Dental Calculus & it’s role in pathogenesis of periodontal diseases


Dental calculus is calcified dental plaque, composed primarily of calcium phosphate mineral salts deposited between and within remnants of formerly viable microorganisms. The plaque formation serves as an organic matrix for the subsequent mineralization of the deposit. Calcification of dental plaque biofilm results from mineral ions provided by bathing saliva or crevicular fluids. Supersaturation of saliva and plaque fluid with respect to calcium phosphates is the driving force for plaque mineralization. Both salivary flow rate and plaque pH appear to influence the saturation degree of calcium phosphates. Inorganic components of calculus include Brushite, dicalcium phosphate dihydrate, octacalciumphosphate, hydroxyapatite and whitlockite. Supragingival calculus formation can be controlled by chemical mineralization inhibitors, applied in toothpastes or mouthrinses. These agents act to delay plaque calcification, keeping deposits in an amorphous non-hardened state to facilitate removal with regular hygiene. For detailed description on plaque and it’s role in pathogenesis of periodontal diseases please read ” Plaque as biofilm and Ecological plaque hypothesis” and ” Microbiology of periodontal diseases”.

Severe dental calculus deposition

After Scaling and root planing


A few definitions of calculus are given here,

Calculus can be defined as a hard concretion that forms on teeth or dental prostheses through calcification of bacterial plaque. (Glossary of periodontal terms (2001). 4th edn. Chicago: The American academy of periodontology).

Calculus consists of mineralized bacterial plaque that forms on the surface of natural teeth and dental prosthesis. (Carranza’s Clinical Periodontology 11th edition).

Calculus is essentially a mineralized plaque covered on its external surface by vital, tightly adherent, non mineralized plaque .(Genco)

When dental plaque calcifies, the resulting deposit is called calculus. (Grant)


Recognition of calculus as a clinical entity in some way related to periodontal Diseases can be traced as far back as the 10th centuryThe discovery of tooth picks of gold and silver in Sumerian tombs dating as back as 3500 B.C. implies the importance given to oral hygiene and the removal of tooth deposits through out the ages. Perhaps the first formal association between dental deposits and oral disease can be found in the writings of Hippocrates (460 -377 B.C.), the Greek physician who founded modern medicine. He noted the deleterious effects on the teeth and germs of  ‘pituita’ (calculus), which insinuated itself, on the roots of the teeth.

It was Albucasis (936 – 1013), however, an Arabian physician and surgeon, who most clearly enunciated the relationship between calculus and disease and the need for removal of the deposits. He designed a set of scaling instruments for the purpose of removing calculus in patients afflicted with periodontal disease.

In 1535 Paracelus, (a Swiss) – German physician and alchemist, introduced the term ‘tartar’ as a designation for a variety of stony concretions that form in humans, noting their physical comparability to the deposits that develop at the bottom of wine casks. He observed that these tophi could be found about the teeth, in the urinary bladder, in the gallbladder and in gouty joints. Paracelus looked on tartar a; a principal cause of certain maladies, which be termed “tartaric diseases”. (Prinz. 1921) until very recently most dentists agreed with Paracelus and considered periodontal disease to be appropriately placed in the category of tartaric disease. In past 25 years, however calculus has been deposed by plaque in the etiologic hierarchy, and the hardened ‘criminal’ has come to viewed by many as a fossilized remmanant of minor significance (Mandel 1974)-an unfortunate and premature relegation to the ash heap, since the calcified deposits do contribute to the development of pathologic conditions.

Pierre Fauchard in 1728 termed it tartar or slime and referred to it as “a substance which accumulates on the surface of the teeth and which becomes, when left there, a stony crust of more or less considerable volume. Common cause of the loss of teeth is the negligence of these people who do not clean their teeth when they might, and that they perceive the lodgment of this foreign substance which produces diseases of the gums”.


Organized calculus consists of mineralized bacterial plaque. It is classified according to its relation to the gingival margin as,

  • Supragingival calculus.
  • Subgingival calculus.

Supragingival Calculus:

The calculus deposited on the teeth coronal to the gingival margin. Usually lighter in color (unless stained) and less dense than subgingival calculus. Supragingival calculus almost always occurs predominantly on the lingual surface of the 6 lower anterior teeth, with lesser amounts on the buccal surface of the upper molars. It is usually white or whitish, has hard clay like consistency and is easily detached from the tooth surface. It is also called as salivary calculus as most of its mineral component is derived from saliva.

Subgingival Calculus:

The calculus deposited on the tooth structure and found apical to the gingival margin within the periodontal pocket is designated as subgingival calculus. It is usually dense, dark brown or greenish black and has a hard or flint like consistency and it is firmly attached to the tooth surface. It is also known as seminal calculus based on the assumption that subgingival calculus derived from the blood gingival fluid.

 Differences between supragingival and subgingival calculus

Features    Supragingival     Subgingival
Definition Tightly adhering calcified deposit that forms on the crowns of the teeth above the free gingival margin. Calcified deposit that forms on the tooth surface below the free margin of gingival and extends into the periodontal pocket.
Also known as Salivary calculus Seruminal calculus
Visibility Visible in the oral cavity Below the crest of marginal gingiva, usually in periodontal pocket, not visible
Location Most abundant opposite the opening of major salivary glands, lingual surfaces of lower anteriors, buccal surfaces of upper first molars Usually seen in proximal surfaces of teeth and with less frequency on buccal surfaces
Prevalence Usually common upto the age of 9 years0-15 yrs: 37-70%
16-21 yrs: 44-88%
Above 40 yrs: 86-100%.
Slightly lower than that of supragingival, but approaches a range of 47- 100% after age of 40 yrs.
Color White or whitish yellow can be influenced with exposure to food, tobacco and with age Dark brown /green black. Not influenced by food and tobacco
Consistency Hard clay-like Dense flint-like
Attachment Lightly attached to the surface Firmly attached
Source of minerals Salivary secretions GCF
Plaque overlying Composed of primarily filamentous organism oriented perpendicular to underlying calcified deposit Consist of cocci, rods, filaments with no distinct pattern of alignment
Composition Mainly brushite and octacalcium phosphate More amount of magnesium whitlokite, less of brushite and octacalcium phosphate. 
Higher concentration of Ca, Mg and F than supragingival calculus
Salivary protein Found Not found
Sodium content Decreased Increased

Composition and Structure of Dental Calculus:

Dental calculus is composed of inorganic as well as organic components. The organic component of calculus consists of a mixture of protein polysaccharide complexes, desquamated epithelial cells, leukocytes and various types of microorganisms whereas inorganic content is composed of minerals, two thirds of which is crystalline in structure.

Organic components:

1. Amino acid content

The most thorough analysis of the protein constituents of dental calculus was carried out by Osuoji and Rowles 1, when they investigated the amino acid content of demineralized acid hydrosylates of mixed supra and subgingival calculus and subgingival calculus separately. Seventeen amino acids were detected with glutamic, aspartic, glycine. alanine, valine and leucine forming the largest proportion of the total residue isolated. The sulphur containing amino acids, methionine and cysteine were present in only trace amounts. Neither cysteine nor hydroxyproline were detected suggesting the absence of keratin or collagen.

This information agrees closely with the earlier work of Little et al 2  who additionally noted differences between the lower lingual and upper molar calculus samples where the amino acid concentration of the former was found to be lower and of a different composition. The nitrogen contents of the upper molar samples was also consistently higher than that of the lower anterior calculus.

2. Lipid Content

        The lipid content of dried calculus was studied by Osuoji and Rowles 1, using chloroform-methanol extraction. A combination of thin layer chromatography and gas liquid chromatography showed the presence of a variety of lipid components and fatty acids. The lipid content was 15.3% of the dry weight of the decalcified calculus and included phospholipids, cholesterol esters, diglycerides, triglycerides and free fatty acids. The free fatty acids represented the largest component of the lipid fraction and the predominant acids detected were palmitic, stearic and oleic, with smaller amounts of the unsaturated fatty acids, linoleic and linolenic.

3. Carbohydrate Content

Studies by Little et al 2 on acid hydrosylates of decalcified calculus indicated the presence of a variety of constituent surgars including glucose, glactose, glactosamine. glucuronic acid, galacturonic acid, glucosamine galactosamine rhamnnose and sometimes arabinose. No difference in carbohydrate content either chemically or chromatographicaly were found between calculus sites or different mouths. The constituent sugars yield some information on the source of origin of the calculus components. Hexuronic acid is a notable component of glycosaminoglycans present in connective tissue. it is not found in the saliva or in the cell wall of oral micro-organisms. It is however a basic component of capsular streptococcus and limes where it is present as hyaluronic acid and other unidentified uronides. The absence of deoxyribose and ribose preclude the presence of nucleic acids calculus and indicated that the oral microorganisms undergo extensive degradation leaving only the cell wall for calculus formation.

Macromolecules in Dental Calculus

During calculus formation conceivably most salivary components particularly those with ionisable groupings are able to interact with the amphoteric surface of calcium phosphate during its maturation stage, although may not necessarily be involved during the initial nucleation or seeding stage. A variety of compounds have been detected in plaque and pellicle and some of these constituents either in their native or modified form could be present in calculus.

a) Salivary glycoproteins

Histochemical studies and carbohydrate and amino acid profiles have implicated the presence of salivary glycoproteins in calculus. Embery 3 reported the presence of a sulphate glycopeptide in supragingival calculus which contained a high amount of ester sulphate, hexose, equal amounts of galactosamine and glucosamine and a small quantity of peptide.

b) Glycosaminoglycans

Although uronides are present in certain bacteria; their detection as glycosaminoglycans in calculus has been considered unusual. Studies by Embery and Whitehead 4  have indicated that sulphated glycosaminoglycans, hyaluronic acid is present in supragingival calculus whereas the sulphate glucosaminoglycans, chondroitin sulphate and dermatan sulphate are additional components in subgingival calculus.

c) Collagen and Keratin

Neither of these molecules nor their degradation products have been identified in calculus. 

Differences in composition of supra and subgingival calculus:

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 octacalcimn phosphate.
  • The ratio of calcium to phosphate is higher subgingivally, and the sodium content increases with the depth of periodontal pockets.
  • Salivary proteins present in supragingival calculus are not found subgingivally. Dental calculus, salivary duct calculus and calcified dental tissues are similar in inorganic composition.
  • In volume percentage of mineral in supragingival calculus can very from 16- 80% and that of subgingival calculus from 46 to 88%.

Inorganic components:

The process of mineralization is not fully understood but involves localized supersaturation, nucleation, crystal growth and the transformation of precursor phases such as dicalcium phosphate dihydrate, octocalcium phosphate and amorphous calcium phosphate into more stable, crystalline deposits of hydroxyapatite and whitlockite 5. Supragingival and subgingivalcalculus contain 37% and 58% mineral content by volume, respectively 6. . At least two thirds of the inorganic component is crystalline in structure. The four main crystal forms and their percentages are :

                        Hydroxyapatite, approximately                                     58%

                        Magnesium whitlockite, approximately                         21%

                        Octacalcium phosphate, approximately                        21%

                        Brushite approximately                                                  9% 

It has been demonstrated that octacalcium phosphate [Ca8(PO4)4(HPO4)25HO](OCP), hydroxyapatite [Ca10(PO4)6(OH)2] (HAP) and ß-tricalciumphosphate or whitlockite [Ca10(HPO4)(PO4)6] (WHT) form the inorganicpart of both supragingival and subgingival calculus. Brushite[CaHPO4-2H2O: dicalcium phosphate dihydrate] (DCPD) is presentonly in the early-stage supragingival calculus 7.  The percentage of inorganic constituents in calculus is similar to that in other calcified tissues of the body. The principal inorganic components are

        Calcium                                     39%

        Phosphorus                                19%

        Carbon dioxide                          1.9%

        Magnesium (Mg)                         0.8%

Trace amounts of sodium, zinc, strontium, bromine, copper, manganese, tungsten, gold, aluminum, silicon, iron and fluorine are also present . 

The organic matrix of dental calculus and its interaction with mineral

The mechanisms by which the mineralization of dental calculus is initiated are not fully understood. In contrast to the molecular events which occur in the homeostasis of bone & dentine, dental calculus represents a surface phenomenon and is therefore outside the normal cellular, neural and hormonal controlling influences. As such there is no remodeling and calculus will form and increase in bulk via accretion due to surface activity. Limits on size will be imposed by shear forces in the mouth, particularly by fragmentation due to masticatory forces.

Along with the calcification systems which occur in physiologic systems, the organic components present are considered to play an important role in the mineralization process. The major part of the organic matrix is derived from saliva, gingival sulcus fluid and oral bacteria, with a contribution from cell debris such as polymorphonuclear leukocytes.

In 1975 Mandel and Levy suggested a role for protein polysaccharides complexes in the formation of calculus. These workers demonstrated the presence of carbohydrate protein molecules in supragingival calculus using histochemical procedures alone. Further studies by this group and by Little et al. 8  yielded valuable information on the carbohydrate and amino-acid constituents of acid hydrolysates of the supragingival calculus from the molar and lingual areas of a large number of individual samples. 

The role of the organic phase in mineralisation

Many reviews have dealt with calculus formation and its prevention, one of them is article by Mandel 9 . A number of theories have been put forward including the ‘booster’ mechanism where the local ph, calcium and phosphate concentrations are high leading to calculus phosphate deposition, the epitactic theory etc. These are discussed later in discussion.

Ennever et al 10 contended that the initiator of claculus matrix calcification is proteolipid. The presence of glycosaminoglycan-rich proteoglycan metabolites in calculus are also potential nucleators due to their high number of sulphate and carboxyl goups which can attract calcium. These molecules in addition to concentrating calcium ions, may attract water molecules and thereby locally increase the metastability of calcium phosphate solution leading to deposition around the organic macromolecules which then feature as template.

These molecules can also inhibit or certainly regulate calcium phosphate formation. Chen & Boskey 11 have shown that coating hydroxyapatite seed crystals with proteoglycan, chondroitin sulphate and dextran sulphate decreased the mount of hydroxyapatite precipitated as a function of time, whereas the desulphated analogues showed less inhibition. On the other hand the removal of sulphate may include conformational changes indicating that charge may not be the only determinant.

The sliding of the negatives sites on the hydroxyapatite surface may be one controlling determinant. In vivo, the metabolism of such molecules must not be overlooked since protease and glycoside enzymes are present in high amounts. The presence of enzymes on the surface of calculus may also be important in controlling its formation, particularly since enzymes increase their turnover activity in the immobilized form.

Rate of calculus formation & accumulation

The starting times and rates of calcification and accumulation of calculus vary from person to person, in different teeth, and at different times in the same person. On the basis of these differences, persons may be classified as:

1) Heavy calculus formers.   
2) Moderate calculus formers.
3) Slight calculus formers. 
4)  Non calculus formers.

The average daily increment in calculus formers is from 0.10% – 0.15% of by weight 12-13. Calculus formation continues until it reached a maximum, after which it may be reduced in amount. The time required to reach the maximal level has been reported as 10 weeks 14 and 6 months 15. The decline from maximal accumulation is referred to as “reversal phenomenon” which can be explained by vulnerability of bulky calculus to mechanical wear from food and from the cheeks, lips and tongue.

Adhesional aspects of dental calculus formation

The adhesional bond strength of calculus to enamel and dentin surfaces determines the ease with which calculus can be removed by daily tooth brushing or professional dental treatment. Briefly following mechanisms of attachment of calculus to tooth surface have been proposed: 

  • Attachment by means of organic pellicle.
  • Mechanical inter locking between the surface irregularities such as resorption lacunae and caries.
  • Penetration of calculus bacteria into cementum.
  • Close adaptation of calculus under surface dispersions to the gently sloping mounds of the unaltered cementum surface.

Various studies have been done on animal and human models to evaluate the calculus attachment to different surfaces of tooth. Beagle dog models have been extensively used for this purpose. It is important to emphasize at this point that two major differences exist between the beagle dog model employed and the human oral cavity regarding calculus formation. Firstly, calculus formed in beagle dogs is known to possess high amount of calcium carbonates, whereas human calculus consistently contains calcium phosphates 16 . Secondly, the calculus surface in the dog model is rougher than generally observed in human due to lack of regular brushing  17. This aspect may lead to increased rates of formation of calculus in dogs under the present experimental conditions compared to man.

The firmer adhesion of calculus to high surface free energy materials is evidenced by brushing and ultrasonic instrumentation can be explained on the basis of the high surface free energies of both interacting surfaces, which of is a thermodynamically favorable situation for adhesion. From a clinical point of view it s important to realize that calculus removal can be facilitated by polishing and surface free energy reduction, since easier removal leads to a smaller loss of sound tissue during instrumented treatment. A major requirement for prevention of calculus formation is a smooth tooth surface. Once this is achieved, calculus formation may not be completely inhibited. As a second preventive measure, the tooth surface free energy may be reduced by adsorption of amine flouride or perfluoroalkyl surfactants to facilitate easier removal 18 . 

Theories regarding calculus formation:

Mineralization theory:

The saliva is super saturated with respect to the salts and thus it is able to support crystal growth, but that spontaneous precipitation does not occur unless the solution is seeded. Crystals for this nucleation process are present in the tooth surface but since they are covered by a pellicle they cannot be used for this function .

Bacterial theory:

The importance of bacteria in the formation of calculus has historically received considerable endorsement. They may

  • Form phosphatases which increase the local concentration of phosphates and hereby lead to calcification.
  • Affect the pH of plaque and saliva and destroy protective colloidal action of the after.
  • Attach the calculus to the tooth.
  • Provide chemicals that induce mineralization.

An alternative view is that bacteria may only passively involved in calculus formation and simply are calcified along with the other components of plaque. The occurrence of calculus formation in germ free animals lends credence to such an opinion, but does not rule out active participation by bacteria had they been present. Viability of organisms is not necessary for participation in mineralization, since non viable organisms calcify readily. Decrease in metabolic activity with reduced production of organic acids that result from glycolysis may be a prerequisition before bacteria can mineralize. 

Carbon dioxide theory:

It claims that freshly secreted saliva leaving the opening of the salivary ducts has a CO2 tension of about of 60 mm Hg , expired air is lower than that it is about 29 mm Hg, the atmosphere is 0.3 mm Hg , this discrepancy will result in the escape of CO2 from saliva, the pH will rise , when the pH of saliva increase, less Ca and phosphorous can be accommodated in the ionized form and consequently spontaneous precipitation may occur, once crystallites are present the physiological super saturation accounts for this growth. This theory explains the formation of calculus near the orifice of the major salivary gland in copious amount. It cannot explain the formation of sub gingival calculus , which may be formed from the salts in the gingival exudates. 

Ammonia theory:

Ammonia is a break down product of urea and might result in a local pH increase in plaque, the pH of plaque is actually frequently above that of saliva and this is attributed to proteolytic activity which may result in the formation of amines, urea and ammonia. Proteolytic enzymes are present in plaque and a positive correlation has been found between their proteolytic activity and calculus formation. 

Booster concept:

Mineral precipitation results from a local rise in the degree of saturation of calcium and phosphate ions, which may be brought about in several ways. ‘Booster mechanism’ or a rise in the pH of the saliva causes precipitation of calcium phosphate salts by lowering the precipitation constant.

  • The pH may be elevated by loss of carbon dioxide and by the formation of ammonia by dental plaque or by protein degradation during stagnation 19-20 .
  • Colloid proteins in saliva bind calcium & phosphate ions and maintain a supersaturated solution with respect to the calcium phosphate salts. With stagnation of saliva. colloids settle out; the supersaturated state is no longer maintained, leading to precipitation of calcium phosphate salts 21. 

Epitactic theory: 

Seeding agents induce small foci of calcification that enlarge and coalesce to form a calcified mass 22This concept has been referred to as the ‘epitactic concept’, or more appropriately, ‘heterogeneous nucleation’. The seeding agents in calculus formation are not known, but it is suspected that the intercellular matrix or plaque plays an active role 23. The carbohydrate protein complexes may initiate calcification by removing calcium from the saliva (chelation) and binding with it to form nuclei that induce subsequent deposition of minerals. Plaque bacteria have also been implicated as possible seeding agents.

Epitactic refers to crystal formation (e.g. hydroxyapatite) through seeding by another compound. The second compound has a molecular configuration that is similar to the crystal lattice of hydroxyapatite so that calcium salts precipitate on to it from the metastable solution in saliva. The organic matrix of plaque is assumed to provide sites with molecular configurations capable of including an oriented precipitation of hydroxyapatite not requiring the solubility product for hydroxyapatite to be surpassed. Other reports point to a more likely seeding of hydroxyapatite by transformation from brushite or octacalcium phosphate.

Attention has also been centered around the significance of lipid component of organic matrix for the mineralizaion of plaque, since in vitro experiments in the decalcified calculus reveal that extraction of the lipid component prevents remineralization of the calculus matrix 24. 

Inhibition theory:

Another approach considers calcification occurring at specific sites because of the existence of an inhibiting mechanism at noncalcifying sites. Where calcification occurs the inhibitor is apparently altered / removed. One possible inhibiting substance is thought to be pyrophosphate (possibly other polyphosphates) and among the controlling mechanisms is the enzyme alkaline phosphate 25 . The pyrophosphate inhibits calcification by preventing the initial nucleus from growing, possibly by “poisoning” the growth centers of the crystals. 


A most attractive hypothesis is the idea that hydroxyapatite need not arise exclusively via epitaxy and nucleation. Amorphous non-crystalline deposits and brushite can be transformed to OCP and then to hydroxyapatite. It has been suggested that the controlling mechanism in the transformation process may be pyrophosphate 26It may well be that all theories might explain some part of the calcification mechanism, especially in calculus, where calcium exists in a variety of forms. In salivary calculus brushite may develop spontaneously as a result of local elevation of pH, calcium and phosphate and then in the maturing process be modified to crystals of higher calcium to phosphate ratios. Early amorphous deposits could be transformed to a more crystalline material. Nucleating substances arising from the bacterial activity or salivary proteins and lipids could also initiate calcification and account for the hydroxyapatite in early deposits.

Various indices used for calculus recording

Oral calculus index (OCI) (Greene and Vermillion 1964)It is component of the oral hygiene index. An explorer is used to estimate the surface area covered by supra-gingival calculus and to probe for the subgingival calculus. Scores are assigned according to the following criteria,

0. No Calculus

1. Supragingival calculus covering no more than one-third of the exposed tooth surface.

2. Supragingival calculus covering more than  one-third but not more than two-third of tooth surface.

3. Supragingival calculus covering more than two-third of exposed tooth surfaces and/or a continuous band of subgingival calculus

After the scores for debris and calculus are recorded, the Index values arc calculated. For each individual, the debris scores are totaled and divided by the number of surfaces scored.

Calculus index – CI (Ramfjord 1959)

The scores on calculus for each individual tooth examined are added and the sum divided by the number of teeth examined to yield the index on calculus. The following teeth were selected as indicators of the periodontal condition within the dentition: maxillary right first molar 16. maxillary left central incisor 21. Maxillary left first bicuspid 24. mandibular left first molar 36. mandibular right central incisor 41 and mandibular right first bicuspid 44. Calculus recording,

0. No Calculus.

1. Supragingival calculus extending only slightly below the free gingival margin (not more than 1 mm).

2. Supragingival calculus covering more than one-third but not more than two-thirds of tooth surfaces

3. Supragingival calculus covering more than two-thirds of exposed tooth surfaces

Calculus surface index (CSI) (Ennener et al. 1961)

CSI assesses the presence or absence of calculus on the four surfaces of the four mandibular incisors. Each surface is given a score of 1 for the presence of calculus or 0 for the absence of calculus. Maximum score for each subject is 16. In applying the scoring method, calculus was considered to be present in any amount, supragin­gival or subgingival, and it could be detected either visually or by touch. If the examiner was uncertain about the presence of calculus on a given surface, the surface was called calculus free.

Calculus rating (Volpe and Manhold 1962)

Calculus formation in vivo is performed using a coloured periodontal probe placed against the lingual surface of the anterior tooth that will be scored with the probe and placed at the most inferior border of any calculus present (supra- or sub-gingival). With the different colours at the probe end representing units, the amount of calculus present can be measured as,

O U no calculus

1 U I mm of calculus

2 U 2mm of calculus

3 U 3mm of calculus

4 U 4 mm of calculus

Marginal line calculus index (MLC-I)(Muhlanann and Villa 1967)

0. no calculus                                           

1. calculus observable, but less than 0.5mm in width and/or thickness

2. calculus not exceeding I mm in width and/or thickness

3. calculus exceeding 1 mm in width and/or thickness.

Detection of Calculus:

Periodontal treatment comprises of non surgical and surgical treatment. The non surgical periodontal therapy comprises of thorough removal of plaque and calculus from root surfaces. Detection of calculus and its complete removal is mandatory to achieve a clean tooth surface. Most common calculus detection modalities are based upon tactile sense of the operator. Visibility is a major factor that limits detection of sub-gingival calculus. Hence operator has to rely on either periodontal probe or explorer or curette to detect the presence of subgingival calculus. The end result of scaling and root planing is smooth and clean root surface. Studies have shown that excess amount of root surface is removed by clinicians to achieve a smooth root surface in case of subgingival scaling and root planing 27.

Conventional calculus detection techniques:

Most common clinically used technique for detection of subgingival calculus is use of an explorer to feel the continuity of root surface with the help of tactile sensation. But due to lack of visibility there are chances that some calculus may be left undetected.

Another technique is radigraphical method which is based upon the principle that on a radiograph the calculus can be seen as a radio opaque discontinuity on the root surface.

Advances in calculus detection techniques:

Calculus detection systems

Calculus detection and removal systems


(Fiberoptic Endoscopy Based Technology)


(Spectro-Optical Technology)


(Auto fluorescence Based Technology)


(Ultrasound technology)



(Laser Based Technology)

Following is the brief description of various calculus detection and calculus detection and removal systems, 

Perioscopy™ (Perioscopy Inc., Oakland, California)

Perioscopy system is modification of medical endoscope. It is exclusively used for periodontal pourposes. This was developed in year 2000. It consists of a fiberoptic bundle surrounded by multiple illumination fibres, a light source and irrigation system. Its miniature nature causes minimal tissue trauma. Fiberoptic system permits visualization of the subgingival root surface, tooth structure and calculus in real time on a display monitor 28. 

DetecTar™ (Ultradent Inc. South Jordan, Utah)

DetecTar™ uses a Spectro-optical approach in order to detect subgingival calculus by utilizing a light emitting diode and fiberoptic technology. This involves an optical fibre which recognizes the characteristic spectral signature of calculus caused by absorption, reflection and diffraction of red light 28. 

Diagnodent™ (KaVo Dental, Charlotte, NC)

This system is based on the fact that the composition and structure of calculus and tooth surface is different. This structural difference gives a typical fluorescence to both these structures. Calculus contains various non-metal as well as metal porphyrins and chromatophores which make it able to emit fluorescent light when irradiated with a light of certain wavelength. Diagnodent™ makes use of this property of calculus to detect its presence. Calculus and teeth fluoresce at different wavelength region of 628-685 nm & 477-497 nm respectively. Diagnodent™ involves use of an indium gallium arsenide phosphate (InGaAsP) based red laser diode which emits a wavelength of 655nm through an optical fibre causing fluorescence of tooth surface and calculus 28. 

Keylaser3™ (KaVo Dental, Charlotte, NC)

It is a laser system that combines a 655 nm InGaAsP diode for detection of calculus and a 2940 nm Er: YAG laser for treatment. Previous versions of this system (i.e. Keylaser 1 and 2) can be used for removal of calculus only. A scale of 0-99 is used for detection of calculus. Values exceeding 40 indicate definite presence of mineralized deposits. Er: YAG laser is activated as a certain threshold is reached. As soon as the value fall below threshold level Er: YAG laser is switched off. Studies done to assess the efficacy of this device have shown that it produces tooth surface comparable to hand and ultrasonic instruments. Cost factor can be a limiting aspect for using lasers for detection and treatment 28. 

Perioscan™ (Sirona, Germany)

It is an ultrasonic device that works on acoustic principles. It is similar to tapping on a glass surface with a hard substance and analysing the sound produced to find out the cracks that are present on glass. Tip of the ultrasonic insert is oscillating continuously. Different voltages are produced due to changes in oscillations depending on the hardness of the surface. Hardness of the calculus differs from the hardness of the tooth surface. This difference in hardness can be used to generate the information of the surface that is being touched by the device. It can differentiate between calculus and healthy root surfaces. It also has a treatment option that can be used to remove these calculus deposits immediately. This combination of detection and removal mechanism is advantageous since calculus can be removed just by switching the mode from detection to removal. The advantage lies in the fact that relocating the previously located calculus is not necessary 28. 

Pathogenic potential of calculus:

Etiological Significance:

It is difficult to separate the effects of calculus and plaque on the gingiva, because calculus is always covered with non-mineralized layer of plaque. There is always a positive correlation between the presence calculus and prevalence of gingivitis, but this correlation is not as great as that between plaque and gingivitis. Young person’s periodontal condition is more closely related to plaque accumulation than the calculus, but the situation is reversed with age 29.

Longitudinal studies 30 have been carried out to deter­mine the prevalence of plaque, calculus, gingival bleeding and type of tooth cleaning device, amongst school children in Morogoro, Tanzania. Results showed that the prevalence of calculus increased with increasing age. while the gingival bleeding was not age-dependent.

Regardless of its primary or secondary relationship in pocket formation, and although the principal irritating features of calculus is it surface plaque rather than its calcified interior, calculus is a significant pathogenic factor in periodontal disease.

Supragingival Calculus:

Until 1960, the prevailing view was the calculus was the major etiologic factor in periodontal disease. Its pathogenicity was attributed to its rough outer surface, which mechanically irritated the adjacent tissues. The cumin view emanated by Shroeder 31, is that the initial damage to the gingival margin in periodontal disease is due to immunologic and enzymatic effects of the microorganisms in plaque. The process is enhanced, however, by supragingival calculus, which provides further relation and thus promotes new plaque accumulations. It is still not clear however, whether calculus plus plaque provokes greater reaction than plaque alone, although there is some suggestive evidence for the former 32 . There is no question however, that the mineralized deposits,

  • Bring the bacterial overlay closer to the supporting tissues.
  • Interfere with local self cleansing mechanisms.
  • Make plaque removal more difficult for the patient.

Partial inhibition of plaque mineralization can be accomplished by chemical agents, but there has been no demonstration in humans of a reduction of gingivitis 33. It remains to be established what level of inhibition, if any, is required to have inure than a cosmetic effect.

Subgingival Calculus:

A number of studies support the view that the presence of subgingival calculus contributes to the chronicity and progression of periodontal disease 32. Clinical studies attest to the importance of frequent and thorough removal of root deposits by scaling and root planing to prevent attachment loss 34.  Morphologic studies show that calcified deposits are porous and could as a reservoir for irritating substances. Experimental studies have established the permeability of subgingival calculus to endotoxin (Baumhammersand Rohrbaugh, 1970) and the presence in the deposition of high levels of toxic stimulators of bone resorption and antigens from Bacteroides gingivalis (Patters et al, 1982). When coupled with increasing build up of PQ on the surface of Cal+, the combination has the potential for increasing the rate of displacement of the adjacent junctional epithelium and extending the radius of destruction of bone beyond that of PQ alone 32 .Thorough removal of porous bacterial retentive subgingival calculus is a key phase in periodontal therapy.

Anti-calculus Agents Used in Commercial Dentifrices:

Triclosan with a PVM/MA copolymer

Triclosan is a broad-spectrum antibacterial agent active on both Gram-positive and -negative micro-organisms. At bacteriostatic concentration, triclosan prevents bacterial uptake of essential amino acids, while at bactericidal concentrations, triclosan destroys the integrity of the cytoplasmic membrane and causes leakage of cellular contents 35 . It is also a potent inhibitor of both cyclo-oxygenase and lipoxygenase pathways 36.

Pyrophosphate and PVM/MA copolymer

Pyrophosphate is a small molecule that has been reported to inhibit crystal growth by binding to the surface of crystal. Pyrophosphate binds to two sites on the hydroxyapatite [Ca10(PO4)6(OH)2]  crystal surface, and one of the two sites needs to be bound by phosphate ion to permit crystal growth to occur. If this site is bound by pyrophosphate, phosphate ion cannot absorb onto crystal, and thus crystal growth is inhibited. To inhibit crystal growth effectively, the concentration of pyrophosphate has to reach a critical level. Below this level, the addition of NaF can induce a short period of slow precipitation, which is followed by rapid crystal growth 37. 

Zinc ions

Zinc is added to toothpastes and mouth rinses, as an anti-bacterial agent to help to control plaque, to reduce oral malodour and to reduce calculus formation through crystal-growth modification/inhibition 38-40. Zinc ions have been found to reduce the acidogenicity of plaque and inhibit its formation 41. There is evidence that zinc ions may inhibit both the adsorption of bacteria to the tooth surface and growth of existing plaque 42-43 .

Zinc competes with calcium for bacterial binding sites which implies that it reduces plaque formation. Zinc has good oral substantivity. Following application, relatively large amounts of the applied zinc dose are retained in the mouth, with reported values typically between about 15-40%  44-48


From the above discussion it is clear that calculus removal is important to achieve a smooth and plaque free tooth surface. As far as it’s etiological potential is concerned, it provides a harboring surface for plaque accumulation.  So, it has an indirect role in pathogenesis of periodontal diseases.  For further discussion on etiology of periodontal diseases please read ” Immunology of periodontal diseases” and ” Host response”.



  1. C I Osuoji, S. L. Rowles. Studies on the organic composition of dental calculus and related calculi. Calcif. Tiss. Res. 16, 193-200 (1974).
  2. Little MF, Bowman L, Cascinani CA, Rowley J (1966). The composition of dental calculus 111; supragingival calculus—the amino acid and saccharide component.Arch Oral Biol 11:385–386.
  3. G. Embery. A sulphated Glycopeptide in Human Supragingival calculus extracts. Calc. Tiss. Res. 23; 13-17.1977.
  4. Embery, G.; Whitehead, E. Hyaluronic acid in supragingival dental calculus . Calc. Tiss. Res. 1977.
  5. White DJ, Bowman WD, Nancollas GH. Physical-chemical aspects of dental calculus formation and inhibition: in vitro and in vitro studies. Oxford: IRL Press, 1989: 175-188.
  6. Friskopp J, Isacsson C (1984). A quantitative microradiographic study of mineral content of supragingival and subgingival dental calculus. Scand J Dent Res 92:25–32.
  7. Rowles SL (1964). Biophysical studies on dental calculus in relation to periodontal disease. Dent Pract Dent Rec 15:2–7.
  8. Little et al. The lipids of supragingival calculus.. J Dent Res. 43:645;1966.
  9. Mandel I. D. (1988) Chemotherapeutic agents for controlling plaque and gingi­vitis. Journal of Clinical Periodontology 15, 488-498.
  10. Ennever J, Boyan-Salyers B, Riggan LJ (1977) Proteolipid and bone matrix calcification. J Dent Res 56:967-970.
  11. Chen CC, Boskey AL, Rosenberg L (1984) The inhibitory effect of cartilage proteoglycans on hydroxapatite growth. Calcif Tissue Int 36:285-290.
  12. Sharawy A. , Sabharwal K., Socransky S. et. Al. A quantitative study of plaque and calculus formation in normal and periodontally involved mouths. J Periodontol 37:495,1966.
  13. Turesky S, Renstrup G, Glickman I: Effects of changing the salivery environment on progress of calculus formation. J Periodontol 33:45, 1962.
  14. Conroy C, Sturzenberger O: The rate of calculus formation in adults, J Periodontol 39: 142,1968.
  15. Volpe A, Kupczak L, King W et. Al. In vivo calculus assessment. Part IV. Parameters of hu,mman clinical syudies, J Periodontol 40:76, 1969.
  16. Racquel Z. Legeros, Ira L. Shannon. The Crystalline Components of Dental Calculi: Human vs. Dog. JDR December 1979 vol. 58 no. 12, 2371-2377.
  17. Knut N. Leknes, Tryggve Lie, Ulf M.E. Wikesjö, Gary C. Bogle and Knut A. Selvig. Influence of Tooth Instrumentation Roughness on Subgingival Microbial Colonization. J Periodontol April 1994, Vol. 65, No. 4, Pages 303-308.
  18. F. J. G. van der Ouderaa. Anti-plaque agents. Rationale and prospects for prevention of gingivitis and periodontal disease. J Clin Periodontol Volume 18, Issue 6, pages 447–454, July 1991.
  19. Bibby B. The formation of Salivary calculus., Dent Cosmos 77: 668;1935.
  20. Hodge H.C, Leung S. Calculus formation, J Periodontol 21:211,1950.
  21. Prinz H. The origin of salivary calculus. Dent Cosmos  63;321, 1921.
  22. Neuman WF, Neuman MW: The chemical dynamics of bone. 1958:pp 169-187 University of Chicago Press, Chicago .
  23. Zander HA, Hazen SP, Scott DB. Mineralization of dental calculus. Proc Soc Exp Biol Med. 1960 Feb;103:257-60.
  24. Ennever J, Boyan-Salyers B, Riggan LJ (1977) Proteolipid and bone matrix calcification. J Dent Res 56:967-970.
  25. Russell RGG, Kislig AM, Casey PA, Fleisch H, Thornton J, Schenk R, Williams DA (1973) Effect of diphosphonates and calcitonin on the chemistry and quantitative histology of rat bone. Calcif Tissue Res 11:179-195.
  26. Fleisch, H., Russell, R.G.G. & Straumann, F. (1966) Effect of pyrophosphate on hydroxyapatite and its implications in calcium homeostasis. Nature (London), 111, 901-903.
  27. Meissner G, Kocher T. Calculus detection technologies and their clinical application. Periodontol 2000 2011;55:189-204.
  28. Meissner G, Kocher T. Calculus detection technologies and their clinical application. Periodontol 2000 2011;55:189-204.
  29. Green J. Oral hygiene and periodontal disease. Am J Public Healthn53:913;1963.
  30. Frencken JE, Truin GJ, van’t Holf MA, Konig KG et al. Plaque, calculus and gingival bleeding and type of tooth cleaning device in a Tanzanian child population in 1984, 86 and 88. J Clin Periodontol. 1991: 18;592-7.
  31. Shroeder H: Formation and inhibition of dental calculus. Berne,1969. Hans Huber.
  32. Mandel ID, Gaffar A. Calculus revisited. A review. J Clin Periodontol. 1986 Apr;13(4):249-57.
  33. P. S. Hull. Chemical inhibition of Plaque. J Clin Periodontol, Volume 7, Issue 6, pages 431–442, 1980.
  34. U. Zappa, B. Smith, C. Simona, H. Graf,* D. Case and W. Kim. Root Substance Removal by Scaling and Root Planing. J Periodontol December 1991, Vol. 62, No. 12, Pages 750-754.
  35. Regos J, Hitz HR (1974). Investigations on the model of action of triclosan, a broad spectrum antibacterial agent. Zbl Bakt Hyg 226:390–401.
  36. Gaffar A, Scherl D, Afflitto J, Coleman EJ (1995). The effect of triclosan on mediators of gingival inflammation. J Clin Periodont 22:480–484.
  37. Moreno EC, Aoba T, Gaffar A (1989). Physical chemistry of calculus formation. In: Recent advances in the study of dental calculus. Oxford: IRL Press at Oxford University Press, pp. 129-142.
  38. Cummins D, Creeth JE. Delivery of anti-plaque agents from dentifrices, gels and mouthwashes. J Dent Res 1992 71: 143–149.
  39. Young A, Jonski G, Rölla G. Inhibition of orally produced volatile sulfur compounds by zinc, chlorhexidine or cetylpyridinium chloride-effect of concentration. Eur J Oral Sci 2003 111: 400–404.
  40. Segreto V A, Collins EM, D’Agostino R et al. Anti-calculus effect of a dentifrice containing 0.5% zinc citrate dihydrate. Community Dent Oral Epidemiol 1991 19: 29–31.
  41. Afseth J, Rolla G (1980). The in vivo effect of glucose solutions containing Cu++ and Zn++ on the acidogenicity of dental plaque. Acta Odontol Scand 38:229-233.
  42. Harrap GJ, Best JS, Saxton CA (1984). Human oral retention of zinc from mouth washes containing zinc salts and its relevance to dental plaque control. Arch Oral Biol 29:87-91.
  43. Saxton CA (1986). The effects of a dentifrice containing zinc citrate and 2,4,4'-trichloro-2'-hydroxydiphenyl ether. J Periodontol 57:555-561.
  44. Gilbert RJ, Tan-Walker RLB, van der Ouderaa FJG. Delivery of zinc and triclosan to micro-reservoirs of anti-bacterial activity. J Dent Res 1989 68 (Sp Iss): 1706–1707.
  45. Gilbert RJ, Ingram GS. The oral disposition of zinc following the use of an anti-calculus toothpaste containing 0.5% zinc citrate. J Pharm Pharmacol 1988 40: 399–402.
  46. Tan-Walker RLB, Gilbert RJ. Oral delivery of zinc from slurries and separated supernatant fractions of dentifrices. J Dent Res 1989 68 (Sp Iss): 1708–1709.
  47. Creeth JE, Abraham PJ, Barlow JA et al. Oral delivery and clearance of antiplaque agents from Triclosan-containing dentifrices. Int Dent J 1993 43: 387–397.
  48. Afseth J, Helgeland K, Bonesvoll P. Retention of Cu and Zn in the oral cavity following rinsing with aqueous solutions of copper and zinc salts. Scand J Dent Res 1983 91: 42–45.

Leave a Reply

You must be logged in to post a comment.