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14. THE ROLE OF DENTAL CALCULUS AND OTHER LOCAL

PREDISPOSING FACTORS

For a comprehensive reading on this topic, please refer to CHAPTER 13 – THE ROLE OF
DENTAL CALCULUS AND OTHER LOCAL PREDISPOSING FACTORS from Carranza’s
Clinical Periodontology, 13th ed., 2018.

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.

1. 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 incisors. The color is influenced by contact with substances such as tobacco and food
pigments. It may be localized 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 (Fig. 13.1) and the lingual surfaces of the mandibular anterior teeth
(Fig. 13.2) (37).
Subgingival calculus is located below the crest of the marginal gingiva and therefore is not
visible on routine clinical examination. The location and the extent of subgingival calculus may be
evaluated by careful tactile perception with a delicate dental instrument such as an explorer.
Subgingival calculus is typically hard and dense; it frequently appears to be dark brown or greenish
black in color (Fig. 13.3), 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 (Fig. 13.4A). Thus, supragingival calculus can be composed of both the initial
supragingival calculus and previous subgingival calculus.
Both supragingival calculus and subgingival calculus may be seen on radiographs. Highly calcified
interproximal calculus deposits are readily detectable as radiopaque projections that protrude into the
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interdental spaces (Fig. 13.5).

Composition
Inorganic Content: dental calculus is primarily composed of inorganic components (70% to 90%)
(59) and the organic components constitute the rest. The major inorganic proportions of calculus are
calcium phosphate (Ca3[PO4]2), calcium carbonate (CaCO3), magnesium phosphate (Mg3[PO4]2),
carbon dioxide, and traces of other elements such as sodium, zinc, strontium, bromine, copper, manganese,
tungsten, gold, aluminum, silicon, iron, and fluorine (132, 206). The percentage of inorganic constituents
in calculus is similar to that of other calcified tissues of the body (Table 13.1). At least two-thirds of the
inorganic component is crystalline in structure (103). The four main crystal forms and their approximate
percentages are as follows: hydroxyapatite, magnesium whitlockite, octacalcium phosphate, and
brushite.
Organic Content: the organic component of calculus consists of a mixture of protein–
polysaccharide complexes, desquamated epithelial cells, leukocytes, and various types of
microorganisms (116). Salivary proteins include most amino acids. Lipids appear in the form of neutral
fats, free fatty acids, cholesterol, cholesterol esters, and phospholipids (110). The composition of
subgingival calculus is similar to that of supragingival calculus, with some differences.

Formation

Calculus is mineralized dental plaque. The soft plaque is hardened by the precipitation of mineral
salts, which usually starts between the 1st and 14th days of plaque formation. Calcification has been
reported to occur within as little as 4 to 8 hours (192). Calcifying plaques may become 50% mineralized in
2 days and 60% to 90% mineralized in 12 days (131, 170, 179). All plaque does not necessarily undergo
calcification.
Saliva is the primary source of mineralization for supragingival calculus, whereas the serum
transudate called gingival crevicular fluid furnishes the minerals for subgingival calculus (80, 188).
The calcification of supragingival plaque and the attached component of subgingival plaque begins
along the inner surface adjacent to the tooth structure. Calculus is formed in layers, which are often
separated by a thin cuticle that becomes embedded in the calculus as calcification progresses (118). The
initiation of calcification and the rate of calculus accumulation vary among individuals, among tooth
variety in the same dentition, and at different times in the same person (132, 195). On the basis of these
differences, persons may be classified as heavy, moderate, or slight calculus formers or as noncalculus
formers. The average daily increment in calculus formers is from 0.10% to 0.15% of dry weight calculus
(179, 195). Calculus formation continues until it reaches a maximum, after which it may be reduced in
amount.

Role of Microorganisms in the Mineralization of Calculus: Mineralization of plaque

generally starts extracellularly around both Gram-positive and Gram-negative organisms, but it may
also start intracellularly (99). Bacterial plaque may actively participate in the mineralization of calculus
by forming phosphatases, which change the pH of the plaque and induce mineralization (43, 114), but
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the prevalent opinion is that these bacteria are only passively involved (60, 162, 205), and are simply
calcified with other plaque components.

Etiologic Significance

Distinguishing between the effects of calculus and plaque on the gingiva is difficult, because
calculus is always covered with a non-mineralized layer of plaque (169). A positive correlation between
the presence of calculus and the prevalence of gingivitis exists (156), but this correlation is not as great
as that between plaque and gingivitis (62). The initiation of periodontal disease in young people is
closely related to plaque accumulation, whereas calculus accumulation is more prevalent in chronic
periodontitis found in older adults (62, 106).
Calculus does not contribute directly to gingival inflammation, but it provides a fixed nidus for the
continued accumulation of bacterial plaque and its retention in close proximity to the gingiva (Fig. 13.12).
Periodontal pathogens such as Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and
Treponema denticola have been found within the structural channels and lacunae of supragingival and
subgingival calculus (136, 137).
Subgingival calculus is likely to be the product rather than the cause of periodontal pockets. Plaque
initiates gingival inflammation, which leads to pocket formation, and the pocket in turn provides a
sheltered area for plaque and bacterial accumulation. The increased flow of gingival crevicular fluid
associated with gingival inflammation provides the minerals that mineralize the continually accumulating
plaque, resulting in the formation of subgingival calculus (Fig. 13.13).
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 constitutes the cornerstone 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 areas where plaque
removal is impossible.

2. 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 (211, 214).
Characteristics of dental restorations and removable partial dentures 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,
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- the contour of the restorations

- the occlusion
- the materials used in the restoration
- the restorative procedure itself
- the design of the removable partial denture.

a. 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 (2) inhibiting the patient’s access to remove
accumulated plaque. The location of the gingival margin of a restoration is directly related to the health
status of the adjacent periodontal tissues (181). Numerous studies have shown a positive correlation
between restoration margins located apical to the marginal gingiva and the presence of gingival
inflammation (58, 76, 85, 159, 183). Even high-quality restorations with clinically perfect margins, if
placed subgingivally, will increase plaque accumulation, gingival inflammation (98, 101, 129, 134, 160,
182) and the rate of gingival crevicular fluid flow (13, 63). Margins placed at the level of the gingival
crest induce less severe inflammation, whereas supragingival margins are associated with a degree of
periodontal health similar to that seen with non-restored interproximal surfaces (52, 181).
Roughness in the subgingival area is considered to be a major contributing factor to plaque
buildup and subsequent gingival inflammation (181).
b. Retained Cement and Periimplantitis
Periimplantitis is an inflammatory disease of the tissues around dental implants resulting in
progressive bone loss (Fig. 13.20A and B), whereas periimplant mucositis is a reversible inflammatory
change of the soft tissues around implants without bone loss (107). Presumably periimplantitis infectious
organisms arise from the sulcular microbiota of the natural dentition (7). Local factors such as retained
residual cement or inadequate seating of the implant abutment or prosthesis can lead to bone loss around
an implant (see Fig. 13.20C–E).
c. Contours and Open Contacts
Overcontoured crowns and restorations tend to accumulate plaque and handicap oral hygiene
measures in addition to possibly preventing the self-cleaning mechanisms of the adjacent cheek, lips, and
tongue (6, 95, 130, 209) (Fig. 13.21). Restorations that fail to reestablish adequate interproximal
embrasure spaces are associated with papillary inflammation. Undercontoured crowns that lack a
protective height of contour do not retain as much plaque as overcontoured crowns and therefore may
not be as detrimental during mastication as once thought (209).
d. Restorative Materials
In general, restorative materials are not in themselves injurious to the periodontal tissues (6, 88).
One exception to this may be self-curing acrylics (203) (Fig. 13.22). Plaque that forms at the margins of
restorations is similar to that found on adjacent non-restored tooth surfaces. The composition of plaque
formed on all types of restorative materials is similar,with the exception of that formed on silicate
(1350. Although surface textures of restorative materials differ with regard to their capacity to retain
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plaque (206), all can be adequately cleaned if they are polished and accessible to methods of oral
hygiene (138, 184).

e. Design of Removable Partial Dentures

After the insertion of partial dentures, mobility of the abutment teeth, gingival
inflammation, and periodontal pocket formation all increase (18, 29, 174). This is because
partial dentures favor the accumulation of plaque, particularly if they cover the gingival
tissue. Partial dentures that are worn during both night and day induce more plaque formation
than those worn only during the daytime (18). These observations emphasize the need for
careful and personalized oral hygiene instruction.

f. Restorative Dentistry Procedures

The use of rubber dam clamps, matrix bands, and burs in such a manner as to lacerate
the gingiva results in varying degrees of mechanical trauma and inflammation. Although such
transient injuries generally undergo repair, they are needless sources of discomfort to the
patient. The forceful packing of a gingival retraction cord into the sulcus to prepare the
subgingival margins of a tooth or for the purpose of obtaining an impression may
mechanically injure the periodontium and leave behind impacted debris that is capable of
causing a foreign body reaction.

Malocclusion

The irregular alignment of teeth as found in cases of malocclusion may facilitate plaque
accumulation and make plaque control more difficult. However, uneven marginal ridges of
contiguous posterior teeth have been found to have a low correlation with pocket depth, loss
of attachment, plaque, calculus, and gingival inflammation (90).
Roots of teeth that are prominent in the arch (Fig. 13.23) - such as in a buccal or
lingual version or that are associated with a high frenal attachment and small quantities of
attached gingiva - frequently exhibit recession (1, 124).
Tongue thrusting exerts excessive lateral pressure on the anterior teeth, which may
result in the spreading and tilting of the anterior teeth (Fig. 13.24). Tongue thrusting is an
important contributing factor to tooth migration and the development of an anterior open bite
(30). Mouth breathing may be observed in association with a habit of tongue thrusting and an
anterior open bite. Marginal and papillary gingivitis is frequently encountered in the
maxillary anterior sextant in cases that involve an anterior open bite with mouth breathing.
Restorations that do not conform to the occlusal pattern of the mouth result in
occlusal disharmonies that may cause injury to the supporting periodontal tissues. More
issues involving deeper initial probing depths, worse prognoses, and greater mobility have
been observed for teeth with occlusal discrepancies as compared with teeth without initial
occlusal discrepancies (69, 139).
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Periodontal Complications Associated with Orthodontic Therapy

Orthodontic therapy may affect the periodontium by favoring plaque retention, by directly
injuring the gingiva as a result of overextended bands, and by creating excessive forces,
unfavorable forces, or both on the tooth and its supporting structures.

a. Plaque Retention and Composition: Orthodontic appliances tend to retain bacterial plaque and
food debris, thereby resulting in gingivitis (Fig. 13.25), and they are also capable of modifying
the gingival ecosystem.

b. Gingival Trauma and Alveolar Bone Height: Orthodontic treatment is often started soon after
the eruption of the permanent teeth, when the junctional epithelium is still adherent to the enamel
surface. Orthodontic bands should not be forcefully placed beyond the level of attachment,
because this will detach the gingiva from the tooth and result in the apical proliferation of the
junctional epithelium with an increased incidence of gingival recession (146).

The mean alveolar bone loss per patient for adolescents who underwent 2 years of orthodontic
care during a 5-year observation period ranged between 0.1 and 0.5 mm (21). This small
magnitude of alveolar bone loss was also noted in the control group and therefore is considered to
be of little clinical significance. However, the degree of bone loss during adult orthodontic care
may be higher than that observed in adolescents, especially if the periodontal condition is not
treated before the initiation of orthodontic therapy (113). Orthodontic treatment in adults with
active periodontitis (evidenced by deep pockets and bleeding on probing) has been shown to
accelerate the periodontal disease process (8, 45, 212).

c. Tissue Response to Orthodontic Forces: Alveolar bone is remodeled by osteoclasts that induce
bone resorption in areas of pressure and by osteoblasts that form bone in areas of tension.
Although moderate orthodontic forces ordinarily result in bone remodeling and repair, excessive
force may produce necrosis of the periodontal ligament and the adjacent alveolar bone (149-151).
Excessive orthodontic forces also increase the risk of apical root resorption (25, 26). Risk factors
associated with root resorption during orthodontic treatment include the duration of treatment, the
magnitude of the force applied, the direction of the tooth movement, and the continuous versus
intermittent application of forces (148) (Fig. 13.26).

Extraction of Impacted Third Molars

The extraction of impacted third molars often results in the creation of vertical defects distal to the
second molars (9, 96, 121). This iatrogenic effect is unrelated to flap design (1530, and it appears to
occur more often when third molars are extracted from individuals who are more than 25 years old (9,
96, 121). Other factors that appear to play a role in the development of lesions on the distal surface of
second molars - particularly in those who are more than 25 years old - include the presence of visible
plaque, bleeding on probing, root resorption in the contact area between the second and third molars,
the presence of a pathologically widened follicle, the inclination of the third molar, and the close
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proximity of the third molar to the second molar (96) (Fig. 13.29).

Habits and Self-Inflicted Injuries

Patients may not be aware of their self-inflicted injurious habits that may be important to the
initiation and progression of their periodontal disease. Mechanical forms of trauma can stem from the
improper use of a toothbrush, the wedging of toothpicks between the teeth, the application of fingernail
pressure against the gingiva (Fig. 13.31), pizza burns, and other causes (20). Sources of chemical
irritation include the topical application of caustic medications such as aspirin or cocaine, allergic
reactions to toothpaste or chewing gum, the use of chewing tobacco, and concentrated mouthrinses
(177). Accidental and iatrogenic gingival injuries may be caused by a variety of chemical, physical, and
thermal sources, yet they are generally self-limited. Iatrogenic injuries are often acute, whereas factitious
injuries tend to be more chronic in nature (157).
a.Trauma Associated With Oral Jewelry
The use of piercing jewelry in the lip or tongue has become more common among teenagers and
young adults (Fig. 13.32A). However, piercings are associated with potential complications including
gingival injury or recession (70, 100, 104, 213, 217); damage to teeth, restorations, and fixed porcelain
prostheses (48, 54, 70, 104); increased salivary flow (54, 197); interference with speech, mastication, or
deglutition (84, 198); scar tissue formation (197); and development of metal hypersensitivities (93).
b. Toothbrush Trauma
The gingival changes that are attributable to toothbrush trauma may be acute or chronic. The acute
changes vary with regard to their appearance and duration, from scuffing of the epithelial surface to
denudation of the underlying connective tissue with the formation of a painful gingival ulcer (Fig.
13.33). Diffuse erythema and denudation of the attached gingiva throughout the mouth may be a striking
result of overzealous brushing. Signs of acute gingival abrasions are frequently noted when the patient
first uses a new brush.
Chronic toothbrush trauma results in gingival recession with denudation of the root surface.
Interproximal attachment loss is generally a consequence of bacteria-induced periodontitis, whereas
buccal and lingual attachment loss is frequently the result of toothbrush abrasion (185). The improper use
of dental floss may result in lacerations of the interdental papilla.
c. Chemical Irritation
Acute gingival inflammation may be caused by chemical irritation that results from either
sensitivity or nonspecific tissue injury. In allergic inflammatory states, the gingival changes range
from simple erythema to painful vesicle formation and ulceration. Severe reactions to ordinarily
innocuous mouthwashes, dentifrices, and denture materials are often explainable on this basis.
Acute inflammation with ulceration may be produced by the nonspecific injurious effect of
chemicals on the gingival tissues. The indiscriminate use of strong mouthwashes, the topical
application of corrosive drugs such as aspirin (Fig. 13.34) or cocaine, and accidental contact with
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drugs such as phenol or silver nitrate are common examples of chemical exposures that cause
irritation of the gingiva.

Smokeless Tobacco
Snuff and chewing tobacco constitute the two main forms of smokeless tobacco. Snuff is a fine-cut
form of tobacco that is available loosely packed or in small sachets. Chewing tobacco is a more coarse-
cut tobacco that is available in the form of loose leaves, a solid block, a plug, or a twist of dried leaves.
Chewing tobacco is typically placed in the mandibular buccal vestibule for several hours, during which
time saliva and dilute tobacco are periodically expectorated (204). The perceive benefits of chewing
tobacco are those derived from nicotine, including improved mental alertness, diminished reaction time,
muscle relaxation, and reduced anxiety and appetite (65, 163).
The use of smokeless tobacco is associated with at least localized gingival recession, clinical
attachment loss, leukoplakia, and possibly enhanced susceptibility to severe periodontitis.

Radiation Therapy
Radiation therapy has cytotoxic effects on both normal cells and malignant cells. The total dose
of radiation is usually given in partial incremental doses, and this is referred to as fractionation.
Fractionation helps to minimize the adverse effects of radiation while maximizing the death rate for the
tumor cells (51).
Radiation treatment induces an obliterative endarteritis that results in soft tissue ischemia and
fibrosis; irradiated bone becomes hypo- vascular and hypoxic (119). Adverse effects of head and neck
radiation therapy include dermatitis and mucositis of the irradiated area as well as muscle fibrosis and
trismus, which may restrict access to the oral cavity (166). The mucositis typically develops 5 to 7 days
after radiation therapy is initiated. The severity of the mucositis can be reduced by asking the patient to
avoid secondary sources of irritation (e.g., smoking, alcohol, spicy foods) to the mucous membrane. The
use of a chlorhexidine digluconate mouthrinse may help to reduce the mucositis (155). Xerostomia
results in greater plaque accumulation and a reduced buffering capacity of saliva. Effective oral hygiene,
professional dental prophylactic cleanings, fluoride applications, and frequent dental examinations are
essential to control caries and periodontal disease.
Among cancer patients who were treated with high-dose unilateral radiation, periodontal
attachment loss and tooth loss were reported to be greater on the irradiated site compared with the
nonradiated control side of the dentition (44). Patients with oral cancer and who require radiation
therapy should ideally be assessed for dental needs (i.e., mucositis, xerostomia, faulty restorations,
periapical lesion, coronal and cervical decay, and periodontal status) before the initiation of radiation
treatment (68). The treatment and prevention of trismus, oral fungal infections, odontogenic infections,
osteoradionecrosis, decay, and periodontal disease are critical to minimize oral morbidity for these
patients. Dental and periodontal infections have the potential to be severe risks for patients who have
been treated with head and neck radiation.
Oral conditions that increase the risk of osteoradionecrosis for patients about to undergo
radiation therapy for oral malignancies include periodontal probing depths of more than 5 mm, dental
plaque score of more than 40%, and alveolar bone loss of more than 60% (87). Non-restorable teeth and
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teeth with significant periodontal problems should be extracted before radiation therapy to reduce the
risk of postradiotherapy osteoradionecrosis (91).
The risk of osteoradionecrosis must be evaluated before the performance of atraumatic
extractions or limited periodontal surgical procedures in previously irradiated sites. Therefore, the
dentist may choose to consult with the patient’s oncologist before the initiation of dental therapy.
The administration of the combination of pentoxifylline with vitamin E as antioxidant therapy
currently shows the greatest promise for revascularization and treatment of osteoradionecrosis sites (39).