CHAPTER 7
The Role of Dental Calculus and Other Local
Predisposing Factors
James E. Hinrichs and Vivek Thumbigere Math
CHAPTER OUTLINE
Calculus
Other Predisposing Factors
The primary cause of gingival inflammation is bacterial plaque.
Other predisposing factors include calculus, faulty restorations,
complications associated with orthodontic therapy, self-inflicted
injuries, and the use of tobacco, in addition to several others. These
will be discussed in turn.
Calculus
Calculus consists of mineralized bacterial plaque that forms on the
surfaces of natural teeth and dental prostheses.
Supragingival and Subgingival Calculus
Supragingival calculus is located coronal to the gingival margin
and therefore is visible in the oral cavity. It is usually white or
whitish yellow in color; hard, with a claylike consistency; and
easily detached from the tooth surface. After removal, it may
rapidly recur, especially in the lingual area of the mandibular inci-
sors. The color is influenced by contact with such substances as
tobacco and food pigments. It may localize on a single tooth or
group of teeth, or it may be generalized throughout the mouth.
The two most common locations for the development of supra-
gingival calculus are the buccal surfaces of the maxillary molars
(Figure 7-1) and the lingual surfaces of the mandibular anterior
teeth (Figure 7-2).34 Saliva from the parotid gland flows over the
facial surfaces of the upper molars via the parotid duct, whereas
the submandibular duct and the lingual duct empty onto the
lingual surfaces of the lower incisors from the submaxillary and
sublingual glands, respectively. In extreme cases, calculus may
form a bridgelike structure over the interdental papilla of adjacent
teeth or cover the occlusal surface of teeth that are lacking func-
tional antagonists.
Subgingival calculus is located below the crest of the marginal
gingiva and therefore is not visible on routine clinical examination.
The location and extent of subgingival calculus may be evaluated
by careful tactile perception with a delicate dental instrument such
as an explorer. Clerehugh and colleagues31 used a World Health
Organization no. 621 probe to detect and score subgingival calcu-
lus. Subsequently, these teeth were extracted and visually scored
for subgingival calculus. An agreement of 80% was found between
these two scoring methods. Subgingival calculus is typically hard
and dense; it frequently appears to be dark brown or greenish black
116
in color (Figure 7-3), and it is firmly attached to the tooth surface.
Supragingival calculus and subgingival calculus generally occur
together, but one may be present without the other. Microscopic
studies demonstrate that deposits of subgingival calculus usually
extend nearly to the base of periodontal pockets in individuals with
chronic periodontitis but do not reach the junctional epithelium.
When the gingival tissues recede, subgingival calculus becomes
exposed and is therefore reclassified as supragingival (Figure 7-4,
A). Thus, supragingival calculus can be composed of both supra-
gingival calculus and previous subgingival calculus. A reduction in
gingival inflammation and probing depths with a gain in clinical
attachment can be observed after the removal of subgingival plaque
and calculus (Figure 7-4, B; see Chapter 46).
Prevalence
Anerud and colleagues4 observed the periodontal status of a group
of Sri Lankan tea laborers and a group of Norwegian academicians
for a 15-year period. The Norwegian population had ready access
to preventive dental care throughout their lives, whereas the Sri
Lankan tea laborers did not. The formation of supragingival calcu-
lus was observed early in life in the Sri Lankan individuals, prob-
ably shortly after the teeth erupted. The first areas to exhibit
calculus deposits were the facial aspects of maxillary molars and
the lingual surfaces of mandibular incisors. The deposition of
supragingival calculus continued as individuals aged, and it reached
a maximal calculus score when the affected individuals were
around 25 to 30 years old. At this time, most of the teeth were
covered by calculus, although the facial surfaces had less calculus
than the lingual or palatal surfaces. Calculus accumulation appeared
to be symmetric, and, by the age of 45 years, these individuals had
only a few teeth (typically the premolars) without calculus. Sub-
gingival calculus appeared first either independently or on the
interproximal aspects of areas where supragingival calculus already
existed.4 By the age of 30 years, all surfaces of all teeth had sub-
gingival calculus without any pattern of predilection.
The Norwegian academicians received oral hygiene instruc-
tions and frequent preventive dental care throughout their lives.
The Norwegians exhibited a marked reduction in the accumulation
of calculus as compared with the Sri Lankan group. However,
despite the fact that 80% of teenagers formed supragingival
 CHAPTER 7 The Role of Dental Calculus and Other Local Predisposing Factors
Figure 7-1 Supragingival calculus is depicted on the buccal sur-
faces of maxillary molars adjacent to the orifice for the parotid
duct.
Figure 7-2suEpxrtaegnisnigvieval calculus is present on the
lingual surfaces of the lower anterior teeth.
Figure 7-3piDgamrkented deposits of subgingival calculus are
shown on the distal root of an extracted lower molar.
calculus on the facial surfaces of the upper molars and the lingual
surfaces of lower incisors, no additional calculus formation
occurred on other teeth, and its presence did not increase with the
individuals age.4
Both supragingival calculus and subgingival calculus may be
seen on radiographs (see Chapter 32). Highly calcified interproxi-
mal calculus deposits are readily detectable as radiopaque projec-
tions that protrude into the interdental spaces (Figure 7-5). However,
the sensitivity level of detecting calculus by radiographs is incon-
sistent.24 The location of calculus does not indicate the bottom of
the periodontal pocket, because the most apical plaque is not suf-
ficiently calcified to be visible on radiographs.
Composition
Inorganic Content. Supragingival calculus consists of inor-
ganic (70% to 90%52) and organic components. The major inor-
117
A
B
Figure 7-4 A, A 31-year-old white man with extensive supragin-
gival and subgingival calculus deposits throughout his dentition is
shown. B, One year after receiving thorough scaling and root
planing to remove supragingival and subgingival calculus deposits,
followed by restorative care. Note the substantial reduction in
gingival inflammation.
ganic proportions of calculus have been reported as approximately
76% calcium phosphate, (Ca3[PO4]2); 3% calcium carbonate
(CaCO3); and traces of magnesium phosphate (Mg3[PO4]2) and
other metals.176 The percentage of inorganic constituents in calcu-
lus is similar to that of other calcified tissues of the body. The
principal inorganic components have been reported as approxi-
mately 39% calcium, 19% phosphorus, 2% carbon dioxide, and 1%
magnesium as well as trace amounts of sodium, zinc, strontium,
bromine, copper, manganese, tungsten, gold, aluminum, silicon,
iron, and fluorine.113
At least two thirds of the inorganic component is crystalline in
structure.89 The four main crystal forms and their approximate
percentages are as follows: hydroxyapatite, 58%; magnesium whit-
lockite, 21%; octacalcium phosphate, 12%; and brushite, 9%.
Two or more crystal forms are typically found in a sample of
calculus. Hydroxyapatite and octacalcium phosphate are detected
most frequently (i.e., in 97% to 100% of all supragingival calculus)
and constitute the bulk of the specimen. Brushite is more common
in the mandibular anterior region, and magnesium whitlockite is
found in the posterior areas. The incidence of the four crystal forms
varies with the age of the deposit.16
Organic Content. The organic component of calculus con-
sists of a mixture of proteinpolysaccharide complexes, desqua-
mated epithelial cells, leukocytes, and various types of
microorganisms.99
Between 1.9% and 9.1% of the organic component is
carbohydrate, which consists of galactose, glucose, rhamnose,
mannose, glucuronic acid, galactosamine, and sometimes arabi-
nose, galacturonic acid, and glucosamine.92,98,161 All of these organic
118 PART 1 Biologic Basis of Periodontology
Figure 7-5 bAitewing radiograph illustrating subgingival calculus
deposits that are depicted as interproximal spurs (arrows).
components are present in salivary glycoprotein, with the excep-
tion of arabinose and rhamnose. Salivary proteins account for 5.9%
to 8.2% of the organic component of calculus and include most
amino acids. Lipids account for 0.2% of the organic content in the
form of neutral fats, free fatty acids, cholesterol, cholesterol esters,
and phospholipids.93
The composition of subgingival calculus is similar to that of
supragingival calculus, with some differences. It has the same
hydroxyapatite content, more magnesium whitlockite, and less
brushite and octacalcium phosphate.142,165 The ratio of calcium to
phosphate is higher subgingivally, and the sodium content increases
with the depth of periodontal pockets.94 These altered compositions
may be attributed to the origin of subgingival calculus being
plasma, whereas supragingival calculus is partially composed of
saliva constituents. Salivary proteins present in supragingival cal-
culus are not found subgingivally.11 Dental calculus, salivary duct
calculus, and calcified dental tissues are similar in inorganic
composition.
Attachment to the Tooth Surface
Differences in the manner in which calculus is attached to the tooth
surface affect the relative ease or difficulty encountered during its
removal. Four modes of attachment have been described.85,145,152,181
Attachment by means of an organic pellicle on cementum is
depicted in Figure 7-6, and attachment on enamel is shown in
Figure 7-7. Mechanical locking into surface irregularities, such as
caries lesions or resorption lacunae, is illustrated in Figure 7-8. The
fourth mode of attachment consists of the close adaptation of the
undersurface of calculus to depressions or gently sloping mounds
of the unaltered cementum surface,161 as shown in Figure 7-9, and
the penetration of bacterial calculus into cementum, as shown in
Figures 7-10 and 7-11.
Figure 7-6atC
taaclhcuedlutso the pellicle on the enamel surface
and the cementum. An enamel void (E) has been created during
the preparation of the specimen. C, Cementum; CA, calculus;
P, pellicle.
E
CA
P
D
CEJ
C
Figure 7-7 Non-decalcified specimen with calculus (CA) attached
to enamel (E) surface just coronal to the cementoenamel junction
(CEJ). Note plaque (P) on the surface of the calculus; dentin (D)
and cementum (C) are also identified. (Courtesy Dr. Michael Rohrer,
Minneapolis, MN.)
Formation
Calculus is mineralized dental plaque. The soft plaque is hardened
by the precipitation of mineral salts, which usually starts between
the first and fourteenth days of plaque formation. Calcification has
been reported to occur within as little as 4 to 8 hours.166 Calcifying
plaques may become 50% mineralized in 2 days and 60% to 90%
mineralized in 12 days.112,146,156 All plaque does not necessarily
undergo calcification. Early plaque contains a small amount of
inorganic material, which increases as the plaque develops into
calculus. Plaque that does not develop into calculus reaches a
 CHAPTER 7 The Role of Dental Calculus and Other Local Predisposing Factors
Figure 7-8 Calculus (CA) attached to a cemental resorption area
(CR) with cementum (C) adjacent to dentin (D).
Figure 7-9 Undersurface of subgingival calculus (C) previously
attached to the cementum surface (S). Note the impression of
cementum mounds in the calculus (arrows). (Courtesy Dr. John Sot-
tosanti, La Jolla, CA.)
Figure 7-10 Subgingival calculus (C) embedded beneath the
cementum surface (arrows) and penetrating to the dentin (D),
thereby making removal difficult. (Courtesy Dr. John Sottosanti, La
Jolla, CA.)
119
Figure 7-11anPdlaqcu
aleculus on the tooth surface. Note the
spherical areas of focal calcification (FC) and the perpendicular
alignment of the filamentous (F) organisms along the inner surface
of plaque and cocci (C) on the outer surface.
plateau of maximal mineral content within 2 days.147 Microorgan-
isms are not always essential in calculus formation, because calcu-
lus occurs readily in germ-free rodents.59
Saliva is the source of mineralization for supragingival calcu-
lus, whereas the serum transudate called gingival crevicular fluid
furnishes the minerals for subgingival calculus.71,163 The calcium
concentration/content in plaque is 2 to 20 times that found in
saliva.16 Early plaque of heavy calculus formers contains more
calcium, three times more phosphorus, and less potassium than that
of noncalculus formers, thereby suggesting that phosphorus may
be more critical than calcium for plaque mineralization.99 Calcifica-
tion entails the binding of calcium ions to the carbohydrateprotein
complexes of the organic matrix and the precipitation of crystalline
calcium phosphate salts.97 Crystals form initially in the intercellular
matrix and on the bacterial surfaces and finally within the
bacteria.53,182
The calcification of supragingival plaque and in the attached
component of subgingival plaque begins along the inner surface
adjacent to the tooth. Separate foci of calcification increase in size
and coalesce to form solid masses of calculus (see Figure 7-11).
Calcification may be accompanied by alterations in the bacterial
content and staining qualities of the plaque. As calcification pro-
gresses, the number of filamentous bacteria increases, and the foci
of calcification change from basophilic to eosinophilic. There is a
reduction in the staining intensity of groups that exhibit a positive
periodic acidSchiff reaction.
Sulfhydryl and amino groups are also reduced and instead stain
with toluidine blue, which is initially orthochromatic but which
becomes metachromatic and disappears.172 Calculus is formed in
layers, which are often separated by a thin cuticle that becomes
embedded in the calculus as calcification progresses.101
The initiation of calcification and the rate of calculus accumula-
tion vary among individuals, among tooth variety in the same
dentition, and at different times in the same person.113,168 On the
basis of these differences, persons may be classified as heavy,
moderate, or slight calculus formers or as noncalculus formers. The
120 PART 1 Biologic Basis of Periodontology
average daily increment in calculus formers is from 0.10% to
0.15% of dry weight calculus.156,168 Calculus formation continues
until it reaches a maximum, after which it may be reduced in
amount. The time required to reach the maximal level has been
reported to be between 10 weeks32 and 6 months.170
The decline from maximal calculus accumulation, which is
referred to as the reversal phenomenon, may be explained by the
vulnerability of bulky calculus to mechanical wear from food and
from the cheeks, lips, and tongue.
Theories Regarding the Mineralization of Calculus.
The theoretical mechanisms by which plaque becomes mineralized
can be stratified into two categories.114
1p.reMcipiniteartaioln results from a local rise in the degree of
saturation of calcium and phosphate ions, which may be brought
about in the following several ways:
A rise in the pH of the saliva causes the precipitation of
calcium phosphate salts by lowering the precipitation con-
stant. The pH may be elevated by the loss of carbon dioxide
and the formation of ammonia by dental plaque bacteria or
by protein degradation during stagnation.15,66
Colloidal proteins in saliva bind calcium and phosphate ions
and maintain a supersaturated solution with respect to
calcium phosphate salts. With the stagnation of saliva, col-
loids settle out, and the supersaturated state is no longer main-
tained, thereby leading to the precipitation of calcium
phosphate salts.130,149
Phosphatase liberated from dental plaque, desquamated epi-
thelial cells, or bacteria precipitates calcium phosphate by
hydrolyzing organic phosphates in saliva, thereby increasing
the concentration of free phosphate ions.175 Esterase is another
enzyme that is present in the cocci and filamentous organisms,
leukocytes, macrophages, and desquamated epithelial cells of
dental plaque.9 Esterase may initiate calcification by hydro-
lyzing fatty esters into free fatty acids. The fatty acids form
soaps with calcium and magnesium that are later converted
into the less-soluble calcium phosphate salts.
2ag.eSnetsediinndguce small foci of calcification that enlarge
and coalesce to form a calcified mass.115 This concept has been
referred to as the epitactic concept or, more appropriately, as
heterogeneous nucleation. The seeding agents in calculus for-
mation are not known, but it is suspected that the intercellular
matrix of plaque plays an active role.100,112,182 The carbohydrate
protein complexes may initiate calcification by removing
calcium from the saliva (chelation) and binding with it to form
nuclei that induce the subsequent deposition of minerals.97,171
Role of Microorganisms in the Mineralization of
Calculus. Mineralization of plaque generally starts extracellu-
larly around both gram-positive and gram-negative organisms, but
it may also start intracellularly.87 Filamentous organisms, diphthe-
roids, and Bacterionema and Veillonella species have the ability to
form intracellular apatite crystals (see Figure 7-11). Mineralization
spreads until the matrix and the bacteria are calcified.53,183
Bacterial plaque may actively participate in the mineralization
of calculus by forming phosphatases, which changes the pH of the
plaque and induces mineralization,40,97 but the prevalent opinion is
that these bacteria are only passively involved53,137,175 and are
simply calcified with other plaque components. The occurrence of
calculus-like deposits in germ-free animals supports this opinion.59
However, other experiments suggest that transmissible factors are
involved in calculus formation and that penicillin in the diets of
some of these animals reduces calculus formation.10
Figure 7-12ulCuaslc (CA) penetrates the tooth surface and is
embedded within the cementum (C). Note the plaque (P) attached
to the calculus.
Etiologic Significance
Distinguishing between the effects of calculus and plaque on the
gingiva is difficult, because calculus is always covered with a
nonmineralized layer of plaque.147 A positive correlation between
the presence of calculus and the prevalence of gingivitis exists,132
but this correlation is not as great as that between plaque and gin-
givitis.55 The initiation of periodontal disease in young people is
closely related to plaque accumulation, whereas calculus accumu-
lation is more prevalent in chronic periodontitis found in older
adults.55,90
The incidence of calculus, gingivitis, and periodontal disease
increases with age. It is extremely rare to find periodontal
pockets in adults without at least some subgingival calculus being
present, although the subgingival calculus may be of microscopic
proportions.
Calculus does not contribute directly to gingival inflammation,
but it provides a fixed nidus for the continued accumulation of
plaque and its retention in close proximity to the gingiva (Figure
7-12). Subgingival calculus is likely to be the product rather than
the cause of periodontal pockets. Plaque initiates gingival inflam-
mation, which leads to pocket formation, and the pocket in turn
provides a sheltered area for plaque and bacterial accumulation.
The increased flow of gingival fluid associated with gingival
inflammation provides the minerals that mineralize the continually
accumulating plaque that results in the formation of subgingival
calculus (Figure 7-13). Over a 6-year period, Albandar and col-
leagues observed 156 teenagers with aggressive periodontitis.2
They noted that areas with detectable subgingival calculus at the
initiation of the study were much more likely to experience a loss
of periodontal attachment than sites that did not initially exhibit
subgingival calculus.
Although the bacterial plaque that coats the teeth is the main
etiologic factor in the development of periodontal disease, the
removal of subgingival plaque and calculus constitute the corner-
stone of periodontal therapy. Calculus plays an important role in
maintaining and accentuating periodontal disease by keeping
plaque in close contact with the gingival tissue and by creating
 CHAPTER 7 The Role of Dental Calculus and Other Local Predisposing Factors
Figure 7-13elSeccatrnonninm
g icroscope view of an extracted
human tooth showing a cross-section of subgingival calculus (C)
separated (arrows) from the cemental surface during processing of
the specimen. Note the bacteria (B) attached to the calculus and the
cemental surfaces. (Courtesy Dr. John Sottosanti, La Jolla, CA.)
Figure 7-14oT
bacco stains on the apical third of the clinical crown
caused by cigarette smoking.
areas where plaque removal is impossible. Therefore, the clinician
must not only possess the clinical skill to remove the plaque and
calculus, but he or she must also be very conscientious about per-
forming this task.
Materia Alba, Food Debris, and Dental Stains
Materia alba is an accumulation of microorganisms, desquamated
epithelial cells, leukocytes, and a mixture of salivary proteins and
lipids, with few or no food particles; it lacks the regular internal
pattern observed in plaque.148 It is a yellow or grayish-white, soft,
sticky deposit, and it is somewhat less adherent than dental plaque.
The irritating effect of materia alba on the gingiva is caused by
bacteria and their products.
Most food debris is rapidly liquefied by bacterial enzymes and
cleared from the oral cavity by salivary flow and the mechanical
action of the tongue, cheeks, and lips. The rate of clearance from
the oral cavity varies with the type of food and the individual.
Aqueous solutions are typically cleared within 15 minutes, whereas
sticky foods may adhere for more than 1 hour.88,169 Dental plaque
is not a derivative of food debris, and food debris is not an impor-
tant cause of gingivitis.39,75
Pigmented deposits on the tooth surface are called dental stains.
Stains are primarily an aesthetic problem and do not cause inflam-
mation of the gingiva. The use of tobacco products (Figure 7-14),
121
A B
Figure 7-15 A, Radiograph of an amalgam overhang on the distal
surface of the maxillary second molar that is a source of plaque
retention and gingival irritation. B, Radiograph that depicts the
removal of excessive amalgam.
coffee, tea, certain mouthrinses, and pigments in foods can con-
tribute to stain formation.95,162
Other Predisposing Factors
Iatrogenic Factors
Deficiencies in the quality of dental restorations or prostheses are
contributing factors to gingival inflammation and periodontal
destruction. Inadequate dental procedures that contribute to the
deterioration of the periodontal tissues are referred to as iatrogenic
factors. Iatrogenic endodontic complications that can adversely
affect the periodontium include root perforations, vertical root
fractures, and endodontic failures that may necessitate tooth
extraction.180,181
Characteristics of dental restorations and removable partial den-
tures that are important to the maintenance of periodontal health
include the location of the gingival margin for the restoration, the
space between the margin of the restoration and the unprepared
tooth, the contour of the restorations, the occlusion, the materials
used in the restoration, the restorative procedure itself, and the
design of the removable partial denture. These characteristics are
described in this chapter as they relate to the etiology of periodontal
disease. A more comprehensive review with special emphasis on
the interrelationship between restorative procedures and the peri-
odontal status is presented in Chapter 67.
Margins of Restorations. Overhanging margins of dental
restorations contribute to the development of periodontal disease
by (1) changing the ecologic balance of the gingival sulcus to an
area that favors the growth of disease-associated organisms (pre-
dominantly gram-negative anaerobic species) at the expense of the
health-associated organisms (predominantly gram-positive faculta-
tive species)88 and (2) inhibiting the patients access to remove
accumulated plaque.
The frequency of overhanging margins on proximal restorations
has varied in different studies from 16.5% to 75%.18,51,70,121 A highly
significant statistical relationship has been reported between mar-
ginal defects and reduced bone height.18,60,70 The removal of over-
hangs allows for the more effective control of plaque, thereby
resulting in a reduction of gingival inflammation and a small
increase in radiographic alveolar bone support54,63,159 (Figure 7-15).