KAR 2010) © McCall's festoons are life preserver shaped enlargement of the marginal gingiva Stillmanis clefts breach in the continuity ‘of marginal gingiva. Neither of them is due to trauma from occlusion, (PGI 1999, 2002,2003, KAR 2009, MAN 1999, 2000) (AIPG 2009) © The two eailiest signs of gingival inflammation are: (AP 2010, AIPG 1991, MAN 2000, Increased GCF production rate PGI2003, AP 2005, COMEDK 2011) Genes Contour changes during gingival inflammation ee rolled, and blunt. contour Acute Gingival Infections NUG (necrotizing ulcerative gingivitis) Primary herpetic gingivostomatitis = Pericoronitis © Acute necrotizing ulcerative gingivitis: (ALPG 2003) - NUG is an inflammatory, rapidly destructive disease of gingiva, Non-communicable Complex etiology. Other names: (KAR 2009, COMEDK 2011, MAN 1994, ALIMS 1998, PGI 2001) Vincent’ infection, Acute ulceromembranous gingivitis, ‘Trench mouth, Ulcerative gingivi Vincent’ stomatitis, Plant- Vincent's stomatitis, Stomatitis ulcerosa, Fusospirillary gingivitis, Fetid stomatitis, Paueclomembraneous angina etc. ° ° ° ° ° ° ° ° Listgarten (1965) described following 4 zones, which blend with each other and may not be all present in every case (COMEDK 2006, MAN 2001, MAHE 2011) seen in canine region © Zone 1: Dactertal zone: "The most superficial, consists of varied bacteria including a few spirochetes of the small, medium and larger types. (AIPG 2009) © Zone 2: Neutrophil rich zone: Contains numerous leukocytes, preponderantly neutrophils, with bacteria including many spirochetes of various types, between the leukocytes. > Zone 3: Necrotie zone: Consists of disintegrated tissue cells, fibrillar material, remnants of collagen fibers and numerous spirochetes of the med and larger types with few other organisms > Zone 4: Zone of spirochetal infiltration: Consists of well preserved tissue infiltrated with medicum and larger spirochetes, without other organisms. Spirochetes have been found as deep as 300 microns from the surface (COMEDK 2011, MAN 2002, KAR 1998, 2000, MAHE 2010, KAR 2009) Psychosomatic factors: positive correlation has been shown between stress and ANUG Characteristic lesions of NUG include: © Punched out, crater like depression at the crest of interdental papillae, subsequently extending to the marginal gingiva and rarely to attached gingiva, (AIPG 1990, 1992, 1998, 2003, 2005, 2006, AP 2002, PGI 2002) www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 553 Gray, psuedomembranous slough covering \ Contd gingival craters and demarcated from rest of Stage 5: Necrosis into buceal ot labial Nem gingiva by a pronounced linear erythema. cars (6%) uleerative (AIMS 2008, AIPG 2001, 2002, COMEDK Stage 6: Necrosis exposing alveolar sromatie 2011) bone (1%) Red, shiny and hemorrhagic gingival margin if sage 7 Necrosis peforting Noma denuded of psuedomembrane covering, of gingiva and Progressive destruction, periodontal structures. Spontancous gingival hemorrhage or pronounced bleeding on slightest stimulation Fetid odor Excessive salivation = Cogen (1990) summarized the clinical features of ANUG as 5 Necessary diagnostic criteria = Interproximal and ulceration (punched out crater like depressions in papil- le) ~ Paingul gingivae + Bleeding (spontaneous or on slight provoca tion) > Other - Psuedomembrane (Fibrin, debris) ~ Fever, malaise, lymphadenopathy = Fetor oris ©. Symptoms = Lesions are extremely sensitive to touch, ~ Constant radiating or gnawing pain, intensi fied by eating hot 'n’ spicy food and chewing (PGI 2005, 2008, 2009) ~ Metallic foul taste in mouth, ~ Excessive amount of thick, pasty saliva, © Clinical course: Pindborg and colleagues (1966) have described following stages in the progress of NUG: ~ Only tip of interdental papilla is involved, ~ Lesion extends to marginal gingiva and cause panched-out papilla ~The attached gingiva is also affected Bone is exposed. Horning and Cohen (1995) extended this staging of oral necrotizing diseases as follows: (KAR 2010, 2011, PGI 2008) Stage 1: Necross of ip of interdental papilla (83%) NUG Stage 2: Necross of entice papilla (19%) Stage 3: Necrosis extending (o marginal NUGINUP gingiva (21%) Stage 4: Necrosis extending to atached singiva (1%) NUP. cheek (0%) © Primary herpetic gingivostomatitis (Fever blisters, cold sores, herpes labialis) (AIPG 2002,2009) = Etiology © Herpes simplex virus (HSV), DNA virus - type T © Type 2 (HSV-2) usually affecting genitals and lower skin, = Herpes virus Infections © 80 known herpes viruses, and eight of them are known to cause infection in humans: ~ Herpes simplex virus (HSV) 1 and 2, Varicella-zoster virus, Cytomegalovirus ~ Epstein-Barr virus, and ‘Human herpes virus 6 (HHV6) © All herpes viruses contain a deosyribonucleic acid (DNA) mucleus and can remain latent in host ‘neural cells, thereby evading the host immune response, “The herpes simplex virus is composed of four layers: = Aninner core of linear double-stranded DNA, ‘A protein capsid, = Ategument, and ~ Allipid envelope containing glycoproteins that is derived from the nuclear membrane of host als, © ‘The two major types, HSVI and 2 can be distinguished serologically or by restriction endonuclease analysis of the nuclear DNA, © Humans are the only natural reservoir of HSV infection, and spread occurs by direct intimate contact with lesions or secretions from an asymptomatic earier. © The virus is transported from mucosal or cutaneous nerve endings by neurons to ganglia where the HSV viral genome remains present in a nonreplicating state. During the latent phase, herpes DNA is detectable, but viral proteins are not produced” occurs when HSV switches to a replicative state © Clinical features: (AIG 2001) = The onset is abrupt ° Reactivation of the latent virusfree ebooks ==> www.ebook777.com 554 Review of All Dental Subjects anterior cervical lymphadenopathy, chills, fe- ver (103° to 105°F), nausea, anorexia, iritabil- ity and sore mouth lesions. ‘The sranifestations may vary from mild wo se verely debilitating Hio previous exposure with herpetic infection may be elicited. ~ The affected gingiva often exhibits distinctive punched-out lesions along the mid facial free gingival margins Satellite vesicles of perioral kin are fairly com- ~ Diffuse, erythematous, shiny discoloration and. edematous enlargement of gingivae with aten- dency to wards bleeding make up the clinical picture. ~The course of the disease is limited to 7 - 10 days scarring does not occur in the areas of healed ulcerations. > Histopathology of the lesio ~The virus targets epithelial cells which exhibit! ballooning degeneration’ consisting of acan- tholysis, nuclear cleaning and nuclear enlarge- ‘ment. The acantholytc clls are called Teanck cells = Infected epithelial cells fuse, forming multinu- cleated cells and intercellular edema leads to formation of intraepithelial vesicles that rup- ure and develop a secondary infanmatory response with a fibropurulent exudates a Site of ulcers Interdental papilla, Marginal gingiva Character of ulcors + Punched out, crater ike doproscion covered by yellow! whitelgray slough *+ Bleed readiyspontaneously ‘Painful on stimulation Fever Doub sight only ‘Symptoms Painful gums! dead feeling teeth Duration of ulcers ané Short lived (1-3 days), with appropriate ‘discomfort therapy Etiology Interaction between host and bacteria, ‘mast probably fusospirochetes Age [Uncommon in children contagious Non contagious Immunity No demonstrated immunity Chronic Desquamative Gi GGingva, No predilection for nterdantal papilla entire oral mucosa? "+ Muttiplo vocicioe that coalacce and form challow ‘bin ‘covered regular shaped uoers. ‘+ Nomarked tendency to bleed Non tender 20° © for more) Sove mouth More than 1 week, even with therapy Specie viral etiology More fequenty in ciléren Contagious ‘An acute episode results in some degree of immunity (war 2011) ‘© The majority of patients are females (80%) and in the fourth through sixth decade of life. ‘© Prina frst used the term ‘chronic diffuse desquamative gingivitis'in 1932. (MAHE 2010) © Classification: MC thy (1960) suggested a provisional classification based on etivlogic considerations: ~ Dermatoses © Lichen Planus 5 Mucous membrane pemphigoid © Bullous pemphigoid © Pemphigus = Endocrine Imbalance © Estrogen deficiency in females following hyst © Testosterone deficiency in males. = Aging (senile atrophic gingivitis) Metabolic disturbances © Nutritional deficiency (gingivosis) ectomy with oopherectomy or after menopause. www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 555 Miopathic Chronic infections © Tuberculosis © Chronic candidiasis © Histoplasmosis Drug Reactions © Toxic-antimetabolites > Allergic-barbiturates, antibiotics ete Abnormal response to irritation (modification of chronic marginal gingivitis) © Clinical Features: IGT itfuse erythema ofthe Ep Ty es ME eae To mmerainal,interertal ac lof bright rea ana gray areas areas if ynich the arava Bs deo Ski stiches orcs inveluing the raroinal end red in epcesrere. + Ususlly painless attacned Snaiva ‘+ Gives 2 speckled appearance. + Mest Fequerty in females + Tre surface is smooth 2nd ‘+ Tre surface eaithelimis shredded and friable src between 47 and 23 years of age shiny and the gingivais softin —_caniee peelec offin smell cetcre consistency. + Trete is slight pitting won creseure, 21d te cote isnot femly adherent to the snoerbyng B88 + Masssairg te gincis with the {ingor results in peeling of the epithelium ard exces. of Me ncerlying bless CT suface, Tis s torre ‘Nikolshy's ‘sign’ ane corsiss in 2 slepirg Corpeeiing of te tissue atthe Ccermakepicermel unction unde slgntisteral esse. al Enlargement Classification: According to the etiologic factors and pathologic factors © Inflammatory enlargement Chronic Acute Drug induced gingival enlargement Idiopathic gingival fibromatosie Enlargements associated with systemic disease © Conditioned enlargement (MP 2009, AIPG 2005, AP 2003) (MAN 2001) (PGI 1999) = Pregnancy ~ Puberty, = Vitamin C deficiency = Plasma cell gingivitis ‘Nonspecific conditioned enlargement (granu Jomatous pyogenicum) ‘+ Surface vessels ese cecasionally wrio nite, feleasing a thin, aqueous fuid and exposing an sncetying sirface tat ised anc av ‘+ Ablast car drected ate gincis cases elevation fhe epitielim anc the consequent formation of ourble, ‘+ Tre areas cfirvolvenent seer to shit to diferent location an ne gi ‘+ Tre muccus memorane oe than te ginsiva is “smooth and shiny and may presenta fssuring in the ‘cheek aelacent te te lire of 2ocl.sicn, Systemic diseases causing gingival enlargement = Leukemia (AP 1998, PGI 2008) Granulomatous diseases (Wegener's granulo- tosis, sarcoidosis) ‘Neoplastic enlargement (gingival tumors) ~ Benign tumors = Malignant tumors False enlargement Scoring of Gingival Enlargement Grade 0: No signs of gingival enlargement Grade 1: Enlargement confined to interdental papilla Grade I Enlargement involves papilla and ‘marginal gingiva Grade IM: Enlargement covers three quarters or ‘ore of the crown, © Pyogenic Granuloma Non specific conditioned gingival enlazgementfree ebooks ==> www.ebook777.com 556 Review of All Dental Subjects = Discrete bright red or purple tumor like lesion of the interdental papilla and extends to the facial and and is friable with surface ulceration and purulent lingual gingival margins (PGI 1998) exudation, ie. granulation tissue growth (KAR 1997) + The marginal and papillary enlargements unite and cover Its considered as an exaggerated response to minor _a considerable portion of the crowns, which interfere with, ‘trauma. occlusion, (BHU 2009) © Puberty gingival enlargement = Conditioned gingival enlargement occurs due to exaggerated response to local irritants = Related to hormonal changes = Microbiota seen are © Capnocytophaga species © Biintermedia © Bonigresens = Can be prevented with good oral hygiene Clinical features © Pronounced inflammation of marginal gingiva and interdental papilla (AIPG 2006) +> Bluish red discoloration and edematous gingiva © Lesion is mulberry shaped, firm, pale pink and resilient with no tendency to bleed, when uncomplicated by inflammation © Common and severe in maxillary and mandibular anterior regions. © Enlargement is chronic and slowly increases in size, Histological Features © There is acanthosis of epithelium and elongation of rete pegs. In connective tissue, there are foci of chronic inflammatory cells particularly plasma cells and large ‘number of fibroblasts and new blood vessels, = Plasma cll Gingivitis (Aire 1983) Drug Induced Gingival Enlargement (AIMS MAY is aaa 2013, AIPG 1996, KAR 1997, PGI 2000, 2001) © Temay be associated with cheilits and glossits = Anticonvulsant drugs associated with gingival > Plasma ell gingivitisisacontacthypersensitvity colargement ater Phenytoin, Phenobarbital reaction most frequently attxbuted to cinnamon flavored chewing gum. Carbamazepine, Sodium Valproate, Primidone and Felbamate — Antihypertensive drugs associated with gingival = Marginal gingival enlargement is seen in cages we, sede, “Amide > RE ‘Nimodipine, Nicardine, Nitrendipine, Diltiazem, ° Sregnancy elie 2 RE acsaengy : 3. Werner: gondononpaptary ype) — Immunosuppressive drugs associated with gingival enlargement ate: Cyclosporine o _ Drug induced = Diffuse gingival enlargement seen in Clinical Features © Leukemic gingivitis © Initially the growth is painless, beadlike enlargement © Idiopathic fibromatosis of gingiva Pocket (AlIMS 2009, AP 1998,2000,2003, AIPG 2003, KAR 1996, 1998) ‘+ Reladonship of tissue val cf tre 20: 2h level fatvectar bane fete ah e the arauiar cater cf the ad acent bone, They exterd from 3 erzcrtal ‘he cement beneath the case of fe coceet along tne bore a3 Normal horesntakabliqe course sf PerDsteUM. between te tooth and fe cove www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 557 Pathogenesis of Pocket: © Zone of semi destroyed connective tissue fibres apical to the JE-zones 3, 4 and 5 compose the so called plaque free zone seen in extracted teeth, Periodontitis lnflammatory changes inthe connective tissue of gingival sulcus Collagenases Activate Trobasts ‘and MIPS. for phayocytzing callagen ¥ val collagen fber destruction Proiferaton of apical calls of junctional ‘epithelium along the root PIN volume reach 60% or more Detachment of the Eoronal parton of {unetional epithelium fom the root bens emote te eet] Inisepiheil cleft and pocket progression) Correlation of clinical features and histopathologic features of pocket (AIPG 2008) Cees Pees ‘Bluish rea colour + Cicuatery stsqnation ‘iscoloration 1+ Destrsctionf te connective Fiacciaity tissue foros ‘Smooth shiny surface + Edema ard atopy of te hither ‘+ Edema anc decereration of eee) the cornectve tissue Pink and firm gingival Fibrliccre ces predominst> soft tissue wall ‘ver exudation ard cecereration + Bleeding elicited by ‘gentle probing + Inner aspect che 2cckel wall is paint or 2rcbirg + Pusexpressedan digital pressure bration ofthe inrer aspect of the pocket wall ‘Suppuratveinfammaton ofthe ‘ner wall of te pocket, ‘Morphology of the tooth wall: © Periodontitis is an inflammatory disease of the gingiva and the deeper periodontal tissues. It involves the destruction of gingival and periodontal fibers, resorption of alveolar bone, and proliferation of junctional epithelium. ©The clinical feature that distinguishes gingivitis from periodontitis is the presence of clinically detectable attachment los. At the 1999 international classification workshop, the different forms of periodontitis were re-classified into 3 (COMEDK 2006) ‘major forms - Aggressive periodontitis Chronic periodontitis ‘Necrotizing forms of periodontal diseases and into periodontal manifestations of systemic diseases. Pathogenesis Periodontal pathogens (LPS) Macrophage | _Tiymohocyte | Neviropil Interleukin t, NF] IL-1 lymphotoxin] IL“, Cathepsins| ‘alpha, PGE2, Hye enzyme, Enhanced prontammatory and catabole ates + Periodontal tissue destructon Periodontitis) Aggressive Periodontitis — The following zones can be seen at the bottom of a periodontal pocket © Cementum covered by caleulus: I exhibits all the root surface changes. © Attached plaque-It covers calculus and extends apically from it to a variable degree, probably 100- 504m, > Zone of unattached plague-tt surrounds attached plaque and extends apically © Zone of attachment of junctional epithelium to the tooth-in normal suldi its extension is more than 500qm but this is usually reduced in periodontal pockets to less than 100um, Historical background © Gottleib-1923: "Diffues atrophy of alveolar bone’ © Gottleib in 1928 gave the term “Deep Cementopathia” and attributed it to its inhibition of continuous cementum formation. © Wannenmacher in 1938 described the classic incisor-first molar involvement and coined the term "Parodontitis marginalis progressiva’. © Orban and Weinmann - 1942: "Periodontosis (AIPG 1993, PGI2003) © Chaput 1967, Butler 1969: Introduced the termfree ebooks ==> www.ebook777.com 558 Review of All Dental Subjects “Juvenile periodontitis” (AIPG 1990) ‘The amount of destruction manifested is not > Baer in 1971 defined Juvenile periodontitis ‘commensurate with the amount of local iritants” as “a disease of the periodontium occurring © 1999 International Classification Workshop: in an otherwise healthy adolescent which is renamed it as Ageressive periodontitis, characterized by arapidlossofalveolarboneabout Classification of Aggressive Forms of Periodontitis more than 1 tooth of the permanent dentition, ETI Novaretuiryrecea sey Prantl recipes Foolish + Resid attacrment loss anc bone destruction periodontal tissue destruction ae an + Elevated aroportons cf Agarecatisactor actinemyoetemoomitars. and in some fer east coculatiors, Porshyomoves gingivalis o RESET Seca cere taeeare artes eee er aa eae eee es + Progressior of attachment loss endlaene loss maybe sett sxrestig lized Aggressive Periodontitis (AIMS MAY 2008) ee + Circunpubertal onset + Usiallyafectng cesens uncer 30 years of age, but patie ‘+ Localized firsvincisor presentation wit terrcximal rrayoe olfer attzctment oss 07 atleast vo perrererttesty, ore of wnicn «Generalized interproximal attachment loss affectira atleast ‘Sa first molar, and iavoWing no more than two leet other than vee permanent eth ater than fist molars and incsors first molars ana incisors. (AIPG 1990) Poro.nced episodic nature of the destruction of stscimert + Robust serum antibody response to nfecine ecerts and aheciar bore ‘+The first clinical sign is tooth mobility and pathological + Pact serum antibody response to ifecting agers migration © Bacterial etiology >) = Localized Aggressive periodontitis: Primarily Aggregatibacter Actinomycetemcomitans (AIG 2009, 2011) ~ Generalized aggressive periodontitis has been frequently associated with the detection of Porphyromonas gingivalis, Bacteriode forsythus and Aggregatibacter Actinomycetemcomitans ~ Aggregatibacter Actinomycetemcomitans has been shown to possess the ability to translocate across the junctional epithelium and invade the underlying connective tissues, = The enzymes produced the micro-organisms include: © Proteases which can digest collagen, fibrin, fibronectin ete (> Arg tproesse © Inflammatory responses have been characterized by: 4. Intense recruitment of PMNs within the tissue and the pocket b. B-cells and Plasma cells, especially increased amounts of IgG producing and less IgA producing cells. € Depressed T-helper to T-suppressor ratio when compared to healthy gingiva and peripheral blood, 4. High levels of PGE2 T1-1a, and IL-1 Bin GCF and tissues ‘+ ‘The abnormalities of the PMNs in LAP are: Reduced chemotaxis in 70-75% of the cases (AIG 2009) = Reduced receptor expression Reduced Phagocytosis and killing of Aa Signal transduction abnormalities ~ Increased superoxide production www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics Refractory Periodontitis Cases that do not respond to therapy oF recur soon after adequate treatment ‘Term is no longer used. Prominent periopathogens such as Pgingivalis, Bfforsythus, Fnucleatum, Pamicros, E.corrodens and S.intermedius have been found to elevated in refractory periodontitis, (BHU 2009) Often patients identified as refractory to treatment hhave other factors, particularly smoking, that may contribute to the disease process Prepubertal Periodontitis is Seen in Papillon Leferve syndrome Hypophatasia Downs syndrome (AIP 2002) Chediak Higashi syndrome Leukemias Neutropenia Can occur before years of age Gingival Abscess Localized, painful rapidly expanding lesion of sudden onset Itis limited to marginal gingival or interdental papilla It is due to foreign substance carried deep into the tissues such as a toothbrush bristle, a piece of apple core or a lobster shell Gingival abscess involves marginal and interdental gingiva, whereas periodontal abscess involves, attached gingiva (AP 2002) Periodontal Abscess Defined as suppurative lesion associated with periodontal breakdown and localized accumulation of pus within the gingival wall ofa periodontal pocket, (AP 2001) Microbiology: © Gram-negative anaerobic species are non. fermentative and display moderate to strong proteolytic activity mainly Porphyromonas gingivalis, Prevotella intermedia, © Strictanaerobic, gram positive bacterial speciesin. periodontal abscesses include Peptostreptococeus micros, Actinomyces spp. Pulp weaity © Vial + Noval + Associated with + Peevstirg + Deep pericccrtal resteration (Clinical features often ita 8 fistlous opening in the aoical ates. may | be ay for Seldom with 2 3 tooth fata ‘Symptoms. + Painis dull, Painis severe. constant throboing and ay Ibcslzedard —lastfor cays, May ‘ne atiertcar be located aay ssyally beste fro tie cfferdne frecfierding tect. tot Pain on + Lesssevere — Neresexere percussion Treatment + Drainsoe Endodontic fellowec by management ericdrtal meneperert | BONE DESTRUCTION PATTERNS Horizontal defeets Vertical or angular defects = Based on number of walls remaining, can be further classified as (AIPG 2003) © One walled defect: one wall remaining also called hhemiseptum Minimum regenerative capacity © Two walled defect: two walls remaining © Three walled defect: three walls remaining also called intrabony defect. Maximum regenerative capacity (AIPG 2006,A1IMS May 2009) = Ledges Ramps = Buttressing bone formation = Exostosis | TRAUMA FROM OCCLUSION Traumatic occlusion introduced by Stillman denotes abnormal stresses capable of producing the injury to dental or periodontal structures is called occlusal trauma TRO refers to tissue injury that occurs when occlusal forces exceed the adaptive capacity ofthe tissues (MP 2011, AIPG 2001)free ebooks ==> www.ebook777.com 560 Review of All Dental Subjects © Primary TO occurs due to excessive abnormal occlusal Torces acting on normal periodontium © Changes produced by primary trauma do not alter the level of connective tissue and do not initiate pocket formation, “This is probably because the supracrestal gingival fibres are nol affected and thus prevent apical migration of the junctional epithelium. (AIPG 1991, AP 1996, MAN 1998) © Secondary trauma from occlusion occurs when the adaptive capacity of the tissues to withstand normal ‘occlusal forces is impaired by bone loss resulting from marginal inflammation. Here normal forces are causing injury in impaired periodontium. © Compression of fibres, stasis of blood flow; hemorrhage, thrombosis and necrosis of blood vessels are early signs of ‘trauma from occlusion © The necrotizing pressure areas, undergoing bone resorption and endosteal bone formation are seen in occlusal trauma, (AIPG 2001, Man 1997, AIIMS 1992, 2000) © Signs / Symptoms (AIMS MAY 2013, KAR 2001) = Tooth pain, sensitivity to percussion = Wear facets (aipG 2011) = Increased tooth mobility _(AIPG 2011, 2009, 1997, 1989, AIIMS 1992, MAHE 1998, COMEDK 2007) = Cementum tears = Widening of periodontal space = Root resorption ickening of lamina dura Vertical or angular bone defects (aIpG 2001) © Bone Remodeling Caused By Trauma From Occlusion: = TO can produce destruction in the presence or absence of inflammation, = In the absence of inflammation, the changes caused by TRO may vary from - compression and tension of periodontal ligament and increased osteoclast activity of alveolar bone to nectosis of PDL and resorption of bone and tooth structure. These changes are reversible; persistant TFO, results in funnel shaped widening of erestal portion of PDL with resorption of alveolar bone. = When combined with inflammation, TFO aggravates the bone resorption caused by inflammation and results in bizarre bone pattera. Remodeling and Mediators of Periodontal Osseous Destruction © MODELING- represents a process that allows a change in the initial bone architecture; external demands (such as oad) on bone tissue may initiate modeling. + REMODELING - represents a change that occurs within the mineralized bone without a concomitant alteration of the architecture ofthe tissue. © Modeling and remodeling occurs throughout life to allow bone to adapt to external and internal demands © The alveolar bone undergoes remodeling on one side of the socket and modeling on the opposite side as the tooth migrates atthe rate of 6.7jim per day. Periodontal ligament (PDL) width, however remain constant, Because of this very high turnover rate, this bone is a very good model to study modeling and remodeling activities + Remodeling of alveolar bone affects ~height, contour and density. BONE REMODELING CYCLE Releases PTH ‘Stimulates osteoblasts Releases IL-1 and IL-6 “Monocytes to migrate into mukinucteated osteocia Release calcium ions from Hydroxyapatite nto the blood Noxmalizes the blood evel of calcium Feedback mechanism of normal bloed levels of Calolumtums off the secretion of PTH © Bone Coupling = Osteoclasts resorb organic matrix along with hydroxyapatite When collagen breaks down from organic matrix it releases vatious organic substrates, which are covalently bound to collagen; Stimulates differentiation of osteoblasts, which deposit bone ~ This interdependency of osteoblasts and osteoclasts is remodeling ~ Coupling. © Reversal Phase Between the resorptive and formative phase is aperiod termed - Reversal Phase, Its estimated that the adult skeleton contains moze then 1 million BMUs at any time with nearly 5-fold more occuring in trabecular bone versus cortical bone © Bone resorption is a complex process morphologically related to the = Appearance of eroded enamel surfaces (Howship lacunae), ~ Large, multinudeated clis(osteoclasts) www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 561 © Cellular events in remodeling of bone = Chemotaxis: Attraction of osteoblast precursor, = Proliferation of osteoblast precursors. = Differentiation of mature cells synthesizing the proteins of bone. = Mineralization of this matrix. © In metabolic bone diseases, there are abnormalities in the coordinated activity of bone forming and bone resorbing cells ~ imbalance between precursors of bone resorption and bone formation. capable of Mediators of Bone Resorption eae ees Fee Bee eee Pay o Rae ee Syctospom Systemic Biochemical Markers of Bone Resorption (NET 2013) Hydroxyproline Hydroxylysine glycoside. Pyridinum cross: Links and related collagen fragments (telopeptides) Bone sialoproteins (BSP). Hydroxyproline (OHPr): Amino acid; mainly in fibrillar collagen: its urinary level reflects collagen turnover in bone and other tissues. Hydroxylysine: Unique to collagen; reflects mainly breakdown of bone collagen. Collagen pyridinium crosslinks: Pyridinoline or promote apoptosis of ECM producing cells; reduce the number of osteoblasts and fibrotic cells. available for repair of resorbed alveolar bone. Cardinal Features of Osteoporosis Include: © Reduced Bone strength © Reduced bone mineral density (BMD)free ebooks ==> www.ebook777.com 562 Review of All Dental Subjects © Altered Macro geometry, © Prone for fracture ‘The current gold standard for diagnosing osteoporosis is the bone mineral density (BMD) test as it is the best predictor of individuals likely to suffer fractures of the hip or spine. Bone mineral density i usually measured using a dual energy x-ray absorptiometry (DEXA) examination. Buttressing Bone Formation © Bone formation some times occurs in an attempt to buttress bony trabaculae weakened by resorption, When, it occurs on the external surface ~ peripheral buttressing bone formation. Bulging of the bone contour is called LIPPING. Orthodontic Tooth Movement © Its believed to result in site-specific bone remodeling in. the absence of inflammation, © Tensional forces stimulate formation and activity of osteoclastic cells, whereas compressive forces promote osteoclastic activity (ATMS MAY 2009) © Postmenopausal osteoporosis: Is a common disorder characterized by an increase in bone resorption, relative to bone formation, generally im conjunction with an increased rate of bone turnover. In PMO: Lack of estrogen leads to increased number of bone multi-cellular units and to uncoupling of bone formation and bone resorption, resulting in too little bone laid down by osteoblasts compared with the amount of bone resorbed by osteoclasts © Inflammatory process in the vicinity of the skeleton eg marginal and apical periodontitis, will affect the remodeling of the nearby bone tissue in such a way that, in most patients, the amount of bone resorbed exceed that being formed, resulting in net bone loss (inflammation- induced osteolysis). © In some patients however, inflammation-induced bone formation exceeds bone resorption and a sclerotic lesion will develop. © Bone remodeling is a complex regulated by systemic and local factors. © There are 4 possible pathways by which systemic bone loss may lead to more severe periodontal destruction, ~ Decreased BMD caused by systemic bone loss. = Modified local tissue response; increased production of cytokines and inflammatory mediators. = Genetic factors. = Certain lifestyle factors, © Bone mineral density (BMD): Amount of matter per square centimeter of bones. = BMD Test: Measures density of minerals in your bones using a special X-ray, computed tomography = Reduced bone mineral density is the strongest predictor of the several risk factors for fractures, © Tissue response to orthodontic forces: = Orthodontic tooth movement is possible because the periodontal tissues are responsive to externally applied forces. = Alveolar bone is remodeled by osteoclasts inducing bone resorption in areas of pressure and osteoblasts forming bone in areas of tension. Moderate orthodontic foree- bone remodeling and repair, = Excessive force - © Necrosis of Pal and adjacent alveolar bone © Risk of applied root resorption, © Diagnostic Potentials for Periodontal Bone Resorption = A graduated periodontal probe-traditional periodontal diagnosis; PD, G Recession, CAL. Number of factors influence. = Radiographs-height of alveolar bone margin, = Shape and form of its outline. = Sensitivity to detect early change is poor, but BIOCHEMICAL MARKERS can detect changes in a short time, = Sophisticated techniques-subtraction radiography and computer-assisted image analysis detect small changes, but have not found a place in routine clinical practice Collagenase and Related Metalloproteinases © MMPs such as-collagenases, stromelysin and elastase = are found in tissues or inflammatory exudates in periodontal lesions, Since these enzymes can specifically cleave and degrade collagen and connective tissue matrix macromolecules they are considered as attractive candidates as markers of periodontal destruction, © Collagenase is also considered as a diagnostic marker of periodontal bone destruction around endosseous dental implants. Levels of collagenase, gelatinase and elastinase around dental implants are similar to natural tooth “© But the diagnostic sensitivity and specificity values for active collagenase asa predictor of attachment loss are still considered low. www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 563 Extracellular Matrix Components: Cer) Is nomcallagencus calcium binding 2rtein associates wit the ECM of rary tss.6, especialy ore ands tho.cit fo elay 2 role remocelg ard real ‘Also know as SPARC (secreted atch acidic ard rich ir cyte} nd beserrent merbrare oct Is single-chain polypepice: ines strongly to hydroxy apatite, js berated fom mary cifferert cell ypes as 2 heat shock ort; stcies show trat heat, @ major Ginical sign ofinfammation, induces their synthe ON i GC, relates to inflammation in general; Fence it May ciscrminate poorly cetveen sircivel inflammation and bone resorpive disease. rere} Nowccllepenase.Ca' sbirdina, highly abnsyleted extzoel crctein produced by ostecblast, ‘osteoclast 211 mac-sphsoes vith increased levels inactive sites of bone vetaboisr. DPN = increases ret ory atthe staoe of mat maturation anc mineralization *ostecélast ier Dutalso at the site of bone resorption. As its produces ey coln ostecblst and cetecclast. i reds ¢ dual function in tot vinerslzaticn ard “Tetsration 3s well s.607e “escmpion. Could ve detected in CCF ard inceeasedl OPN levels cohcided wih ncressec prong deeth measures. ‘Altough atlticnal onastrre scspecive stes are needed. OPN cles ormise ase sossiblebiomerker of pericdontal cisease proavessic, tition Cerny) ‘Another ECM orcten; associated with bone formation. Not detectable in erevicular fluid of gingivitis ls 200 te £09 times higher r sun of untested sericconts ties rer (oon) ‘Suleular ud is ich in metabolctdegradative factors of proteoglycans, Site specificity of various GAG: = Suleular uid-metsoaicicearadatve products of protecalyears, = Ghaival Connesive tissueen in dernstar sulle. = _Avecler bone-in in cronscotn sult, 2 major GAG components-hyalurcnian are chandkoitindesulfate Dot blot assays ard ELISA provice ar accurate assessment of he GAC levels wit the simply of @ ‘chair side” appcation. ADVANCES IN PERIODONTAL DIAGNOSIS Therinusmanuni robes designedincuds Willa l Periodontal probe, Michigan ‘O° probe, Glickmai (COMEDK 2010, 2011, KAR 2011, 2008) Fee en eee crekman Premier ‘O° probe, CPITN probe, Marquis M-1 ‘probe, Naber’s probe, LL 20 probe ete. Pressure sensitive probes (Second generation probes): = Vine valley probe: his is an electronic pressure sensitive probe, which allows control of insertion Clinical Diagnosis © Periodontal PROBES . “The National Institute of Dental Research (NIDR) proposed the following criteria for an ideal periodontal probe: 1. Aprecision of 0.1mm. ‘Arrange of 10mm Constant probing force ‘Non invasive, light weight and comfortable to use [Able to access any location around all teeth ‘A guidance system to ensure probe angulation Complete sterilization of all portions entering the mouth, 8. No bio-hazard from material or electrical shock. 9. Digital output ‘Manual probes (First generation probes) ~ Manual probing is the most commonly used method. pressure and permits use of diferent types of probe tips. It allows usage of pressure force within a range of sensitivity of 5 - 100 gms. = Viva care TPS probe: This isa true pressure sensitive all plastic periodontal probe with disposable probing hhead which aids in detection of CEJ, calculus, irregularities of root form and overhangs, Automated and computerized periodontal probe (Third _generation probes): Recently developed automated probes ‘commonly feature controlled force, direct computer input and reference landmark recognition for relative or clinical attachment levels564 free ebooks ==> www.ebook777.com Review of All Dental Subjects Automated Blovide probe: It consists of a probe hand piece, a digital xead out, a foot switch and a computer interface and computer. It utilizes a reproducible occlusal landmark or customized stent margin asa reference land ark and can detect alos of attachment level ofless than 11mm change with a certainly of 9% = The Foster Miller automated probe: This vtlizes CE] as its attachment level landmark and can determine clinical attachment levels with a repeatability of 0.2mm in a vitro study of odontolype mounted teeth (AIPG 2006)(AIPG 2008) ~The other electronic probes include > The interprobe has an optical transduction clement and is designed to measure probing depth. © Toronto probe works by constant air pressure and uses the occlusal surface as its reference point to measure gingival attachment levels Temperature probe: A heat sensing periodontal probe was recently developed called Periotemp. This ean detect temperature differences of 0.1°C between core body temperature and that of periodontal pocket. Results are shown by one ofthe 3 light emitting diodes. = Green (inactive or low risk sites) ~ Yellow (intermediate) ~ Red (high risk sites) ‘Tooth mobility = This is an important clinical manifestation of an advanced periodontal disease. In practice, the extent ‘of tooth mobility is most often subjectively graded on a scale of 0 - 3. However in researc situations, more objective methods are desirable. Radiographic Diagnosis, Conventional radiographs include = Intra oral periapical radiographs, = Bitewing radiographs, = Panoramic radiographs, = Xeroradiographs ete, Radiographs are not sensitive but may be specific. (COMEDK 2010) Subtraction radiography = In subtraction radiography, a standardized radiographic image is obtained before the appearance ‘of an anatomical change, such as crestal alveolar bone logs and is subtracted from subsequent standardized radiograph, = The structures that have not changed will subtract out and appear as neutral gray, bone loss appearing darker gray and areas of bone gain appearing lighter gray. = Detectability of small osseous lesions compared With the conventional radiographs from which the subtraction images are produced. 5% change in mineral density can be identified. Direct Digital Radiography (Radiovisiography-RVG) = Also called a filmless radiography, radiovisiography uses an intra oral detector similar in concept to a miniature video camera to capture radiographic images of the diagnostic area. It depends on the concept of Charged Couple Device (CCD) consisting of pure selenium chip. = Advantages © Immediate image display. ‘Ihus film processing and indirect digitalizing are eliminated © Contrast and brightness of image can be adjusted after image is exposed so thal artifacts can be avoided © 80-95% reduction in X-ray dose when compared to conventional radiography using D-speed film © Since the image ie digital it may be printed or may be stored in a computer disk 1 absorptiometry = It is a non-radiographic method introduced by Hendrickson which measures the mineral content of alveolar bone with a high degree of accuracy and precision, ~ Iti based on the absorption of a low energy gamma beam, originating from a radioactive source of I by bone. = To improve the study of posterior ateas mainly’ farcations, photodensitometric analysis technique has been developed. Photodensitometric analysis = tis based on the absorption of beam of light by the radiographic film, which also shows the image of an aluminium scale. = also has the ability to transform density reading co millimeter of aluminium equivalent, ‘This is accomplished by a microdensitometer linked to a microcomputer. Computer Assisted Densitometric Image Analysis (capi) = This system appears to offer an objective method for following alveolar bone density changes {quantitatively over time, and when compared with TP absorptiometry and digital subtraction analysis, it has shown a higher sensitivity and a high degree of reproducibility and accuracy Nuclear Medicine Technique (Bone scanning) = Mis one of the most recent advances in the assessment of bone changes in bone metabolism that may precede www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 565 architectural changes. Hence it has the potential to detect the easiest stage of bone los. = Inthis technique, abone seeking radiopharmaceutical diphosphonate compound labeled with Technetium = 99m ( Te) is injected intravenously and following a wailing period, it allows bone uptake and clearance of radio pharmaceutical. The uptake by the bone is measured by means ofa mini probe radiation detector. ined semiconductor Microbial Diagnosis Conventional methods: = Dark ground microscopy = Phase contrast microscopy. (AIPG 2008) (AIPG 2008) = Bacterial cultures-gold standard Immunodiagnostic Methods: = Immunodiagnostic assays utilize antibodies chat recognize specific bacterial antigens to detect target microorganisms. This principle is used in the following diagnostic procedures © Direct immunofluorescent microscopy assays > Indirect immunofluorescent assays > Latex agglutination assay Evalusite; It is a membrane immunoassay, Used to detect Aggregatibacter actinomycet emcomitans, Porphyromonas gingivalis, and Prevotela intermedia. > ELISA Nucleic acid probe assays (COMEDK 2008, KAR 2005, 1996) = DNA probes have been developed to identify nucleotide sequence that is specific for bacteria believed to be of diagnostic significance including suspected periodontal pathogens. = Theyareableto detect the presence ofas few 10 cells in te sample and provide information of the presence of, selected species that is as reliable as culture methods. = Pgingivalis, intermedia, A.actinomycetem comitans, Ecorrodens, Enucleatum, Cxrectus, Bdorsythus and Tdenticola can be detected using radioactively labelled probe. = However DNA probes cannot provide reliable ‘quantitative data and ate limited by the availablity of| probes. Polymerase chain reaction It is a nucleic acid based assay developed by Karl ‘Malls, can detect a single microorganism and has therefore the greatest sensitivity of any microbiological method, = Advantages © Target to specific microorganism © Rapid © Most sensitive assay ~ Disadvantages © Ievequires extensive instrumentation © Reference laboratory testis needed = Restriction Endonuclease Analysis (REA) © REArecognize and cleave double stranded DNA at, specific base pair sequences, The DNA fragments generated are separated by clectrophoresis, tained with ethidium bromide, and visualized swith UV light, © Advantages = REA is a powerful tool for determing the distribution of a specific pathogenic strain wughout a population REA is also used in molecular genetic analy. sis of the oral bacteria like A.a, gingivalis, intermedia, E.corrodens, Enucleatum and Tedenticola - REA helps in studying the transmission pat- terns of putative periodontal pathogens among. family members. Enzyme based Assay: B.A.N.A. (COMEDK 2010, 2011) ~The identification of black pigmented Bacteroides, as it gives a positive trypsin like reaction. B,forsythus, Peingivalis and small spirochetes, Treponema denticola ‘and Capnocytophaga species can be identified with B.ANN.A.as they have in common trypsin like enzyme ~The activity of this enzyme is measured with the hydrolysis of the colorless substrate N Benzoyl D-1 arginine-2-napthylamide (BA.NA.). When hydrolysis takes place, it releases the chromophore Betanapthylamide which turns orange and when a drop of fast garnet is added to the solution. - BAN.A. testis not specific, since it cannot distinguish which of the 3 known BANA species is responsible for the reaction, A commercially available BANA reagent kit is called Perioscan. = Gannot identify Actinomycetemcomitans (KAR 2011) Volatile Sulphur Compounds = Pgingivalis, intermedia, Pmelaninogenica, Bforsythus, Tdenticola and Raucleatum are capable of producing toxic, volatile sulphur compounds such as hydrogen sulphide, methyl mercaptan, dimethyl sulphide and dimethyl disulphide through their metabolic pathways, = Diamond probe/Perio-2000 system is an instrument Which has the features of periodontal probe and can detect volatile sulphur compounds in the periodontal pocket.free ebooks ==> www.ebook777.com 566 Review of All Dental Subjects PROGNOSIS Defined as the prediction of the course, duration, and ‘outcome of a disease and its response to treatment. © Classification: Ey © Novore loss ‘© Excelent ghigial colton + Gocd gatent coocerator + Ne systemioerirormental actors (One or more ofthe following ‘Acea.ete reratring kone supcot ossiilies to certo etiologic factors ard establish 2 rairtanable dentition ‘Aceauete patient cocperation. ro systemic ervrcamerial faces Gre or roe of te folowing Less than acexte rearing toe suport Some tot mebilty Grace I cation ivolonent ‘Reeauele Yarteranoe ocssble _Acoeotable patent coopesin Fresence of rites systemicerermentl faoors (One or rere cf he folowing Medkrate to acvances tone kes Tech mebilty og + Grace 10° fication mvohernrets ‘+ Diffcult to maintain areas or doubtul patient cocperation + Presence of sysleriofewicarertal facts coo © Extactors ielcated + Presence of systevic o” ewirormental factors (Gre or To ef te foowina ‘Acvances cv bss en maintaiacte areas uestion- en . Gre or roe cf te folowing ‘Revarcesi one loss Grace Lor furcation Pwo nents Toot ebity Insocessible eas Fresence of systericenvcrmrertal fats PERIODONTAL TREATMENT ‘Mechanical Plaque Control Father of oral hygiene-Fones (MAHE 2006) ‘Term oral hygiene was coined by Rhein © Mechanical plague contral = Toothbrush Dentifrice = Interdental leaning aids © Dental floss © Toothpick © Interproximal brush = Oralirvigation Toothbrush ADA given specification Length: 1 to 1.25 inches © Width: 5/16 to 3/8 inches © Surface area: 254 to 3.2.em. No. of rows:2 to 4 rows of brushes © No.of tufts: 5 to 12 per row © No. of bristles: 80 to 85 per tut Diameter of bristles range from: (MAHE 2011, AP 2001) © Soft brushes: 0.007 inch o: 0.2mm commonly preferred. (AIPG 2014, AIIMS MAY 2013) Medium brushes: 0.012 inch or 0.3mm © Hard brushes: 0.014 inch or 0.4mm_ © Child brush: 0.1 to 0.15mm © Length of the bristles: 10-11:mm long © Rounded bristle ends cause fewer srateh to gingiva Bass Soft Brush © Straight handle + Nylon bristle + 0.007 inch(0.2:mm) in diameter + 0.406 inch(10.3 mm) in length + Rounded ends © Brows oftuts © Gevenly spaced tufts per row © 80-86 bristles per tuft Powered Toothbrushes © Are not generally superior to manual ones © Powered toothbrushes have been shown to improve oral ‘health = Children and adolescents = Children with physical or mental disabilities = Hospitalized patients ~ Patients with fixed orthodontic appliances www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 567 Ionic Tooth Brush and Its Mechanism of Action © Principle: that every clement in nature has a positive ‘or negative charge. This is called polarity, When the polarities are opposite, the two elements cling together, ‘That's why dust sticks to your coffee table and why plague, which has a positive charge (+), clings stubbornly to your negatively charged (-) teeth. ‘The Ionic Action toothbrush temporarily reverses polarity of the tooth surface from negative (-) to positive (+), drawing plaque towards the negatively charged Ionic ‘Toothbrush head, ‘Tooth Brushing Techniques Horizontal brushing (scrub) Leonard method (vertical) Bass method Modified Bass methods Stillman method (vibratory) Modified Stillman method (roll) Charters method “Methods of cleaning with powered toothbrushes Dentrifice (AIMS 2008, COMEDK 2007, KAR 2006,AP 2002, MAN 1999, 2001) Composition + Abrasives: silicon oxide, aluminium oxide, granular poly vinyl chloride, ca carbonate, ca pyrophosphate, al silicate, diatomacious earth et. Humectant: Glycerine Detergent: Sodium lauryl sulfate Fillers: Na carboxy methyl cellulose (AIPG 2008, 2006) © Antibacterial agents: Ticlosan, Na lauryl sulfate Anti caries agents: Sodium monofluro phosphate Sodium fluorides, stannous flouride Desensitizing agents: Strontium salts, NaF Flavouring agents Colouring agents © Sweeteners: Saccharine © Anti tartar: Pyrophosphate Anticalculus agents: Soluble pyrophosphatase, zinc compounds Embrasure form Cleansing aids TYPE-1 embrasure with tight contact zones and intact papillae Floss ‘TYPE-2 embrasure with concave interproximal surface and Interdental or Proxa ‘Moderate papillary recession brush, ‘TYPE- embrasure with, Unitufted brush complete loss of papillae Interdental Cleansing Agents Pe TDescRITPTION [USES PROCEDURE | SPECIAL INSTRUCTIONS Interdental Brushes Srvlltaperes oyincricalinsh beac teethibitcatons Clean scaces between Noieten rset t ar angle according Cro bance. tosirgial contour Stirulaicn, buccolingusl ctor Apshing chemotherapeutic s9ects End tut Sholeiqous ofsrall Cpenintepodrel teas. Drec interproxial tins Surfaces rent ea, sfairg oben wih terrtiest pressure. Sultler br sting stro Interdental tp Conical, exo Expesec bifurcations. SCxegree argle to Caution against stb cingial use. ‘stimulator usberislestic attached AtSelow gingival marci. lorg aks of tect. SONOT USE or patieris with Keericfrewle! Chen spares. ‘rece shoWval nach. realty tissue. teotbtst Stimulation. Re adeirst teeth as it moves Fst of open spacesfree ebooks ==> www.ebook777.com 568 Review of All Dental Subjects a Wedge cleaner? Matle of woos (cals ‘stimulator “Stine. cer) or plastic Cont” ‘Knitting yar 5 Gauze Swip . Fipe Cleaner : Toothpick in holder = Dental floss holder Noccle lke cevioe with oeering or one end through whieh floss is ‘reales Tongue cleaner = Dental Floss © Multiflament vs, monofilament © Twisted vs. untwisted © Bonded vs. unbonded © Waxed vs, unwaxed © 12.18 inches for use © Suetch: thumb and forefinger © Up-and-down stroke Gingival Massage © Epithelial thickening, increased keratinization, Noicten with saliva Using the flat part ofthe tisrale, te places tonars the Tiseue and inserted with Euccolngtal ‘atin, Chenze if weed becomes spect this could ferce soins into te ours, Intercroximal areas. Massace. For wise scaces where Fole double, roisten. = fos is ool narrow to clean Use same tecnicue 3s effectively flossing Proximal seas rent to ecentulo.s seas owisely 210 68 irc sescedteeth lerat.Yirao ato.ne Usira s shoes sto. Furcations. Checkwireerdic = Expcsec proxtral revert damaze to sutfeces. sirave or scratching of conertal surfaces, buccolingul mctor. Interdertal deersing Whiten vith salva Funcations trace siraival "ash (Oren pationt with art e73, Flacue removed at or just Under gingival margin Grn aoplisroes : Under Pontes Aes that are too tight for ‘oss insertion ssmeke's Lsein postetorto = Coates torques! deeply enteior director fissured Elorgates oacile (nay orate} Increased mitotic activity in epithelium and connective tissue © Emphasizing the importance of altering or removing plaque rather than stimulating or thickening the kkeratinized surface in the plaque control program Chemical Plaque Control Classification Chemical Plaque Control! Agents © FIRST GENERATION Eg: Antibiotics, phenol, quarternary ammonium compounds and sanguinarine » SECOND GENERATION Eg: and" Bsbiguanides(chlotheridine) www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 569 © THIRD GENERATION Eg: Delmopinol SC ToRer Ty Phencl derivative Is synthetic ard ionic Used' a 3 tocical atirie-tial agent Broad scectur of action inducing toh cram postive 21d aram negative oacterias Italscincides myochacterir spores anc Cardia species ‘Mechanism Of Action = Tidkossn fet On Oyeplasric Mevbare ~ nse estege Of Ctl Constiterts = Bacteroiysis “riclosan is inclices in toot paste to reduce olen. foration Used’ slora with Zinc cirate 0” co-solyrer Gante2 b erence its retention with the oral caity “Trclosan delay plaque formation Ieinhts formation of prostaglandins and leukorianes thereby reduces the chance of inammation DSLR AIEULIS |trecuces the alcottc activity ir bacteria ar delays oacteralarovt ors PUN CCatioric arsseptics ara s.rface acthe scents Rta} Elective aoainstorar costve crgsnisms Fostvely charged molecule reacts with regatively charced cell membrane shosptates anc trereoy clsrats the bacterial cell wall sucture Ea: Berzertnoniur chorce ane catyoyrediriam Seno rT) Varcenyein,erytorycin. Ndamycin and Kanamycir Lue to actenal resistance preblems the use of anubnctcs hs beer rece Itis = benzophenanthredine akaloid Poa Inviits olzgve arceth and recuices aingivits ‘Mechanism of action = _lnterTere with plecue mati formation anc aso res.uoes oacterial acnerence = Ihcauses weak onding of clza.e t tooth, ts sing easy "eral ofslza.e by mechanical prooscures = Tis therefore incicated 2s a re crushiry routh rinse + Adverse effect of delmopinal = Staining of toot ans torte = Taste distances = Mucosal soreness ar eresion itis ost effective ageirst ran ve crass Used in meus nse Chlorhexidine (PGI 2009, 2001, AIIMS 2009,1991, AIPG 2004,1997, AP 2001, KAR 1996) © Mechanism of Action = Chlorhexidine isa potent antibacterial substance. The antiseptic binds strongly to bacterial cell membranes. = Ithas a broad antimicrobial activity: Gram ve and gram ~ve bacteria, yeasts and some lipophilli viruses (AIIMS MAY 2009) = Gram +ve bacteria are more susceptible. It is also a potent antifungal(Budlz - Jorgensen). At low concentration results in increased permeability with leakage of intracellular conponents including potassium, hence bacteriostatic. thigh concentration chloshexidine causes precipitation of bacterial cytoplasm and cell death, hence bactericidal * Commonly used concentration is 0.2% viv (AIrG 2001)570 free ebooks ==> www.ebook777.com Review of All Dental Subjects Side effects ~ Reversible brown staining of teeth, tongue, restorations = Transient impairment of taste Ithas low systemic toxicity and no teratogenicity No appreciable resistance develops in microbes Disclosing Agents (MAHE 2011, KAR 2001,MAN 1997) Disclosing agents: Disclosing solution contains a dye or other coloring substance, which imparts its color to calculus, plague and films on the surface of teeth, tongue and gingiva. It isa excellent oral hygiene aids because they can provide the patient with additional motivational tool to improve the elliciency of plaque control procedures. It also conserve operating time by making inconspicuous deposits more evident Factors to be considered in the selection of a disclosing solution are: = Intensity of color = Non-irritating to mucous membrane = Diffusibilty - neither too thin nor too thick = Astringent and antiseptic The various disclosing agents are = Todine, Iodine disclosing solution, Diluted Tincture of Iodine, Berwick’s solution, Buckley's solution, Talbot Iodoglycerol, Metaphen, Basic fuchsin, Bismarck Brown, Easick’s solution, Bender’ solution, Mercurochrome solution, Erythrosin (RDC Red No, 3), DC yellow no. 8 fluorescein, Two tone dye (FDC. red no. 3 and FDC green no.3), Two - tone dye test uses FDC red no, 3 and FDC green ao, 3 solution ‘which stains thick accumulation of plaque as blue and thin deposits are stained red/pink, = Taste Instrumentation © Sickles with straight shanks are used for anterior teeth whereas sickle scalers with contra angled shanks adapt (0) posterior teeth © Tip action of magnetostrictive ultrasonic unit is elliptica/orbital (4 active working susfaces). Piezoelectric is linear (2 active working surfaces) * Scaling motion should initiate in the forearm and transmits from wrist to the hand with slight flexing of fingers Comparison of area-specific(gracey) and universal curettes a Area of use tes designed for specie areas and Ore cuete clesizned for ell areas and Surtees, Cutting Eege Use (One cuttrg eage usec work wih cuter ede ony Bot outing edges used: wore with efter outer or inn ec Curvature Curved in to plares clade cues us ard the ste Cured in ore clare: blade curves Uo, rot to the sie, Blace angle (Offset blade: face of blade beveled ot 60 cearees to lace ret cffset of beveled at 0 dearees to stark, sak, © Gracey curette series Gracey curette number Specific area of use we Artericr teeth 3a Anterior eth www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 571 Aerio teeth ard oremolar 78 Posterior teeth, Facial ar lingual surfaces 110 Posterior teeth, facial af oval srfaces 2 Posterior teeth, mesial surfaces (als 2065) 13/74 Posterior teeth, sista surfaces Number 15-16 is the modification of the standard 11-12 and is designed for mesial surfaces of posterior teeth, It consists of Gracey 11-12 with acutely angled Gracey 13-14 shank ‘Number 17-18 is a modification of 13-14, It has a terminal shank elongated by 3mm and a more accentuated angulation of the shank to provide complete occlusal clearance and better access to all posterior distal surfaces. Extended shank curettes (After five series): The terminal shank is 3 mm longer, allowing extension into deeper periodontal pockets of 5 mm or more, All standard Gracey numbers except forthe no 9-10 are available in After five Mini bladed curettes (Mini five series): Blade are half the length of standard Gracey. All except 9-10 are available inthis design Gracey curvettes: Blade length is 50% shorter than standard Gracey © Sub 0 and no. 1-2: are used for anteriors and premolars © The no:11-12 is used for posterior mesial surfaces (© The no: 13-14 is used for posterior distal surfaces Langer and mini langer curettes: Set of three curettes that combines the shank design of the standard Gracey 5-6, 11-12 and 13-14 curettes witha universal blade angled at 90" Antimicrobial Therapy and only small portion of the total dose actually reaches Systemic Antimicrobial Therapy: limitations © Systemic delivery provides a ready exposure of all periodontal sites to the antimicrobial agent, but it also possesses a risk of adverse reactions to non-oral body sites ©The drug is dissolved by dispersal over the whole body, the subgingival microflora in the periodontal pocket. “Adverse drug reactions area greater concern and are more likely to happen if drugs axe distributed via the systemic Emergence of drug resistant strains also pose a problem, Local drug delivery overcomes many of the above limitations of systemic antimicrobial therapy, Classification of Local Antimicrobial Agent Therapy in Periodontics Personally applied (In patient , home selfcare) Non-sustained subgingival drug delivery (Home oral irrigation) Sustained subgingival drug delivery (Not developed to date) Professionally applied (In dental office) ‘Non -sustained subgingival drug delivery. (Professional pocket irrigation) x Sustained drug delivery system with first order kinetics and “0” order kineticsfree ebooks ==> www.ebook777.com 572 Review of All Dental Subjects © Controlled release local delivery systems can be classified as: = Reserviors without rate controlling system. eg hollow fibers, gels, dialysis tubing = Reservoir with rate contol system. eg. monolithic matrices, acrylic strips, ethylcellulose strips. Local Drug Delivery an =I LE aT or ra Voaseee aaa Es eS Sao SE TA Dentamycin/peric Mincoydlire Biocegradable ‘rixtu’e in syringe = (minceycline microspreres) ST Ee eae SS ee arr (AIPG 2008) =EE CERES era Pharmacological Strategies For Treating Periodontal Bone Loss. © Generally target-bacteria in the lesion or the host response to the bacteria Pevegannenie ame sans Aeon sori pes oe soonaot ie Tae aatonacl LO iL8 OPS Decoy Aatve osteocast Tank, Dillerentason 4 ‘elvan Nonoote J | Precitoret ner Bisphosphonates penne et NEB sphonaos we Resorption TRAP — Inhibitors a Figs49: Renkeanbong axis Potential therapeutic strategies to treat bone resorption: that blocks receptor activator of nuclear factor-kappa + Agents that block the diferentistion or activity of B (NF-KB) ligend (RANKL) and RANK juxtacrine osteoclasts are potential therapeutic agents, interaction. = Osteoprotegerin (OPG) inhibits the differentiation __~_ Nonsteroidal ant-niammatony drugs (NSAIDs) and of osteoclasts through its action as a decoy receptor ther anti-nflaramatory molecules (including pit www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 573 Anti mitogen-activated protein kinase inhibitors, c-jun [N-terminal kinase inhibitors, NF-KB inhibitors, and the specific, high-affinity IL-1 inhibitor IL-1 (TRAP]) can inhibit the formation of hematoprogenitor cells to preosteoclasts. Antibodies (o RANKL can also block this interaction, MMP inhibitors reduce the protease degradation of the organic matrix, and anti-integrins block the initial ‘osteoclast adhesion to the matrix. Bisphosphonates and MMP inhibitors work at the site ofthe osteoclast adhesion zone to the mineralized, ‘matrix in blocking bone resorption (Inflammatory Agents Agents that block cytokine production or activity are the earliest strategies to inhibit bone resorption, NSAIDs have shown promising results in slowing periodontal destruction, But their widespread use has been limited to their adverse reactions, Localized application ~ cut down adverse effects. Inhibition of cycloxygenase 2(COX.2), a mediator of pro-inflammatory prostaglandin activity, prevents alveolar bone loss in experimental animal study. Specifically blocking IL-1 and TNE, dramatically reduces the loss of alveolar bone, Blocking agents were administered by intrapapillary injection 3 times/week over a 6-week period with, significant reductions in radiographic alveolar bone loss. ‘These types of strategies may provide future therapeutic modalities to treat periodontal bone resorption, Bisphosphonates Inhibit osteoclast formation and function. In high concentration its preferentially taken up by bone tissue. Bind/adhere to bone surface. Inhibit resorptive activity by directly acting on osteoclast; promote apoptosis of osteoclast Also affect protein production of osteoclast Low-dose tetracycline = Tetracyelines ~ broadspectrum antibiotics ~ Extensively used in management of periodontal disease © Inibits bacterial protein synthesis. © Blocks tissue destruction enzymes, such as MMPs © Chelate the cations of metalloproteinases that are requited for action. = Other non-microbial mechanisms attributed to tetracyclines include = Inactivation of enzymes that activate etalloproteinases = Scavenging reactive oxygen species. = Blockade of secretion of lysosomal proteinases = Modulation of osteoclast functions and osteoblast apoptosis. (MAHE 2008) ~ Low-dose tetracyclines have been shown to reduce collagenase activity in gingival tissue extracts and ce ~ Long-term tetracycline therapy resulted in undesirable effects; hence CHEMICALLY MODIFIED TETRACYCLINES were developed which ~ eliminate the antimicrobial properties BUT maintains its activities on MMPs = This modification produces a molecule that has no antimicrobial activity but inhibits collagenase activity and reduces tissue breakdown. = Currently CMT appear to have promising therapeutic potential in the treatment of periodontitis, Estrogen And Selective Estrogen Receptor Modulators (SERMS): = Estrogen deficiency > accelerated bone resorption, characteristic of postmenopausal osteoporosis = Estrogen withdrawal > Increase in bone resorption; Enhanced osteoclast formation and reduced osteoclast apoptosis, Has inhibitory effect on both MMP-1 and MMP-3; this blocks the initiating step in the bone resorptive process, Bisphosphonate-complexed implants results in better osteoconduction and repair in animal models, suggesting that inhibition of bone resorption facilitates bone healing. In naturally occurring periodontitis-no effect. In ligature-induced periodontitisit reduced the amount of attachment loss and prevented loss of bone density = Treatment with estrogen > Tahibits bone loss and bone turnover; increases bone mineral density ~ Anew class of drug ie, SERMs: That exert estrogen fleets on various tissues has been MOA of SERMs is same as that of estrogen — blocking production of cytokines that promote osteoclast differentiation and by promoting osteoclast apoptosis. ~ Estrogen deficiency. and osteoporosis: Increased ‘oral bone resorption , attachment loss and bone Ios.free ebooks ==> www.ebook777.com Review of All Dental Subjects Increased loss of interproximal alveolar bone height: In deficiency. IL-B level in GCF is low in estrogen sufficient patients Estrogen supplementation > decreased gingival inflammation and decreased frequency of CAI. © Osteoprotegrin (OPG): Microbial. stimulation by Aa induced RANKL expression on the surface of CD4* cells and in vivo inhibition of RANKL function with the decoy receptor OPG diminished alveolar bone destruction and decreased the number of osteoclasts after ‘microbial challenge, Peptides that specifically inhibit MMPs reduce MMP activity and bone loss and may have therapeutic benefit with future study Gingivoplasty and Gingivectomy Reshaping of the gingiva to create physiologic gingival contours in the absence of pockets (AP 2003) Gingival clefts, raters and the shelflike interdental papilla caused by ANUG ate indications of gingivoplasty (AIMS Nov 2010, MP 2008, AIPG 2002, 2001, 1992, 1991, AP 1990) In gingivectomsy, Kirkland knife isthe first to be used for incisions on facial and lingual surface. (PGI 1999) Orban knife is for supplemental interdental incision Merrifield knife is representative of knives commonly used in interdental areas. Rationale © Pocket elimination for root accessibility Establish physiologic gingival contours Sverabony pockets ‘Ar aoemiate zone of keratrize tissue Fookets greater than 3 74 \Wer bone les is Forizortal anc no neec exists cf osseous surgery Gingival evlargements ‘Ateas of inited scness Unestnetic or ssyrrrstic chal to0e-schy For excos.ce of sft tissue impaction to ernaroe eruption To eats restorative dentistry To estabisr ysologic and ghighal centou's ost acute ‘necrlizing ulcerative gingivils and fap procedures Periodontal Flaps © Objectives of Periodontal Surgery: Access o roots and alveolar bone © Enhance visibility © Increase the effectiveness of scaling and root planning © Lessen tissue trauma Modification of osseous defects (Classification of Flaps: Peso Cory Based On Flap Placement After NorsDispaces Flaps Disclaced Flaos ‘Av inadequate zore of kertrized tissue Pockets thal exterd 2eyond the mucoainighal ire ‘The ree for osseous resection oirdcve techniques: Highly inflamed or edematous issue ‘Areas of estetic compromise ‘Shallow saletal vauit 215 cremnentexterral colo rzes “Treatment ofietrecary pockets Patierts wih coor cral hypiore © Establish physiologic architecture of hard tissues by regeneration oF resection © Augment alveolar ridge defects Repair or regeneration ofthe periodontium Pocket reduction © Enhance maintenance by patient and dentist © Improve long term stability Provide acceptable soft tissue contours © Enbance plaque control and maintenance © Improve esthetics Full THckness (ucoperiostea Flaos PPantal Thioaress (Moose) 6p www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 575 PSone) co + Corventcnal Flops: = Modified widman fap = Unalsplaced fap = Aially displaced flop = _ Flees forrevorstuctive procedures + Foils Preservation Fao = Used for regenerative surgeries = Prefers areas win aesthetic concen (HP 2010, AIIMS 2007, KAR 2008, AIPG 2006, 2004) Modified jidman Flap (AIPG 2010) © Described by Ramfjord and Nissle- 1974 © his difference between modified widman and original widman is that the original widman technique included: = Apical displacement of flaps = Osseous recontouring © Three incisions are used in this technique: = Internal Bevel Incision (o the alveolar crest starting 0.5-Lmm away from the gingival margin parallel to long axis of teeth = Crevicular incision is made from the bottom of the pocket to the bone, to facilitate gentle separation of the collar of pocket epithelium and granulation tissue from the root surfaces = Interdental or thied incision is made after flap is relected in a horizontal direction, close to surface of bone crest separates soft tissue collar of root surfaces from bone. Apically Displaced Flap = Can be used for pocket elimination or widening the zone of attached gingiva (KAR 2011, AIMS 2007, AIPG 1991, 2002) = Has the advantage of preserving outer portion wall and transforming into attached gingiva > Hnceases the length of clinical crown an isnot indicated for palatal pockets, Resective Osseous Surgery CT + vertical Srecving B Radiol blerding s Caer (sero) Flatening interproximal bone + Grasualising marginal bone Furcation ‘Measured by Naber’ probe (AIPG 2004)(AIPG 2008) Classification Reshaning of bore without emcving toch supcotig bere (COMEDK 2006) For comectio’ of shallow craters, bone lecges ard excstoses Done with olay instruments Removal ct tcot suppertng bone For comection of regative architecture cre wall oseeus defects Flaten interoroxial bone ie used ir the teatrent cf herisepta CCetectory provedtites are done with rend istrumerts TE an ENT nes 2 Scar srry = Cereal 1 Recs y xy 1 Gronecemy reece pst P1208, 7150) eee foefree ebooks ==> www.ebook777.com 576 Review of All Dental Subjects Grace! cure sac Noverate cases: Fatal ceretation of prose = Scalia, root slanting aor x = GIRwithcore cians Nayimay aotbe cetectec by Xray ee Advanced casos: = _ Reotresectcn cr hemisedtion Grace m Inter racioutar tone Kees ‘Sealing ard rec sianing Through and through passage of proce + Tunneling (resection aocessibilty) Furcation is coveres by gingiva Roct esedtio ans hemisection Grace iv Grade i furcation with orifice» \ioteveto cases uncovered by gingiva ‘Save as crac Ilwitr oocl.saladustrent + Aevanced cases- extraction tion! Am- Removal cf roctvthcut removal any c-oNn pertor Maxilzy 1st-rolr fs most favorace for root section Resection of distobuccal roct s tre cwoce of tereoy iffurcatcn Inolvementis in between vocal cts. ‘Surgical removal of o7e rcotend the correscordine overtira c-owa. The tact i separated succolinguly ‘ouch te bifucatcn, end te affected cr ciseased prt ofthe toot is rervoved.(MP 2017, AIPG 2002) eer IMolaris simely cutwitoat removal efny pan of crown or rot fllovéd by festorstion 2s te se2erste sits Hemisectior andbsicuspication ae eutable for mandibular mors LUstelly erdorlontic treatment shoule te dore before periocental therapy stch as voct resoratin or emisection, © The term introduced by Friedman © The 1996 World Workshop in Clinical Periodontics renamed Mucogingival surgery as Periodontal Plastic surgery-a term, proposed by Miller in 1993 + Periodontal plastic surgery is defined as “Surgical procedures performed to correct or eliminate anatomic, developmental or traumatic deformities of the gingiva or alveolar mucosa’ Crown Lengthening (MP 2010) Methods of alincal crown lengthening Extension Apealy atecony| —Aptaty Seoeaeny| positioned flap Extension Coronal Extnsion| Post and) Mata With osseous resection) Without osseous] ‘The procedure depends mainly on © Band of attached gingiva © Thickness of marginal alveolar bone (Sato 1989) www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 877 Wit of ataches gingiva Sutiint Ineuficers| Lack of tached grava ae Gosgecony) . ee een THckrargial toe] Tick ono] Tin) APE] APF partial thiekness el Ful thickness) Concept of Biologic Width and Its Significance Biologic width is defined as the physiologic dimension of the junctional epithelium and connective tistue attachment. The average width is 2.04mm; the average epithelial attachment is 0.71- 1.35 mm and the average connective tissue is 1.06-1.08mmn. ‘Biologic width is measured from the bottom of the gingival sulcus to the alveolar crest and is maintained by homeostasis. Impingement on the biologic width may result in “© Gingival inflammation © Pocket formation © Attachment loss ‘ype of Surgical Procedure Distance between the bone and gingival margin >3nm www.ebook777.com 578 Review of All Dental Subjects + Tecnioues fo coverage cf ceruses roots + Technicues to deepen te ve . wes + Techrioues forthe vestibule cf frenum + Frerecary (KAR 2066) “Tamow technique + Semilunarcoronally displaced fop (KAR 2004, AP 2000) Villers technique + Free scft tissue astonrat Langor's technique + Stbsrthetialcornectve tse ort (KAR 2006) Pouch and tunnel technique + VetetofLarge’s teomnioue Regenerative Therapy “© Guided tissue regeneration = Principle: only the periodontal ligament cells have the potential for regeneration of the attachment apparatus of the tooth, Presence of any other cells retards this process (AIPG 2008) = Consists of placing barriers to cover bone and PDL and preventing epithelial migration along the root surface allowing PDL cells to directly bond to the tooth surface = Membranes used are: © Non resorbuble + PTFE (Gorctex membrane) removed 2-6 weeks later © Absorbable membranes: = ascoondstage surzery is not necessary because it does not requite removal, = Fewer ineision line openi of bone regenerated is erea + Collagen membrane. = Polylactic’ polyelycolic acid membrane. ‘omplications if they do cccur, management is more Predictable and the amount alcr than similar complications w ith non-reserbable materials 2 Acco dtl mais = Guided Bone Regeneretion: (COMEDK2007) ~The buries membrane should be placed over « 1 GBR provides mony athe primary key for bone partial gal rather tan an cmpy or lod elt frfingsuch ae (IPG 2006, ANS 2007 fled space A Blood lo, in and of el, doesnot _ . KAR 1995) pattem bone formation under the BM Because 2 Spacemmaimenares flood ots 95% stagnant red blood cells and 5% 2 ieee flood ws Plats the eovrnient to grow boas ied at 8 Gra wabuiation, fed blood cle and rece the pi i the region 9. Belson of brous Ustue nthe galt (KAR 1999) Bone Grafts © Types bone graf(AIPG 1988, 1991, AP 1995, PGT 1996) Asta Ais ore tarsorestomene nso aren postin theory oe care ase ‘Allograft Atissve (bcre) oat trarsferres between individuals of seme soeces, bt ofrcn inertial genetic elspesitic, Alloplast Asyretic hone orfing materel—bone oft scbstitte carat “renters ofiferert species Xenogralt /tissve (bc www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 579 Classification TTT re rrr Cry (AIPG 2006, PGI 1864) Rack) Comte ore cries + Freshfezeatere + ‘Bee ceived + Pebiets + Osseous cnagulum + Mineralised Fydroxyapatite | © Bioceravics S Boreble (APG 2010, 2011, Reezedriedbore —» Oscuum + Ticaldur Phoschate tmaei2005) Magra (FORAY: + clk ee eerie + Bone swacina + como + Avorgericcore + Dense) Non porcus’ Non + Intraoral canoelicus cone and marrow freeze dried hone eo eos + Extaualcaaetoussore ancmarw alegre OFDEA: + Ciranalotm + Porcus! Non resorbble + Have the highest ostecgenic potential Osteoinductive Seon + Resorbable (KAR 2005, MP 2010) + Ostesoonouctne carve asses (M2008, AP 2602) Ossenccrducive (IGNOU 2010, KAR 2003) Mechanism of Action ‘Tre places oral oy the ectcn of factors ooataires in itself Such 8S croteins és crown Factors, induces foxration of “Tre alaced craft acts asa trels ora scaffeld ower which new bore decosts can occur Cotteal ens bscause oftheir relate large Size 1,559 x 1. re viable cels present in places ort material actively forms bone in the ecient sits mon: urseraent sequestration Sources Cssecus coagulum + Exostesis + Lineval noges of mance + Palatal excrecerses + Qsceous tissues cbtzined from cstecplastc proecties, Intra oral cancellous bone andmrarrow + ~esling bony wounds ‘+ Healing extraction sackets (6-12 weeks «Most productive) ‘= Edentulous rcges ‘+ Nencicula retremclar eas + Maxie tiberesty Extraoral cancellous hore anc marrow + Arterior/ Pstero: ac crest (AP 1987) ‘+ Greatest cstecoenic cotetial + Risk of disease transfer in allogenic grafts = Fresh frozen bone allografts one in 2 million = Freeze dried bone one in 28 billion = _Creutzfelét-Jakob disease-Risk is remote if proper exclusionary techniques are followed. © Radiation sterilization must not be used to sterilize DFDBA as it was found to reduce it inductive capacity by 40% © DFDBA isan osteoconductive material while demineralising FDBA exposes BMP-Osteoinductive material © Biocoral calcium carbonate obtained from natural coral genus porites. Pore size 100-200 microns. Bicoral has high osteoconductive potential because no fibrous encapsulation has been reported.free ebooks ==> www.ebook777.com 580 Review of All Dental Subjects Bioactive glasses: = Mode of action a0, Na,O, S102, 2,0, Exposed to sue fluids Covered by double layer 4 Promotes absorption and concentration of proteins + ‘Guides and promotes osteogenesis ‘Currently two forms are available = Perioglas: Particle size 90-710 microns = Biogran: Particle size 300-355 microns advantageous for guiding osteogenesis. Xenogenic bone grafts ~ = Consist of deproteinized cancellous skeletal bone tissue that is harvested from one species and transferred to the recipient site of another species. ~ Unlimited supply of available material = Has the same inherent problems as allografts, and being from different species, it may cause even more pronounced immunological problems. = Disadvantage-only osteoconductive property. Coral-derived granules ~ Natural coral exoskeleton derived from marine reefs (madreporic corals) = Is composed of calcium carbonate. = Has excellent mechanical properties = The calcium carbonate of natural coral can be converted to HA through an hydrothermal exchange process (replamine form) = The volume of porosity affects the rates of biomaterial resorption and bone formation, Another material Phycogene HA is derived from calcified marine algae. Calcium phosphates Similarity in composition to the bone mineral, bioactivity, osteoconductivity and ability to form an unique strong interface with bone The major advantage of being able to readily adapt to the shape of the bone defect. Rapidly integrate into the bone structure and are transformed into new bone by the action of bone cells. (osteoclasts and osteoblasts) responsible for the local bone remodeling, Limitations-mechanical biodegradation in vivo Properties and slow Alloplastic bone grafts or synthetic bone substitutes. ~ Synthetic materials = Developed to replace human bone, = They ate biocompatible and are the most common type of graft materials utilized = Osteoconductive materials. = There are three types of alloplastic substances in clinical use nowadays: CaPs; other ceramics (eg. Hydroxyapatite-HA), Biphasic Calcium Phosphate (BCP), Tricalcium Phosphate (TCP), Calcium Sulfate and Biocompatible Composite Polymers ‘Tricalcium Phosphate = Similar to synthetic hydroxyl apatite ( SHIA ) ~ Formulated into pastes, particles or blocks, ~ Biocompatible and biodegradable — Disadvantage © Unpredictable rate of bioresorption, = Recent formulation: §-TCP (Vitoss, Orthovita, Malvern, Pa) is 3-dimensionally macroporous, containing spaces into which bone ingrowth can ‘occur Italso has a microporosity thats thought to promote diffusion of nutrients and transmission of fluid pressures www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 581 = Used as an ) © Osteoconductive filler © Bone graft extender and © Acarvier of aspirated bone marrow cells. L ph © Biphasic Calcium Phosphate = sila andp-TcP = Recent development of BCP ceramics (HA/B- TCP), has provided materials in which bioactivity is controlled by an association of Hydroxyapatite (Hap: CA10 (PO4)6(OF1)2) and Bericalcium. phosphate {G-TCP: Ca3(PO4)2) in adequate rations. = Bioactive glasses azesilico-phosphate chains = chemically bonds with bone and are supposed to function as small bone regenerative chambers = Bioactive glasses may osteoconductive properties. have © Calcium Sulfate = One ofthe first materials investigated as a substitute forbone graftwasPlasterofParis,the(-hemihydrate form of calcium sulfate (CaSO4-1/2H20, POP), = Itis a biological inert, osteoconductive, resorbable and high biocompatible material = Advantage © Fase of handling, ©. Resorption by osteoclasts and attachment and deposition of osteoid by osteoblasts = Drawbacks © Reduced mechanical support © poor bioactivity. © faster resorption rate of the POP cement is too fast, which may negatively affect bone regeneration, © poor mechanical macroporosity (Osteoactive agents " = An osteoactive agent is a material which has the ability to stimulate the deposition of bone. = ‘These may be classified in three categories: osteoinducers, osteopromoters and _ bioactive peptides. ~ _Urist (1965) in a classical study described ectopic bone induction in intramuscular implantation of (C_Hemineralized bone matrix (DBM) strength and low Bone Morphogenetic Protein = Osteoinductive = BMPs belong to a group of proteins called TGF-B superfamily that regulate many different biological processes including cell growth, differentiation and embryonic pattern formation ~ BMPs2. 4, 6, and 7 (also known as osteogenic protein 1 [OP-1}) are thought to be the most important BMPs for bone formation, Bone Morphogenetic Protein acts as an extracellular molecule that can be classified asa morphogen as its action = Recapitulates embryonic bone formation = One of the challenges in the use of BMP is in its delivery to a site of action. = While recombinant BMP molecules are extremely’ potent, they are difficult to use clinically in powder fr solution, Their handling properties and biologic activity are enhanced when BMPs are delivered with carrier materials, but the best carriers for vatious surgical applications have not yet been determined = More recently biodegradable gels, collagen sponges impregnated with BMP and silica glass have been used as carriers, ‘Transforming Growth Factor 6 Enhance bone healing. TGF-6 has been shown to participate in all phases of bone healing Daring the initial inflammatory phase, TGF-} is released from platelets andstimulates mesenchymal cell proliferation. Its chemotactic for bone forming cells, Stimulates angiogenesis and Limits osteoclastic activity a the revascularization phase ‘Once bone healing enters osteogenesis, © TGF-B increases osteoblast mitoses, regulates osteoblast function and increasing bone matrix synthesis inhibits type II collagen but promoting type I collagen ‘Combinations of BMP and'TGF-B, may enhance the osteoinductivity of an implant, while at the same time, make it osteopromotive. Platelet-Derived Growth Factor = Platelets are known to contain a number of different growth factors which are released into the tissue Aker injury. These include TGE-§, PDGE, IGF and FGE which act as differential factors on regenerating periodontal tissues = The PDGF is angiogenic and is known to stimulate the repr cells and matrix deposition, = Platelet Rich Plasma (PRP) is one potential source of concentrated platelets that could be used in bone regeneration duction and chemotaxis of connective tissuefree ebooks ==> www.ebook777.com 582 Review of All Dental Subjects © Bioactive Polypeptides = Thelast category of bioactive molecules is the polypeptide group, = May act as osteoinducers or osteoenhancers = Two short amino acids chain peptides that have demonstrated a bone activity are known as P-15 and OSA-117MV. P-15 is reported to attract and bind osteoblasts with the bone-grafing matrix. Stem Cell = Human mesenchymal stem cells (MSCs), obtained from the adult bone marrow, are multipotent cells capable of differentiating into various mesenchymal tissues. — From a small volume of bone marrow, MSCs can be isolated and culture expanded into a large number due to their proliferative capacity maintaining their functionality alter cryopreservation. Thus, MSCs aze thought to be a readily available and abundant source of cells for tissue engineering applications — MSCs can be combined with porous, biphasic calcium phosphate ceramics (hydroxyapatite/ f-tricalcium phosphate ~ HA/TCP) ‘Stem cell Stages inthe cilferentation of a ster cell. Erionjcric stem cells are nearly tctinctert. whereas a stem cell + 2 eoultissue ay oe clurcotert (lor exairele, heratorcietic stem cel) cr uriootert(enitelisl cell, for : ‘examole). An adult tissue may cortin the stom cel sor ces separated fom ful clifferetistion ‘oy one or several stevs. The periodontal inerrent nas been shown to certain erecursor cells cr progeriters ‘ 10 cementcblasts. Tae diflerertiated cell may also oorsist of subooculaticns cf the sare cell type. Precursor cell ¥ Differentiated cell Materials For Long-Term Ridge Pres Materials For Transitional Ridge De Ss Ean ieee ct “+ Synthetic nycroxyapatte + Ar organic sovine bore mat. ‘+ Demineralized freeze dried bere allograft + Particulate derse HA. + Rescroable calcium phosphate (CFOBA) + Potots covalline KA. ceramics. ‘+ Autogencus bone wit lovedensity HATO? = Bicectve ass. + Macropcrots bioactive glass. ‘oF ABI product in 2 50:50 o° 75:25 atic. 1+ 0f0Ls polymethyl methacrylate XR Sutures. GMT * Ske where acproxination cf irterdental pails is rot cossiole (AP 2008) COE * "dicated wre multpleintercertal areas are involve suture + This s.tte is often use forte interercximal eas of caster cr for wise inlerdental scaces to procery adeat he iterpximalczcila acaist the ocr. + Two sutures are often necessary + The henzcntal matress suture can oe irocrporsted wih contiiscus. rdepensent sig Stes, (KAR 2008) Corns suture TRCCCICUICAN * Used when the faps are not in close apposiion because of apical Nap postion or non scalloped incisons GET EISLIe | * Another technique to close a fap located in an edentulous area mesial or distal o tooth + Consists of yng a cect suture that closes the proximal lap, carying one ofthe threads around the tooth tBanchor the tissue ageirstthe toot, ard ther tyin the wo treo: TEIN * _nccated where he approximation ofboth labial and lingual Naps are tied independently www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 583 I PERIODONTAL DRESSINGS Function (MAHE 1998) + To obtain and maintain a close adaptation of the mucosal flaps to the underlying bone especially when flap has been repositioned apically to prevent coronal displacement. + To protect the wound post surgically form irritation caused by food, at, tongue or cheek movements ‘To provide additional support to stabilise fee gingival graft ‘Template for healing by preventing excessive formation of granulation tissue by filling interdental space. © Facilitates healing - no curative properties, ‘= Minimises likelihood of postoperative infections and haemmorhage. = Maintenance of debris free area, + Protects the suture. © Splinting of mobile teth, © For the comfort of the patient ‘+ Deseasitize the root surface; protect the exposed root surface from temperature changes. Classification Of Pe \dontal Dressings During the course of time, vatious periodontal dressings have been evolved. Periodontal dressing can be mainly classified into: © BUGENOL based periodontal dressing + NON-EUGENOL based periodontal dressing (Glickman) Se ee en oes era ee eee) ‘© Wards wonder pack © Coenak + Cieais2eck = Patio Care + Golemar's cack PeriPak + Kirklano's pac = Yeo Pak ‘+ Modited Kirkland pack Pete Paty ‘+ Baricad visible isnt curing periocortaloressing + Collagen cessing + Metnacylic cel aressing ‘+ Cyanoacrylote cessing + Powder: + TUBE*I = Rosin=C.52 ome, Zinc oxideaatepetic,astingent = Zire cxise = C4 ams INaD-heles in eettrg ction = Becitracin = 3000 Units \ecetable cetzsticty + Licuies: SSy-thetic rosiraconesiveness = Zrcoxide= 5% Lerthidebfunaicid= = Hycogenate ft o5% + TUBE-I Lid coor ety cic thickened with onlochony CChlorothymol: Bacteriostatic nent Modifiers: Zinc acetate clllose. wax Natural quis: To 20.8 setirs time HEAI IG Factors Involved in He: 9 © Integrins: = Cell-Surface associated dimeric glycoproteins = function as cell to extracellular matrix adhesion receptors,free ebooks ==> www.ebook777.com 584 Review of All Dental Subjects = They play key roles in: re-cpithelization and granulation tissue formation = Regulates a wide range of cell functions during growth, development, differentiation and immune response. M ixbinding subunit Drie alo a cysiene _ tich domains “alin Taman ‘acini binding Figt4.t4: Structure © Epithelial cells can bind and also activate transforming growth fi, through a7, © Laminin-s = Found in basement membrane of skin and other epithelial tissue, = _Itserves asa component of anchoring filaments that span through the basement membrane = Laminin: 5 is also recognized by a, integrin. = Infact laminin: 5 appears to be & motility factor for keratinocytes but when proteolytically processed it starts to function as the nucleator of hemidesmosomes and therefore promotes the formation of basement membrane structures The role of laminin: 5 appears to bec cal even for healing of the blister wounds where lamina densa remains intact. Ccotiagen inaing doar Sing = = omar = xe “ooe Heparin o Cot sutace Foparansutato Sing dome { Sais Sonat Fig.14.18: Structure of Laminin www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 585 © Fibronectin: EIT Aappeats to be present underneath, migrating keratinocytes in vivo, FIBRONECTIN ~ a critical early component of 1. Clot 2. Forming granulation tissue Cellular fibrnoectin - Produced by 1. Keratinocytes 2. Fibroblasts 3. Macrophages Fibronectin vary structurally by alternative splicing of 3 regions namely. 1 EMA 2. ENB 3. VAIlIcs) EIITA Fibronectin -> expressed by migrating keratinocytes in wound EIILB Fibronectin expressed in embryoyonal tissue but not normally in adult connective tissue It is strongly upregulated during granulating tissue formation ‘© Tenascin: C are also found underneath the migrating Keratinocytes. = Function as a modulator of cell adhesion to other ratrix components such as fibronectin — The reorganization of basement membrane is complete at 4 weeks at which time the localization of all basement membrane components such as type IV and VI collagens, laminin ~ 1 and heparan sulphate proteoglycan appear normal — Urokinase type plasminogen activate receptor is able to associated with integrins © Transforming Growth Factor f Transforming growth factors fp are a family of polypeptides that have multiple regulatory actions in cell growth, differentiation and’ developmental ~ Timulate keratinocyte motility by svitching the cells from the differentiating to regenerative phenotype and by inducing their production of fibronectin and laminin - 5 In addition transforming growth factor b, other growth factors like platelet derived growth factor, epidermal growth factor, keratinocyte growth factor, hepatocyte growth factor also regulate wound healing, © Origin of wound fibroblasts Possitle sources of Steps involved wound fbrobias Surouncing comectie Misratior,cifeeniation tissue Fericytes Frolifestion, micration one mar-om Systemic control homirg siflerertition Healing After Periodontal Therapy ‘True _periocontal regeneration is tre reformation of functionally ted pericsotal ligament wth collagen fbres inserting in both rearcen aheciar sore and vefermec acsiler Cemertum cer @ previcusly cIseased rot surece, (uP 2011) Process callec bealing oy scar erests bone ‘cestuctcn witiLt necessarily inceasinc bone beient “erair_follonira cencccrtal_theresy ‘ccturs by the foeation cf ‘© L273 national epitneliur (COMEDK 2010, AIMS Nov 2010) 1+ New core with rcot -eserption or arcsis rb, Cog Now attacment is tre enbeciing of new Periodontal Igament fibres ino new cementum ano the atzcimert ofthe airavalepthelst ‘a tbcth stface creviot sly denuiec by disease, (AP 2005) Ateciment of the ciigiva or te periosental ligamert © areas of the toot fom wich they ‘Tay 62 removed in the course cf teatment cr ‘ounng the preceration cf teeth fer resteratons represents simcle healing or rifacimet of ‘ne periedortir not new ataciment, (AIPG 1993, 1996) “The final outcome of periodontal pocket healing depends on the sequence of events during the healing stage. (AP 2000) = If the epithelium proliferates along the tooth surface hefore the other tissues reach the area, the result will be along junctional epithelium, = the cells from gingival connective tissue are the first to populate the area, the result will be fibres parallel to the tooth surface and remodeling of the alveolar bone with no attachment to the cementum, = If the bone cells arrive first, root resorption and ankylosis may occur. = Finally only when cells from periodontal ligament proliferates coronally is there new formation of ‘cementum and new attachment. 19 Following Curettage Restoration and epithelialization of the sulcus generally require from 2 to 7 days Restoration of the junctional epithelium occurs in animals as early as 5 days after treatment, = Immature collagen fibres appear within 21 days. Healing after curettage results in the formation of a long thin, junctional epithelium with no new connective tissue attachment.free ebooks ==> www.ebook777.com 586 Review of All Dental Subjects Healing After Gingivectomy ~The initial response is the formation of & protective surface clot: = By24 hours, there is an increase in new connective tissue cells, mainly angioblasts, just beneath the surface layer of inflammation and necrosis, = By the third day numerous young fibroblasts are located in the area = After 12024 hours, epithelial cells atthe margins ofthe wound start to migrate over the granulation tissue, separating it from the contaminated surface layer ofthe clot ~ Epithelial activity at the margins reaches a peak in 24 to 36 hours = Surface epithelialization is generally complete after 5 to 14 days, = Complete epithelial repair takes about one month = _Vasodilation and vascularity begin to decrease after the fourth day of healing and appear to be almost normal by the 6th day. = Complete repair of the connective tissue takes about 7 weeks. Healing offre soft tissue grafts STE IEoy * In these trst days of heating a thin layer of exudates prosent between the graft and the recipient bod. During this eu aCe Period the orfies tissue survives with ar avascular plasmatic circulation” From the suvival cf the graft rat = tose contact establish to the urderving recipient aed at the time of cperaticr. + Tre exihelium of the fee raft degenerates early inthe Iilal healing prase 27d subsequerily R cecomes: sesouerates. (AIG 2062, 2003) + 4509s of healing arastemcses are estacisned between the boca ves ecard those inthe vetted tsste. fhe recipi SSCL GRE ° Durincthispe-oc the nurse ot clood vescelsinthe tersplentcecomes advallyredicec, ss ater acproxirately Tetgieieu) — “4daystre vascular system of the aratacpears rormal. Also the epithelium rack ally tures wth te fermation pacers) of axeratr layer dre this Stace trea + Theestaclstmentet colstealrcubtior from aelacentvascula-cordersofthebed allows the healing prerarr=aor oF BRIDGING’ ‘+ Aaotrer healing prenor=nor feqverty observed flloyng fee araftorcoscutes is’ CREEPING ATTACHNENT, is, a corenal micratior of the soft issue margin, Tis ccours 26 2 ocrseauewce of tissue rratuatio Surg & Peticd cf about 1 yeorpost= trestmert. © Neovascularisations stimulated by various growth factors: The most potent angiogenic factors are fibroblast growth factors aswellas TGF - a and TGF - BFGF and oFGF-stimulate endothelial proliferation = aFGF - stimalate tubule formation © Connective Tissue Repair = TGF-B- potent stimulate of fibronectin and collagen production — PDGF and FGF -> increases influx of fibroblasts at wound site and increase extracellular matrix production, PDGF and IGF1 ~ stimulates recruitment and proliferation of fibroblasts = Increased collagen synthesis and maturity + Re-Epthelialization ~ EGF and TGF-a-> directly increases the rate of re-epithelilisation, ~ DEGF and PDGF ~ indirectly enhance epithelialisation by stimulating a healthy bed of new connective tissue ~ TGF. inhibits epithelial cell proliferation but stimulate their migration © Hyperbaric Oxygen Therapy = _ Oxygen is one of the most versatile and powerful agents available to modern practitioner. The therapy used to oxygen sed under pressure is hyperbaric oxygen (HBO,). I assists in wound healing hyperbaric oxygen helps in www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 587 ‘Vasoconstriction Downregulation of inflammatory cytokines ‘Upregulation of growth factors ‘Anibacterial effect © Potential of antbioties = is used successfully im hypoxic or ischemic wounds like diabetic wounds, venous stasis ulcers filing grafts and flaps = In wound healing hypoxia prevents normal healing process. HBO, provides the oxygen needed to stimulate and supplement wound healing tis a safe, non invasive therapy. e000 ll PERIODONTIC - ENDODONTIC CONTINUUM Pathways of Communication Between Pulp and Periodontium GSE ee [ese © Denthal tables + Fereratiors + Lateral anc ecoessory canals Vertical root fracture + Avicalforanen + Palatoginaival roove © Anatomic considerations: DID between pulpal and periodontal disease 2 cuiNoAL es Saree Sees Bes a = Nissan Sees eral Pa Soa EE eal [oer ea chen © [Pee eee Ree eral] allen ae ene Radiographially rm ra aaa cinerea RES ES eae) 3 Peisictieta! ater vetoes a aoa ra = a Junctiorel epithetiyim No aaical Migration Apical Migrate ae Goes deka eng Saaier) eos a SS] ie aol =a Trersoy Treatmentfree ebooks ==> www.ebook777.com 588 Review of All ental Subjects ME HALITOSIS + Halitosisiscausedprimailybyvolatilesulfurcompounds, So specifically hydrogen sulfide, methyimercaptan and © Also termed ae: dimethyl sulfide, which result from bacterial putrefaction = Fetorexore of proteins containing sulfur amino acids = Fetororis (MP 2010, COMEDK 2007) = Oral malodor © Other causes include ~ Diamines (putrescine and cadaverine) = Short chain fatty aids (butyric, valeric and propionic © Are of diagnostic significance © Source may be intraoral or extraoral © Common local source is food stagnation on tongue and a gingival sulcus Classification (Miyazaki 11999) [a + Gonuine haltosis CChvioss Talon wh intersty beyord scillyaccectele level is ce-eivedL = Physoiogichatiosis Tt + Malosr arises trough putefecive cross within the orl cay. Neier specific disease nor pathologic condition that could cause hast founc. ‘righ ie mainly the corscpesteror region of te tone ‘+ Terporaryhaltcsis ste to cietry factors (¢-. garlic) shuld be excluded. = Patrolonic ralitesis ral TN as TN2 ‘+ altosis caused by disease, patocgic conciton. 0° ratfanction cf cral tissues ‘+ Halitosis derived ftom tongue coating, modified by pathologic condliton (e.g pericdoatal disease, xerostomia} is ehiced in ts sucdie, Extecral TNs + Maloccr oiinates from nasal araresal, ancerleryncealrecions + alocer onainates from pulmonary tact cr upeer geste tect * Maloscr originates trom ciscrders anywhere in the beay waereby tre cour BS blood some ard emittes wis liras (69, diabetes Melis, repatic ckrresis, erie. itera blessing) + Pseudo halitesis, Tht awiTNA thers de nctipercee oovicus malecor, although te patient comp existen ‘© Condition is imeroved by courseling (usa iteretre suopert, scucatin, ard ‘xclanatior of examination restts) and simile ral hygiene ‘reasures ofits + Haltophobia TM awINe + Afler treatment for ceruine haltcsis 0” 2seudoralitosis. the patirt persists in believing that heist 725 reliosis + No ohysical or sccial evilenoe exists to suggest tet haltcsis is present Description of various treatment needs Era TN-1 Explanation ofhaltosis ard instructors fo cral hygiene JN2 Gra prrtylaxs, professional clearing, anc treat for crl siscases, especially cericrial ciseases TNS —_Refertalto 3 prysicien N4 Explanation of exenination data fLve orcessicnelirstictio, education and reass.srce TNS Referral to 2 clinical psyoroloait, psychiatrist, o cther psychclocical special. www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 589 © Different methods of assessing the oral malodor are: = Selfexamination = Organoleptic method ~ Gas chromatography (Oral chroma) ~ Dark field or phase contrast microscopy = Saliva incubation test Electric nose + Orgunoleptic scoring, considered as gold standard method for oral malodor. It was introduced by Rosenberg and Meullum. (KAR 2010) © “The organisms implicated in halitosis is Pgingivalis The instrument that detects halitossis Osmoscape (AP 2005) Extra oral sources Eee Ee + Ration eags + Indcative of volatile sulfide compounds main responsible for naliosis + Sveetodourorcesd rice + ver insutloney (KAR 2061) + Acstore eat orton apples + Disbetes + Fist odour My ocour + Kidney nsutiency © Mouthrinses combining cetyl pyridinium chloride with chlorhexidine (CHX 0.05% + CPC 0.05% + zinc lactate 0.14%) significantly reduces plaque and gingivitis indices as well as morning halitoss. (MP 2010) © Haliteis a tongue seraper. Mm LASER Commercially Available Lasers Fresueey covblec Alexerdite Laser Neody riumYag Laser (N&:YAG) Excium Grove EroiumYAG (Er-YAG) EroumYSGG ErySCo, rium, Chromium VSG (ErCar YG) CORfree ebooks ==> www.ebook777.com 590 Review of All Dental Subjects Wave Length Of Main Lasers Car 369 Helumnecn De xnjton Ruby elu Yes egonuoride Krypton fuoride [5 PERIODONTAL MICROSURGERY tors red 128 lofered Be tnfared Red Red creer Greer Red Inrered utes violet uit © Carl Nylen is considered the father of microsurgery. Basically, there are two types of optical magnification available: © Magnifying loupes = Simple loupes = Compound loupes = Prism telescopic loupes © Surgical microscope Advantages of Periodontal Microsurgery © Improved cosmetics, © Rapid healing © Minimal discomfort © Less invasive-As there is reduced incision size, lessened need fe for vertical releasing incisions and smaller surgical sites thus, periodontal microsurgery is considered less invasive procedure © Reduces surgical fatigue and development of spinal and occupational pathology of the operator © Enhanced patient acceptance. Advantages of Loupes Over Microscopes © Less expensive to purchase; © Easier to use © Loupes tend to be less cumbersome in operating field and les likely to breech a clean operative field: and © They are handy in free-lancing practice. = Disadvantage of loupes over microscopes is that the individual light source is required for loupes. = In periodontal surgery a magnification of x 4.5 to x5 for loupe spectacles and x10 to x20 for surgical microscope appears to be ideal, www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 5o1 MISCELLANEOUS . A dendritic cell is any cell that has branching processes ‘The epithelium in addition to the keratinocytes contains. three types of resident cells of the dendritic morphology. ‘These are Langerhans cells, Merkel cells and melanocytes Transseptal fibres ace the only fibres, which are not embedded into bone. They extend interproximally over the alveolar bone crest and are embedded in cementum of adjacent teeth, Transseptal means they are always present across the septum and they are a constant finding because they get reconstructed even after destruction of alveolar bone. (AIPG 2009) Passive eruption is a pathologic process of exposure of teeth by apical migration of gingiva. Gottlieb and orban believed that active and passive ‘eruption occur together (AIPG 2012) © The attachment apparatus of the tooth is composed of periodontal ligament, cementum and alveolar bone. | * Periodontium is composed of gingiva, periodontal ligament, cementum and alveolar bone. Alveolar process is formed at the time of tooth eruption and disappears gradually after the tooth is lost. Alveolar bone proper, which is seen as lamina dura in radiographs, gives attachment to principal fibres |. of periodontal ligament. I is formed of partly dense lamllated bone and party of bundle bone. Inner wall of tooth socket, which is thin compact bone, is formed by alveolar bone proper Bundle bone is the bone adjacent to periodontal ligament that contains great number of sharpey’s fibres. Bone mineralization: osteoid is freshly secreted bone matrix, which is non mineralized. Mineralization process always follows bone matrix (osteoid) formation, Width of attached gingiva increases with age and eruption of teeth, the latter phenomenon is utilized in clinical ‘treatment planning via ortho-perio estheitics, ‘The width of the periodontal ligament space will decrease if the tooth is unopposed or in hypofunction, PDL ground substance = Glycoaminoglycans-hyaluronic acid and proteoglycans (chondroitin and dermatan sulfate) = Glycoproteins - fibronectin and laminin Enlargement in pregnancy is usually generalized and tends to be more prominent interproximally than on, facial and lingual surfaces ‘Tumour like gingival enlargement in pregnancy is not ‘neoplasm but an inflammatory response to bacterial plaque. Pregnancy associated gingivitis is accompanied by increase in steroid hormones in crevicular fluid and dramatic incteate of Bintermedia, No notable changes occur in gingiva during pregnancy in the absence of local dnritants Spirochactes are found to penetrate necrotic tistue and apparently unaffected connective tissue Although the primary source of collagenase in periodontal pockets is host tissue cells, bacterial collagenases may also contribute to collagen degradation in a similar fashion, Calcification begins along the inner surface of supragingival plague and in the attachéd component of subgingival plaque adjacent to the tooth. Caleulus does not mechanically irritate the gingiva but provides fixed nidus for continued accumulation of plaque and retains bacterial flora and their virulence factors in close proximity to the gingiva. Bacterial plaque is a primary etiologic factor in periodontal diseases. Teeth least affected by periodontal disease : lower premolars and upper canines. Composition of plaque formed on all types of restorative material is similar, with the exception of that formed on silicate. The difference isin higher carbolydrate:nitrogen ratio (due to reduced carbohydrate metabolism) and lower nitrogen:calcium ratio. Highest incidence of gingival infiltrative lesions (calargement) is in acute monocytic leukemia (66.7%) > acute myelocytic - monocytic leukemia (18.7%) > acute myelocytic leukemia (3.7%) Bleeding tendency in leukemia specially affects the ‘oral cavity especially gingival sulcus. Bleeding is due to thrombocytopenia resulting from replacement of bone marrow cells by leukemic cells. ‘Trueleukemic enlargement may alsobe seen in subacute leukemia but seldom oceuts in chronic leukemia, Bruxism and periodontal health/disease are independent phenomenon-no association has been shown Peeling of surface occurs in chronic desquamative gingivitis and drug induced gingival overgrowth produces nodular surface. ‘Actual position is the level of epithelial attachment ‘on tooth whereas apparent position is level of crest of gingival margin,free ebooks ==> www.ebook777.com 592 Review of All Dental Subjects + NUG does not lead to periodontal pocket formation) because junctional epithelium is necrotic. Remember that a viable junctional epithelium is amust for sulcus deepening and pocket production. Pericoronitis is a incubation zone for ANUG © Reversed architecture is most common in maxilla, (MP 2010) © Maxillary premolars are least common site for furcation, involvement. © Cuneiform defect is another name for erosion. © Gingivosis is associated with the deficiency of estrogen and progesterone, because it is seen more commonly during menopause and perimenopause phase. (AIPG 2009) “The periodontal (lateral, parietal) abscess is rarely associated with afistulous tract. us is a common feature of periodontal disease but its only a secondary sign. Presence of pus merely reflects the nature of the inflammatory change in the pocket wall. (AIPG 2008) Pas formation is not an indication of the depth of the pocket or severity of destruction of periodontal supporting tissues. (AIG 2006) ‘Transgingival probing predicts features of the underlying bony topography FewTerms to Remember © Macules: Well circumscribed flat lesion that are noticeable because oftheir change from normal skin color © Papule: Solid lesions raised abave the skin surface that ate smaller than 1 cm in diameter + Plaque: Solid raised lesions that are over 1 em in diam, they ate large papules © Nodules: hese lesions are present deep in the dermis, 5: Blevated blisters containing clear uid that are under | emia diameter. © Bullae: Flevated blisterlike lesions containing clear fluid that are over 1 cm in diameter. © Brosions: Moist red lesions often caused by the rupture or bullae as well as trauma. © Pastules: Raised lesions containing purulent material © Uleers: A defect in the epithelium; it is a well- circumscribed depressed lesion over which the epidermal layer lost. © Purpura: Reddish to purple flat lesions caused by blood vessels leaking into the subcutaneous tissue, Classified by size at petechiae or ecchymoses, these lesion do not blanch when pressed, © Petechiae: Purpuric lesions 1 to 2 mm in diameter. Larger purpuric lesions are called eechymoses, Nice to Know Elesronic instunert usec to measure cor Etc ei Fresctictio soliton of chlorexisine Srna Detects pocket terperaire aiffererces Of "0 from 2 referenced sucaingival ‘emperatuie ly magnetized instuments desined val ofbro) + Alsocalledasclectrolyticmedication, lectromedication ‘and ionic medication The introduction by means of electric current of ions ‘of soluble salts into the tissues, usually for therapeutic purposes. ‘Based on the principle of electrolysis, whereby a salt, such as NaB, placed in the solution will undergo ionization, ‘+ The introduction of a positive electrode (anode) and a negative electrode (cathode) into solution, and passing of direct current through the solution will result in concentration of fluoride at the positive pole and sodium ions at the negative pole. When used in dentistry, one electrode is attached to the tooth and other is held in the hand. ‘Percentage of sodium fluoride used in iontophoresis is 2% (AIPG 2006) www.ebook777.comfree ebooks ==> www.ebook777.com Periodontics 593 Pigmentation Leac line (Burtorian tine) Silver Argyria) Bisqruth, arsenic and mercury Nesenteric line Bust red er deeo bite linear pigmentation in ma-chal inca (AIPG 2005, MAN 1994) ‘Viet rarairal Ine Blac marcinl tine (AIPG 2005) Delicate, browr or black ciaertec non carogericplacue foune cn the eran at tre cervical Tarair ofthe toot”