Oral Cavity

Functions mastication, swallowing, speech

Saliva 70% from submandibular gland, 25% from parotid and 5% from sublingual and
accessory glands
Submandibular gland palpated bimanually, differentiates from lymph nodes
Ulcerative and Inflammatory lesions
Aphthous ulcers (Canker sores)
o Extremely common (25%), small (<5 mm), painful, shallow round or oval ulcers.
o Types
Minor most common, <10 mm in diameter, grey/white centre with thin
erythematous halo and heal without scarring within 14 days
Major - >10 mm in diameter, persist for month and heal with scarring
o Appear singly or in groups on nonkeratinized oral mucosa soft palate, buccolabial
mucosa, floor of mouth, lateral borders of tongue
o Common in first 2 decades of life, females and non-smokers
o Triggered by stress, fever, ingestion of certain foods, activation of inflammatory
bowel disease, deficiencies of iron, folic acid or vitamin B12
o Self-limiting, resolve within a few weeks, but may recur in same or different location
o Topical triamcinolone or systemic corticosteroids lessen the duration and severity of
attacks
Herpesvirus infection
o Herpetic stomatitis caused by HSV 1
o Extremely common
o Primary infection asymptomatic but virus persist dormant within ganglia about the
mouth (trigeminal ganglia)
o Reactivation by fever, sun or cold exposure, respiratory tract infection, trauma
o In immunocompromised more virulent disseminated eruption develops herpetic
gingivostomatitis, lymphadenopathy, encephalitis, disseminated visceral lesions
o Keratoconjunctivitis
Oral candidiasis
o Candida albicans normal inhabitant of oral cavity in 30-40%
o Pseudomembranous candidiasis most common fungal infection of oral cavity
o Affects diabetes mellitus, anaemia, antibiotic or glucocorticoid therapy,
immunodeficiency, debilitating illness like disseminated cancer and AIDS
o Morphology adherent white, curdlike, circumscribed plaque anywhere within oral
cavity, pseudomembrane can be scraped off to reveal an underlying granular
erythematous inflammatory base.
o If more vulnerable oesophageal candidiasis, disseminated candidiasis
AIDS
o Develop candidiasis, herpetic vesicles, microbial infections (gingivitis, glossitis), hairy
leukoplakia
o Hairy leukoplakia only in AIDS white confluent patches anywhere on oral mucosa,
have a hairy or corrugated surface due to marked epithelial thickening. Caused by
EBV
Kaposis sarcoma
Bacterial syphilis, tuberculosis
Systemic disease Reactive arthritis, Behcets syndrome, SLE
Trauma dentures
Neoplasia squamous cell carcinoma
Drugs chemotherapy, antimalarials
Skin disease pemphigoid, pemphigus, lichen planus
Leukoplakia
Whitish, well-defined mucosal patch or plaque caused by epidermal thickening or
hyperkeratosis
Cannot be scraped off and cannot be characterized as any other disease
Microscopy vary from banal hyperkeratosis without epithelial dysplasia to mild to severe
dysplasia bordering on carcinoma in situ
Strong association with use of tobacco pipe smoking, smokeless tobacco
Also associated with chronic friction (ill fitting denture, jagged teeth), alcohol abuse, irritant
foods, HPV
Some undergo transformation to squamous cell carcinoma
Variants
o Hairy leukoplakia in AIDS, does not undergo malignant transformation
o Verrucous leukoplakia may harbour malignancy
o Erythroplakia red, velvety, often granular circumscribed areas, Almost invariably
reveals epithelial dysplasia
Tongue
Glossitis red, smooth, sore tongue seen in B12, folate, iron deficiency, infections due to
Candida, riboflavin and nicotinic acid deficiency
Black hairy tongue due to proliferation of chromogenic microorganisms causing brown
staining of elongated filiform papillae.
Geographic tongue familial, erythematous areas surrounded by well-defined, slightly
raised irregular margins, painless.
Cleft Lip and Palate
Most common congenital abnormalities of orofacial structure
Isolated or associated with other conditions like congenital heart disease
High incidence in Oriental groups, low incidence in blacks
Types
o Cleft lip alone 15%, more in males, unilateral, bilateral
o Cleft lip and palate 45%, more in males
o Cleft palate only 40%, more in females, soft palate or soft palate and hard palate
Aetiology
o Genetic predisposition more significant in cleft lip/palate than cleft palate alone
o Environmental component maternal epilepsy, drugs like steroids, diazepam,
phenytoin, smoking, alcohol
Classification LAHSHAL system
Primary Management
o Antenatal diagnosis by US after 18 weeks of gestation
o Feeding sometimes need soft bottles, modified teats, may result in failure to gain
weight
o Retained nasopharyngeal intubation if airway obstruction significant or surgical
adhesion of tongue to lower lip (labioglossopexy)
o Cleft lip surgery between 3-6 months
o Cleft palate surgery between 6-18 months
o Cleft lip and palate two stage procedure
Secondary management for complications
o Hearing should check due to their Eustachian tube dysfunction and also
sensorineural deafness so, assessed for sensorineural and conductive deafness
before 12 months of age. Hearing aid for sensorineural deafness and prophylactic
myringotomy and grommet insertion for conductive deafness
o Speech assessed before 18 months and regularly, problems are velophrayngeal
incompetence (leading to increased nasal airflow and resonance producing nasal or
hypernasal speech due to poor function of soft palate), articulation problems.
o Dental Delayed tooth development, delayed eruption, morphological
abnormalities, hypodontia, hyperdontia may occur.
Dry Mouth/Xerostomia
Causes
o Sjogrens syndrome
o Drugs antimuscarinic, antiparkinsonism, antihistamines, lithium, MAO inhibitors,
TAD, clonidine
o Radiotherapy
o Psychogenic chronic anxiety and depression
o Dehydration, shock, chronic kidney disease
Management preserve what flow remains, stimulate flow, replace saliva (glycerine, lemon
mouthwash, artificial saliva)
Siarlorrhoea
Excessive production of saliva
Rare
Need to swallow more frequently and leaking from mouth
Causes
o Obsessive
o Cerebral palsy
o Mentally subnormal
Complications
o Angular chielitis
o Secondary infections of lip, chin
Management
o Medical physiotherapy, speech therapy, propanthelene, scopolamine patches,
topical antifungals
o Surgery relocated submanidublar ducts posteriorly
Sialothiasis
Stone formation within glands or duct system
80% in submandibular glands (as their secretions are viscous), 19% in parotid gland
80% of submandibular stones are radio-opaque, parotid ducts stones are usually radiolucent
so sialography needed
Stones generally calcium phosphates (hydroxyapatite and carbonate)
Clinical features
o Complete obstruction at opening of duct
Acute painful swelling precipitated by eating
Swelling occurs rapidly and resolves within 1-2 hours after meals
o Partial obstruction at hilum of gland or within the duct
Infrequent, minimal discomfort and swelling, not confined to meal times
o Enlarged firm submandibular gland, tender on bimanual examination, pus draining
from sublingual papilla due to infection
Management
o Stone distal to lingual nerve simple ductoplasty
o Stone proximal to lingual nerve sialadenectomy
Nerves at risk marginal mandibular branch of facial nerve, lingual nerve,
hypoglossal nerve
Complications haematoma, wound infection, nerve injury, transection of
nerve to mylohyoid muscle producing submental skin anaesthesia
o Retrieval of stone by sialadenoscopy or lithotripsy
Sialadenitis
Inflammation of the major salivary glands
Types
o Acute
o Chronic chronic bacterial sialadenitis is rare in parotid
o Acute on chronic
Causes
o Traumatic
o Viral mumps (predominantly parotid, submandibular gland occasionally involved,
diffuse interstitial inflammation, oedema, mononuclear cell infiltration, focal
necrosis, childhood mumps self limited (5-10 days), spreads by airborne droplets of
infected saliva, prodrome of fever, nausea, headache for 2 days, treatment is regular
paracetamol and adequate oral fluid intake , in adults cause pancreatitis, orchitis,
oophoritis, sensorineural deafness, meningoencephalitis), Coxsackie A, B,
parainfluenza 1,3, echo also can cause
o Bacterial secondary to ductal obstruction from stone formation (sialolithiasis),
retrograde entry in severe systemic dehydration like postoperative state. Most
common are S.aureus, Streptococcus viridans, largely interstitial, focal areas of
suppurative necrosis, abscess formation
o Autoimmune causes chronic sialadenitis, in Sjogren syndrome
o HIV associated sialadenitis
o Granulomatous painless, due to Mycobacteria, sarcoidosis
o Associated with radiotherapy
Management in bacterial causes, antibiotics, Incision and drainage if fluctuant
Sialadenosis
Non-inflammatory swelling
Parotid gland mostly affected
Associated with diabetes mellitus, alcoholism, endocrine diseases, pregnancy, drugs
(sympathomimetics), bulimia, eating disorders
Soft swellings and symmetrical
Hamster like appearance
Pathogenesis malnutrition causing glandular atrophy and fatty replacement or neuropathy
interfering with salivary gland function leading to acinar cell atrophy (in diabetes mellitus
and drugs)
Treatment correction of underlying disorder
Sjogrens syndrome
Autoimmune condition causing progressive destruction of salivary and lacrimal glands
Classification
o Primary no connective tissue disorder, more severe symptoms, high incidence of
lymphomatous transformation
o Secondary underlying connective tissue disorder
Females more affected, parotid usually affected
Occasionally painful, kertoconjunctivitis sicca and xerostomia
Progressive lymphocytic infiltration, acinar cell destruction and proliferation of duct
epithelium in all salivary and lacrimal glands.
Management symptomatic
o Artificial tears
o Artificial salivary substitutes
o Drinking enough water
Complications
o Increased risk of lymphoma (B-cell)
o Oral candidiasis
o Periodontal disease