Dental Calculus and Other Contributing Factors :

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HISTORICAL PERSPECTIVE
Albucasis (936–1013 AD), an Arabian physician and surgeon, defined the relationship between calculus and dental disease and explained the need for the thorough removal of deposits. Albucasis described the way to remove calculus from teeth. Paracelsus (1493-1541) developed an interesting theory called as doctrine of calculus. He understood that pathologic calcification occurred in a variety of organs, and he considered these disease conditions to result from a metabolic disturbance whereby the body takes nourishment from food and discards the refuse as “tartarus”, a material that cannot be broken. This tartar consisting of gravel and gluelike components was considered to came from barley, peas, milk, meat and fish, and drinks such as wine, beer, and fruit juice. The amount of tartar formed depended on the region of the body. Paracelsus recognized the extensive formation of tartar on the teeth and related this to toothache. Until the 1960s, the prevalent thinking in dentistry was that dental calculus was the cause of periodontal diseases; that by its roughness it was irritating and that bacteria then had a secondary
influence. However, a series of classic studies on experimental gingivitis published from 1965 to 1968 clearly demonstrated the causative relation between dental plaque and gingivitis. Current thinking is that dental plaque is the precursor of calculus, which is mineralized plaque. Calculus is invariably covered with plaque on its surface.
DEFINITION
Dental Calculus is an adherent, calcified or calcifying mass that forms on the surfaces of teeth and dental appliances.
TYPE/CLASSIFICATION
It is classified according to its relation to the gingival margin as supragingival and subgingival calculus (Table .1).
The various forms of submarginal and subgingival calculus are shown in (Fig. 1).
Spicules: Small isolated pieces of calculus. These are frequently located at line angles and interdental areas.
Ledge: A larger deposit that forms on a section of the tooth and is approximately parallel to the cementoenamel junction (CEJ).
Ring form: A ledge like deposit that encircles the tooth, forming a ring of calculus. In addition to calculus, roughness on the tooth surface may be caused by rough restorations, carious lesion, or necrotic cementum.
TABLE 1: Differences between supragingival calculus and subgingival calculus
Supragingival calculus Subgingival calculus
1-Color
2-Shape
3- Consistency
4-Attachment
5-Location
6-Visibility
7-Composition
8-Source
9-Distribution
White or whitish yellow
Amorphous bulky, shape of calculus is determined
by anatomy of teeth, contour of gingival margin and
pressure of tongue, lips or cheeks
Moderately hard
Easily detached from tooth
Coronal to the gingival margin (Fig.2)
Visible in the oral cavity
More brushite and octacalcium phosphate.
Less Magnesium whitlockite.
Salivary proteins are present.
Sodium content is lesser.
Derived from salivary secretions
Symmetrical arrangement on teeth, more on facial
surface of maxillary molars and lingual surface of
mandibular anterior teeth due to openings of salivary
glands ducts (Fig.4).
Dark brown/genuine black
Flattened to conform with pressure from the pocket wall.
May be crusty, shiny, thin, finger and fern like.
Flint like, brittle
Firmly attached to the tooth surface
Below the crest of the marginal gingiva (Fig. 3).
Not visible on routine clinical examination
Less brushite and octacalcium phosphate.
More Magnesium whitlockite.
Salivary proteins are absent.
Sodium content increases with the depth of pocket.
Formed from gingival exudate
Related to pocket depth, heaviest on proximal surfaces.
                               
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Fig. 1: Forms of subgingival calculus   



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Fig. 2: Supragingival calculus



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Fig.3: Subgingival calculus   



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Fig..4: Calculus at lingual surfaces of mandibular anterior teeth
                         
                              




COMPOSITION OF CALCULUS
1. Inorganic content
a. Elements: Calcium (39%), phosphorus (19%), carbon dioxide (1.9%), magnesium (0.8%) and traces of sodium, zinc, strontium, bromine, copper, manganese, tungsten, gold, aluminium, silicon, iron, fluorine.
b. Compounds: Calcium phosphate (75.9%), calcium carbonate (3.1%) and traces of magnesium phosphate and other metals.
c. Crystals: Hydroxyapatite (58%), magnesium whitlockite (21%), octacalcium phosphate (12%) and brushite ( 9%) are the four main forms of crystals present.
2. Organic content: 1.9 to 9.1% of carbohydrates (galactose, glucose, rhamnose, mannose, glucuronic acid, galactosamine, arabinose, galacturonic acid, glucosamine); 5.9 to 8.2% of proteins; 0.2% of lipids (Neutral fats, fatty acids, cholesterol, phospholipids, cholesterol esters); Protein polysaccharide complexes; Desquamated epithelial cells; Leukocytes and microorganisms.
3. Bacterial content: At periphery – Gram-negative rods and cocci predominate. Filamentous organisms, Diphtheroids, Bacterionema and Veillonella species are also present.
CALCULUS FORMATION
Mineralization consists of crystal formation, namely hydroxyapatite, octacalcium phosphate, magnesium whitlockite, and brushite each with a characteristic developmental pattern. The crystal forms in the intercellular matrix, on the surface of bacteria and finallywithin the bacteria. The mineralization process is considered the same for both supragingival and subgingival calculus. The initiation of calcification and the rate of calculus accumulation vary from person-toperson, for different teeth and at different times in the same person. On the basis of these differences, persons may be classified as heavy, moderate, or slight calculus formers or as noncalculus formers. Heavy calculus formers have higher salivary levels of calcium and phosphorus than do light calculus formers. Light calculus formers have higher levels of parotid pyrophosphate. Pyrophosphate is an inhibitor of calcification.
Theories Related to Mineralization of Calculus
1. Booster/precipitation theory: Loss of carbon dioxide and formation of ammonia leads to increase in the pH which leads to the precipitation of calcium phosphate salts.
2. Epitactic/Nucleation concept: The carbohydrate – protein complexes may initiate calcification by removing calcium from the saliva and binding with it to form nuclei that induce deposition of minerals. Seeding agents induce small foci of calcification that enlarges and unites together to form calcified mass.
3. Inhibition theory: Calcification occurring only at specific site is because of the existence of an inhibiting mechanism at noncalcifying sites. Where calcification occurs, the inhibitor is apparently altered or removed. Inhibiting substance is thought to be pyrophosphate and among the controlling mechanism is the enzyme alkaline pyrophosphatase, which can hydrolyze the pyrophosphate to phosphate. The pyrophosphate inhibits calcification by preventing the initial nucleus from growing, possibly by “poisoning” the growth centers of the crystal.
4. Transformation theory: Amorphous noncrystalline deposits and brushite can be transformed to octacalcium phosphate and then to hydroxyapatite.



CLINICAL ASSESSMENT
The clinical assessment can be done by:
1. Visual examination by use of compressed air: Small amount of supragingival calculus that have not been stained are frequently invisible when they are wet with saliva. Subgingival calculus deposits can sometimes be detected visually by blowing air down the gingival crevice. Dark edge of calculus may be seen at or just beneath the gingival margin. An explorer may be used when visual examination is not definite.
2. Probing: A fine subgingival explorer or probe is needed that can be adapted close to the root surface all the way to the bottom of a pocket. Each subgingival area must be examined carefully to the bottom of the pocket, completely around each teeth. While probing for sulcus/pocket a rough subgingival tooth surface can be felt when calculus is present Although there are other causes of roughness, subgingival calculus is the most common.
3. Radiographs: The deposits may also be visible on radiographs although this is not always reliable.
Radiographs may be useful in diagnosis of subgingival calculus (Fig.5). The location of calculus does not indicate the bottom of the periodontal pocket because the most apical plaque is not sufficiently calcified to be visible on radiographs.
4. Clinical records: The various indices for recording and scoring calculus are explained in chapter no. 7 Epidemiology of Gingival and Periodontal diseases.




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Fig. 5: Subgingival calculus seen in radiograph




MODES OF ATTACHMENT OF CALCULUS TO THE TOOTH SURFACE AND IMPLANT
Helmut A. Zander in 1952 described four types of calculus attachment (Figs .6A to D):
1. Attachment by means of an organic pellicle.
2. Mechanical locking into surface irregularities such as resorption lacunae and caries. This type of attachment make the removal of calculus difficult as calculus embedded beneath the cementum surface penetrates into the dentin.
3. Penetration of calculus bacteria into cementum.
4. Close adaptation of calculus undersurface depressions to the gently sloping mounds of the unaltered
cementum surface.
Shroff later theorized that the type of calculus attachment probably depends on the length of time the calculus has been on the tooth. The attachment of calculus to pure titanium implant is less intimate than to root surface.


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Figs 6A to D: Modes of attachment of calculus



ROLE OF CALCULUS IN PERIODONTAL DISEASE
Calculus may be harmful both physically and chemically to adjacent gingiva. Calculus is permeable and thus, may absorb and adsorb toxic products. Calculus is rough and porous which facilitates the retention of dental plaque. Calculus is always covered with unmineralized plaque which provides further retention and promotes new plaque accumulation and thus, causes periodontal destruction in the following manner:
• Calculus brings bacterial overlay closer to the supporting tissues
• Interfere with local self-cleansing mechanism
• Provide nidus for continuous plaque accumulation.
• Make plaque removal more difficult.


LOCAL CONTRIBUTING FACTORS
1. Anatomic factors
a. Proximal contact relation: The integrity and location of the proximal contacts along with the contour of the marginal ridges and developmental grooves typically prevent interproximal food
impaction. Food impaction is the forceful wedging of food into the periodontium by occlusal forces.
Hirschfeld in 1930 classified vertical food impaction relative to etiologic factors:
Class I – Occlusal wear
Class II – Loss of proximal support
Class III – Extrusion of a tooth beyond the occlusalplane
Class IV – Congenital morphologic abnormalities
Class V – Improperly constructed restorations
Sequelae of food impaction:
• Feeling of pressure and the urge to dig the
material from between the teeth.
• Vague pain which radiates deep in the jaws.
• Gingival inflammation with bleeding and a foul taste in the involved area.
• Gingival recession.
• Periodontal abscess formation.
• Varying degree of inflammatory involvement of the periodontal ligament with an associated elevation of the tooth in its socket, prematurity in functional contact and sensitivity to
percussion.
• Destruction of alveolar bone.
• Caries of the tooth.
Plunger cusps are the cusps that tend to forcibly wedge food into interproximal embrasures of opposing teeth. Distolingual cusps of maxillary molars are the most common plunger cusp. Plunger cusp effect may occur with wear or it may be the result of a shift in tooth positions following the failure to replace missing tooth.
b. Cervical enamel projection (CEP) and enamel pearls: They appear as narrow wedge-shaped extensions of enamel pointing from the cementoenamel junction (CEJ) toward the furcation area. The clinical significance of CEPs is that they are plaque retentive and can predispose to furcation involvement.
c. Intermediate bifurcation ridge: The intermediate bifurcation ridge is a convex excrescence of cementum that runs longitudinally between the mesial and distal roots of a mandibular molar. It may be located at the midpoint between the buccal and lingual surfaces of the area of root division or it may be located in a more lateral position. These ridges are found more frequently on first molars. These irregular contours make plaque and calculus removal more difficult and inadequate plaque and calculus removal can lead to failure of furcation treatment, especially regenerative therapy.
d. Palatogingival groove: The palatogingival groove frequently termed the palatoradicular groove, often begins at the cingulum and extends apically for a variable distance (Fig.7A). Deep pocketing of maxillary incisors, especially isolated, should prompt an examination for this plaque – retentive root anomaly (Fig.7B). If the palatogingival groove is associated with bone loss and attachment loss, the clinician may attempt to remove the groove through odontoplasty or to reduce its depth to minimize plaque retention (Fig 7C).


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Figs 7A to C: (A) Palatogingival groove at the cingulum of lateral incisor. (B) Pocket associated with palatogingival groove (C) Bone loss associated with palatogingival groove




e. Root proximity: Close approximation of tooth roots, with an accompanying thin interproximal septum leads to an increased risk for periodontal destruction.
2. Iatrogenic factors: Inadequate dental procedures that contribute to the deterioration of the periodontal tissues are referred to as iatrogenic factors.
a. Restorative dentistry: The improper use of rubber dam clamps, matrix bands and burs can lacerate the gingiva resulting in varying degree of mechanical trauma and inflammation. Restorations can do more harm than good to the
patient’s oral health if performed improperly (Fig. 8). Overhanging margins of restorations and crowns accumulate additional the patient’s access.


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Fig. 8: Interproximal bone boss associated with overhanging restoration predisposing to plaque retention




b. Prosthesis: Gross iatrogenic irritants such as poorly designed clasps, prosthesis saddles and pontics exert a direct traumatic influence upon periodontal tissues (Fig. 9).




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Fig. 9: Inflammatory gingival changes around fixed partial prosthesis



c. Orthodontic procedures: Orthodontic therapy may affect the periodontium by favoring plaque retention, by directly injuring the gingiva as a result of overextended bands, chemical irritation by exposed cement (Fig. 10) and by creating excessive, unfavorable forces, or both.
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Fig. 10: Gingival hyperplasia in lower anteriors due to chemical irritation by exposed cement



d. Extraction of impacted third molar: The extraction of impacted third molars often results in the creation of vertical bone defects distal to the second molars. Careless use of elevators or forceps during extraction results in crushing of alveolar bone.
3. Malocclusion as contributing factors: Crowded or malaligned teeth can be more difficult to clean than properly aligned teeth. In deepbite, maxillary incisors impinge on the mandibular labial gingiva or mandibular incisors on the palatal gingiva, causing gingival and periodontal inflammation (Fig.11). Failure to replace missing posterior teeth have adverse consequences on the periodontal support for the remaining teeth. When the mandibular first molar is extracted, the initial change is a mesial drifting and tilting of the mandibular second and third molars with extrusion of the maxillary first molar. As the mandibular second molar tips mesially, its distal cusps extrude and act as plungers. The distal cusps of the mandibular second molar wedge between the maxillary first and second molars and open the contact by deflecting the maxillary second molar distally. Subsequently, food impaction may occur and accompanied by gingival inflammation with eventual loss of the interproximal bone between the maxillary
first and second molars.



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Fig. 11: Deep bite causing gingival and periodontal inflammation
4. 

Habits as contributing factors
a. Toothbrush and floss trauma: The toothbrush maycause damage to dental soft and hard tissues. A new toothbrush, and especially a hard toothbrush, can abrade epithelium and leave painful ulcerations on the gingiva. Thin marginal gingiva that is abraded away can lead to gingival recession and exposure of the root surface. The tooth surface, usually the root surface, can be abraded away by improper toothbrushing technique, especially with a hard toothbrush. The abrasives in toothpaste may contribute significantly to this process. The defect usually manifests as V-shaped notches at the level of the CEJ (Fig. 12). Flossing can also cause damage to dental hard and soft tissues. Flossing clefts may be produced when floss is forcefully snapped through the contact point so that it cuts into the gingiva. Also, an aggressive up and down cleaning motion can produce a similar injury.



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Fig. 12 : Toothbrushing abrasion


b. Mouth breathing and tongue thrusting: Mouth breathing can dehydrate the gingival tissues andincrease susceptibility to inflammation. These patients may or may not have increased levels of dental plaque. In some cases, gingival enlargement may also occur. Excellent plaque control and professional cleaning should be recommended, although these measures may not completely resolve the gingival inflammation. Tongue thrusting is often associated with an anterior open bite. During swallowing the tongue is thrust forward against the teeth instead of being placed against the palate. When the amount of pressure against the teeth is great, it can lead to tooth mobility and cause increased spacing of the anterior teeth. This problem is difficult to treat but must be recognized in the diagnostic phase as a potentially destructive contributing factor.
c. Tobacco use: Smoking is one of the most significant risk factors currently available to predict the development and progression of periodontitis (Fig. 13). Rest is explained in chapter no 16. Smoking and Periodontium.


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Fig. 13: Tobacco stains


d. Factitious injuries: Self-inflicted or factitial injuries can be difficult to diagnose because their presentation is often unusual. These injuries are produced in a variety of ways including pricking the gingiva with a fingernail (Fig. 14), with knives and by using toothpicks or other oral hygiene devices.



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Fig. 14: Localized gingival recession due to pricking the gingiva with a fingernail (Courtesy: Dr. Ajay Mahajan)



LANDMARK STUDIES RELATED
Lang NP, Hotz P, Graf H, Geering AH, Saxer VP, Sturzenberger OP, Mechel AH. Effects of supervised chlorhexidine mouthrinses in children. Journal of Periodontal Research 1982; 17: 101-11.
The study was done on 158 children (aged 10–12 years). They were divided into four groups, Group A was assigned to daily mouthrinses 6 times per week using a 0.2% solution of chlorhexidine gluconate, Group B used the same solution only twice per week, and Group C was assigned to daily rinsing using a 0.1% solution of chlorhexidine gluconate. Group D served as control and rinsed daily with a placebo solution. All the rinsings were supervised and timed for 30 seconds. No attempt was made to influence the oral hygiene habits of the children. Prior to the initial prophylaxis and after 6 months of supervised rinsing, plaque was scored using the Plaque Index (PlI), and gingivitis was assessed using the gingival index (GI). Calculus was scored according to the calculus surface index (CSI), and stain was also graded. At the end of the study it was found that plaque was significantly reduced whereas, calculus was increased significantly in all the groups when compared with the controls. Thus, it was concluded that there was statistically significant increase in calculus levels in children rinsing with a 0.2% chlorhexidine gluconate solution. It was postulated that dead bacteria had accumulated on the tooth surfaces, acting as sites for calculus deposition.
Gaare D, Rolla G, Aryadi FJ, Vander Ouderaa F. Improvement of gingival health by tooth brushing in individuals with large amounts of calculus. Journal of Clinical Periodontology 1990; 17: 38-41.
This study was conducted on Indonesian soldiers of 20 - 25 years of age having large amount of calculus. In one half of the subjects (Group A) careful professional prophylaxis was performed, while in the other half (Group B), tooth brushing was the sole oral hygiene aid. Gingival health in both groups improved after 2 months: from 63 to 36% bleeding points in group A, and from 61 to 36% in group B. There was thus no obvious benefit from the professional prophylaxis received by group A. The improvement of gingival health through tooth brushing, in spite of the presence of calculus, supports the contention that plaque, rather than calculus, as a noninflammatory
POINTS TO PONDER
Reversal phenomenon is the decline from maximal calculus accumulation. It is due to vulnerability of bulky calculus to mechanical wear from food, cheeks, lips and tongue.
Calculus can also occur readily in germ free animals.
Calculocementum is the calculus embedded deeply in the cementum and which appears morphologically similar to cementum.
Calculus is the most prominent plaque retentive factor and is a secondary etiologic factor for periodontitis.
BIBLIOGRAPHY
1. Grant DA, Stern IB, Listgarten MA. Calculus. In, Periodontics. 6th ed CV Mosby Company 1988; 198-215.
2. Hinrichs JE. The role of calculus and other predisposing factors. In, Newman, Takei, Carranza. Clinical Periodontology 9th ed WB Saunders 2003; 182-203.
3. Lang NP, Mombelli A, Attstrom R. Dental Plaque and Calculus. In, Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant dentistry. 4th ed Blackwell Munksgaard 2003; 81-105.
4. Mandel ID. Dental calculus. In, Genco RJ, Goldman HM, Cohen DW. Contemporary Periodontics. C.V Mosby 1999; 135-46.
5. Wilkins EM. Dental calculus. In, Clinical practice of the dental hygientist. 8th ed Lippincott 1999; 277-84.



MCQs
1. Mineralized plaque is:
A. Materia alba
B. Calculus
C. Food debris
D. Dental stains

2. Calculus
A. Per se is the irritating cause to gingiva
B. It is always covered with a non-mineralized layer of plaque
C. It is formed as all plaque undergoes mineralization
D. Formation cannot be maintained in germ-free animals

3. The most efficient means of identifying supragingival calculus is by:
A. Visual observation and compressed air
B. Tactile detection and periodontal probe
C. Use of disclosing solution
D. Transillumination

4. Dental calculus contains:
A. Vital microorganisms
B. Non-vital microorganisms
C. Both of the above
D. None of the above

5. The most common crystalline forms present in supragingival calculus are:
A. Hydroxyapatite and magnesium whitlockite
B. Hydroxyapatite and octacalcium phosphate
C. Hydroxyapatite and brushite
D. Magnesium whitlockite and octacalcium phosphate

6. Which of the following crystals is more commonly found in the calculus of mandibular anterior areas?
A. Hydroxyapatite
B. Magnesium whitlockite
C. Octacalcium phosphate
D. Brushite

7. Calculocementum is:
A. Calculus similar in composition to cementum
B. Cementum similar in composition to calculus
C. Cementum appearing morphologically similar to calculus
D. Calculus appearing morphologically similar to cementum
Answers
1. B 2. B 3. A 4. B 5. B
6. D 7. D

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