DENTAL CALCULUS power point presentation

dental calculus

1. M.HARITHA PG1ST YR DENTAL CALCULUS 1

2. CONTENTS INTRODUCTION HISTORY PREVALANCE CLASSIFICATION COMPOSITION ATTACHMENT TO TOOTH SURFACE FORMATION THEORIES OF CALCULUS MINERALIZATION OF CALCULUS ETIOLOGIC SIGNIFICANCE IATROGENIC FACTORS DETECTION OF CALCULUS PREVENTIVE ASPECTS CLINICAL MEASUREMENT REFERENCES 2

3. INTRODUCTION Once a tooth erupts, various materials gather on its surface , these substances are frequently called as tooth accumulated materials/ deposits. They are classified as – Soft deposit Hard deposit SOFT DEPOSIT Acquired pellicle Material Alba Microbial plaque Food Debris HARD DEPOSIT Calculus Stains 3

4. CALCULUS Dental Calculus consists of mineralized bacterial plaque that forms on the surfaces of natural teeth and dental prosthesis. [Carranza ] A hard deposit that forms by mineralization of dental plaque and is generally covered by a layer of unmineralized plaque ( Lindhe ) A deposit of inorganic salts composed primarily of calcium carbonate and phosphate mixed with food debris bacteria and desquamated epithelial cells. (Greene 1967) Calculus is derived from Greek words Calcis -lime stone, Tartar- white encrustation inside casks . 4

5. SYNONYMS TARTAR DISAMIGUATION CALCIS ODONTOLITHIASIS FOSSILIZED PLAQUE MANDEL ET AL CALCULUS REVESISED A REVIEW 2013 5

6. HISTORY Hippocrates (460-377 BC) Albucasis ( 936-1013 ) Paracelsus 1535 6

7. In 1683, van leeuwenhoek described microorganism in tartar, he called them “ANIMALCULES” 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 1970's, the first studies of ancient dental calculus took place on archaeological samples of cattle, sheep, and horse teeth (Armitage, 1975) and revealed the presence of numerous oral phytoliths (silica content of some plant cells) 7

8. PREVALENCE Many studies have been conducted on the prevalence of calculus and these surveys revealed a high prevalence(70-100%) of calculus in virtually every population studied. Longitudinal study was done by Anerud and coworkers (1991) among Srilankan tea laborers and Norwegian academicians for 15 years and all periodontal parameters were recorded Two national surveys by O’Brien(1993) and Bhat M.(1991) have provided data on the prevalence of calculus. 8

9. National Health and Nutrition Examination Survey (NHANES ΙΙΙ ) They evaluated 9689 adults in United States between 1988 and 1994 out of which 91.8 % of subjects had detectable calculus 55.1% had subgingival calculus. 9

10. 10

11. 11

12. CLASSIFICATION According to location - Supragingival calculus - Subgingival calculus According to source of mineralization -Salivary calculus - Serumal calculus (Jenkins, Stewart 1966 ) 12

13. According to surface -Exogenous -Endogenous ( Melz 1950) According to initiation and rate of accumulation, calculus former are classified as -non calculus formers -Slight calculus formers -moderate calculus formers -heavy calculus formers ( Muhler and Ennever 1962) 13 MODERATE HEAVY SLIGHT

14. In extreme cases calculus may form a bridge-like structure along adjacent teeth or cover the occlusal surface of teeth without functional antagonist . F ound nearly 100% in mandibular anterior teeth, decreasing posteriorly to 20% of the third molars. In maxilla, 10% of the anterior teeth and 60% of first molars had supragingival calculus. 14

15. SUPRAGINGIVAL CALCULUS Location – On the clinical crown coronal to the margin of the gingiva and visible in the oral cavity. Distribution – Most frequent sites are on the lingual surfaces of the mandibular anterior teeth opposite Warton’s duct and on the buccal surfaces of the maxillary molars opposite Stenson’s duct. Crowns of teeth out of occlusion; non-functional; or teeth that are neglected during daily plaque removal. Surfaces of dentures and dental prosthesis. 15

16. 16

17. SUBGINGIVAL CALCULUS Location On the clinical crown apical to the margin of the gingiva, usually in periodontal pockets, not visible upon oral examination . Extents to bottom of the pocket and follows contour of soft tissue attachment. Distribution May be generalized or localized on single teeth or a group of teeth. Proximal surfaces have heaviest deposits, lightest deposits on facial surfaces.( Lovdal et al.1958) Occurs with or without associated supragingival deposits. 17

18. Submarginal Calculus Hematogenetic Calculus Serumal Calculus 18

19. 19

20. Distribution of dental calculus on dentition Lingual surfaces of the lower anterior teeth. Buccal surfaces of the upper molars

21. COMPOSITION Supragingival calculus consists of: inorganic (70 to 90 per cent) and organic components (20 to 30%) 21

22. Inorganic portion consist of: 76% calcium phosphate 3% calcium carbonate 4% magnesium phosphate 2% carbon dioxide Traces of other metals Trace elements – sodium tungsten zinc gold strontium aluminium bromine silicon copper iron manganese fluorine INORGANIC CONTENT 22

23. 4 main crystal forms are- Hydroxyapatite -58% Magnesium whitlockite - 21% Octacalcium phosphate – 12% Brushite - 9% 23

24. ORGANIC CONTENT 24

25. Carbohydrate – 1.9% and 9.1% of organic component, consist of : Galactose sometimes : arabinose Glucose galacturonic acid Mannose glucosamine Glucuronic acid Galactosamine Salivary proteins 5.9% to 8.2% of organic component Lipids 0.2% of organic component 25

26. It has composition similar to supragingival calculus, with some differences. More homogenous with equally high density of minerals. Same hydroxyapatite content, more magnesium whitlockite Less brushite and octacalcium phosphate The ratio of calcium to phosphate is higher subgingivally . The sodium content increases with the depth of periodontal pockets. Salivary protein found in supragingival calculus is not found subgingivally SUBGINGIVAL CALCUUS 26

27. MICROBIOLOGY OF DENTAL CALCULUS The percentage of gram positive and gram- negative filamentous organisms is greater within calculus than in the remainder of oral cavity . The microorganisms at the periphery are predominantly gram-negative rods and cocci . Most of the organisms within the calculus is nonviable. 27

28. Friskopp & Hammarstrom (1980) With TEM & SEM found differences in the nature of the microbial coverings. On supragingival calculus filamentous organisms,oriented at right angles to the surface dominated, Subgingival calculus was covered by cocci, rods and filaments with no distinct pattern of orientation. 28

29. Pathogens like A.actenomycetecomitans , P.gingivalis , T.denticola have found within the lacunae Of both supragingival and subgingival calculus Plaque bacteria have been proposed to actively participate in the mineralization of calculus by forming phosphatases, changing the plaque pH inducing mineralization ( Emper et al, 1962) 29

30. SUBGINGIVAL CALCULUS Superficial layers : gram- negative filaments most numerous Deep and middle zones : gram-positive filaments predominant. SUPRAGINGIVAL CALCULUS Predominance of gram-positive filaments. Next in frequency; gram-negative filaments and cocci. 30

31. 31

32. ATTACHMENT TO THE TOOTH SURFACE 32

33. CALCULOCEMENTUM Calculus embedded deeply in cementum may appear morphologically similar to cementum and thus has been termed calculocementum 33

34. ATTACHMENT OF CALCULUS ON IMPLANT Attachment to pure titanium is less intimate than to root surfaces structure . Smooth machined implants have less micro porosities for retention . (This would mean that calculus may be chipped off from implants without affecting it) Matarraso et al 1996 34

35. Acquired pellicle forms on an implant surface when the metal surface initially comes into contact with tissues (Baier, 1982). 1 Adsorption of proteins does not occur on the surface of pure titanium (Ti). 5-6nm oxide layer composed of TiO 2 forms on the surface of Ti when exposed to air. At physiological pH, the TiO 2 layer carries net -ve charges, which enable the TiO 2 layer to bind cations like Ca 2 +

36. This makes the surface of an implant + vely charged and, consequently, attracts the high-weight molecules carrying - ve charges, notably proteins. Some irregularities may also be encountered on oral implant surfaces, The attachment to commercially pure titanium generally is less intimate than to root surface structures.  

37. FORMATION 37

38. 38

39. PELLICLE FORMATION All surfaces of the oral cavity are coated with a pellicle. Following tooth eruption or a dental prophylaxis, a thin, saliva- derived layer, called the acquired pellicle, covers the tooth surface Initial adhesion and attachment of bacteria Transport to the surface – involves the initial transport of the bacterium to the tooth surface . Initial adhesion – reversible adhesion of the bacterium, initiated by the interaction between the bacterium and the surface , through long-range and short-range forces Attachment – a firm anchorage between bacterium and surface will be established by specific interactions. 39

40. W hen the firmly attached microorganisms start growing and the newly formed bacterial clusters remain attached, microcolonies or a biofilm can develop . Gram- positive coccoidal organisms are the first settlers to adhere to the formed enamel pellicle, and subsequently, filamentous bacteria gradually dominate the maturing plaque biofilm ( Scheie , 1994 ). Colonization and Plaque Maturation 40

41. Rate of formation and accumulation   Formation of plaque consist of amorphous and/ or finely granular organic matrix containing mass of variety of gram positive and gram negative coccoid bacteria and filamentous form. The matrix is a form of mucopolysaccride derived from either saliva or bacteria or both. MINERALIZATION 41

42. 42

43. 43

44. C ALCIUM IONS CARBOHYDRATE PROTEIN COMPLEX CRYSTALLINE CALCIUM PHOSPHATE SALT 44

45. RATE OF FORMATION Calculus is formed by the precipitation of mineral salts which can start between 1st to14th day of plaque formation The average daily increment in calculus former-0.10% to 0.15% of dry weight Calculus formation continues until it reaches maximum levels in about 10 weeks to 6 months time Calcification is reported to occur in as little as 4-8 hrs. ( Tibetts 1970) 45

46. THEORIES OF MINERALISATION OF CALCULUS 46

47. BOOSTER MECHANISM Mineral precipitation results from a local rise in the degree of saturation of calcium and phosphate ions A rise in the pH of the saliva causes the precipitation of calcium phosphate salts by lowering the precipitation constant Colloidal proteins in saliva bind calcium and phosphate ions and maintain a supersaturated solution with respect to calcium phosphate salts . Phosphatase liberated from dental plaque, desquamated epithelial cells , or bacteria precipitates calcium phosphate by hydrolyzing organic phosphates in saliva, thereby increasing the concentration of free phosphate ions. 47

48. EPITACTIC CONCEPT / SEEDING THEORY/HETEROGENOUS NUCLEATION ( Mandel 1957) 48

49. INHIBITION THEORY Calcification at specific sites - because of inhibiting mechanism at non-calcifying sites . The site where calcification occur ,the inhibitor is apparently altered or Removed. Alkaline pyrophosphatase enzyme involved in controlling mechanism- --- hydrolyzes pyrophosphate to phosphate (Russell and Fleisch 1970 ). Pyrophosphate inhibits calcification - prevents the initial nucleus from growing, possibly by poisoning the growth centers of the crystals 49

50. TRANSFORMATION THEORY Hypothesis - hydroxyapatite need not arise exclusively via epitaxis or nucleation. Amorphous non-crystalline deposits and brushite Transformed into octacalcium phosphate and then to hydroxyapatite ( Eanes et al 1970). Controlling mechanism in transformation mechanism can be pyrophosphate ( Fleisch et al 1968 ). 50

51. BACTERIOLOGICAL THEORY Oral microorganisms are the primary cause of calculus formaton Involved in the attachment to the tooth surface. Leptotrichia and Actinomyces have been considered most often as the causative microorganism. 51

52. ENZYMATIC THEORY Calculus formation Action of phosphatases derived from either oral tissues or oral microorganism on some salivary phosphate complex (phosphoric ester of hexophosphoric group) 52

53. ROLE OF MICRORGANISM IN THE MINERALIZATION OF CALCULUS Mineralisation of plaque generally starts extracellularly around both gram positive and gram negative organism, but it may also start intracellularly . Mineralisation spreads until the matrix and bacteria are calcified. Bacterial plaque may actively participate in the mineralizaion of calculus by forming phosphatases, which change the pH of plaque and induce mineralization. 53

54. ETIOLOGICAL SIGNIFICANCE The incidence of calculus, gingival inflammation and periodontal disease increases with age.(Greene et al, 1963; Gregory et al, 1965) Calculus does not contribute directly to gingival inflammation, but it provides a fixed nidus for the continued accumulation of of plaque and its retentionin close proximity to the gingiva ENZER reported that only 11%. of examined tooth surfaces containing calculus ( supragingival or subgingival ) exhibited gingivitis, while 75% of the surfaces harbouring plaque exhibited gingival inflammation FRENCKEN et al. (59), in a longitudinal study of Morogoro school children from 1984-1988 in Tanzania, observed that dental calculus increased with increasing age while gingival bleeding remained the same, suggestive of no correlation between calculus and gingival condition. 54

55. Margins of restorations Over Contoured Crown Design Of Removable Partial Dentures Restorative And Endodontic Procedures Iatrogenic Factors 55

56. Margins Of Restorations Over hanging margins increases plaque formation retentive areas Changed the ecologic balance Compromises hygiene practice. Subgingival margins Waerhaug - restorations placed in a sub gingival location - detrimental to periodontal health. Increased plaque, severe gingivitis and deeper pockets. 56

57. Over Contoured Crown Leads to accumulation of plaque and prevent the self-cleaning mechanisms of oral tissues . proximal contacts , contour of the marginal ridges , developmental grooves - prevent interproximal food impaction – prevent periodontal disease. Hancock et al 1980 – food impaction – periodontal pathosis. Jernber G et al 1983 - probing depth , clinical attachment loss – increased in open contact and food impaction. 57

58. Dental Materials Restorative materials are not in themselves injurious to the periodontal tissues Self curing acrylics Silicate Kourkouta et al – highly glazed porcelain – less plaque than enamel Composites – more likely to harbor bacterial plaque. Wang et al 1998 – metal pontics – higher amount of periodontal pathogens than porcelain. Plaque accumulation maintained – finished and polished surfaces. 58

59. Design Of Removable Partial Dentures Favor the accumulation of plaque. Quantitative and qualitative changes Increase in spirochetal microorganisms Mobility of abutment teeth, gingival inflammation, pocket formation increase Studies by Zlataric et al Zlataric et al 59

60. Restorative And Endodontic Procedures Rubber dam clamps, matrix bands, burs – lacerate the gingiva – inflammation Gingival retraction cord – impacted debris – foreign body reaction. 60

61. Miscellaneous Factors – Malocclusion Poorly aligned teeth themselves are not associated with a greater degree of gingivitis complicate oral hygiene procedures - increased plaque accumulation - subsequent gingival inflammation . Behfelt et al - direct relationship between tooth displacement and gingival inflammation Reduced interproximal spaces – less effective removal of plaque Extreme anterior overbite - palatal recession in maxillary incisors. 61

62. Miscellaneous Factors – Vertical Root Fracture Longitudinal , confined to the root of the tooth. Mesiodistal, buccolingual plane – occur at any point along the root. Narrow , isolated periodontal pocket . Recurrent periodontal abscesses. 62

63. Mucogingival deformities – Aberrant frenal attachment Aberrant frenal attachments may be a problem, especially in shallow vestibules or areas of minimal attached gingiva. frenum is stretched - the muscle attachments may pull the marginal tissue away from the tooth - accumulation and apical migration of bacterial plaque – gingival recession 63

64. Miscellaneous Factors – Orthodontic Therapy Orthodontic therapy affects the periodontium by Favouring plaque retention Directly injuring the gingiva as a result of overextended bands Creating excessive forces , unfavourable forces, or both on the tooth and supporting structures. Modify the gingival ecosystem Orthodontic band Excessive orthodontic forces – necrosis of PDL and adjacent alveolar bone , apical root resorption . 64

65. Radiation therapy Cytotoxic effects on both normal cells and malignant cells. >60 Sv – salivary production impaired – xerostomia – greater plaque accumulation and reduced buffering capacity by saliva. Periodontal attachment loss and tooth loss has been reported to be greater in cancer patients who were treated with high-dose unilateral radiation as compared with the non radiated control side of the dentition 65

66. Tobacco smoking Smoking is strongly related to severity of diseases and to recurrent and refractory diseases. Numerous studies have shown the association of smoking with periodontitis. 66

67. FACTORS AFFECTING THE RATE OF CALCULUS FORMATION   Diet and nutrition – the significance of diet in calculus formation depends more upon its consistency than upon its content. Increased calculus formation has been associated with deficiencies of vitamin A, niacin, or pyridoxine , and with an increase in dietary calcium, phosphorus, bicarbonate, protein and carbohydrate.

68. Age – there is an increase in calculus deposition with an increasing age .(Schroeder et al,1969 ). 5 This increase, is not only increase in the number of surfaces, but also the size of calculus deposits. This may be due to change in quantity and quality of saliva with age, favouring the mineralization properties.

69. Habits – In populations that practice regular oral hygiene and with access to regular professional care have low tendency for calculus formation. Smoking- is associated with an elevated risk for supragingival calculus deposition . Smoking may exert its influence systemically (elevated levels of salivary calcium and phosphorus) or locally via a conditioning of tooth surfaces.

70. Salivary pH- increase pH increases the calculus formation.   When the calcium phosphate crystals in solution are in kinetic equilibrium, the rate of precipitation is equal to that of dissolution. If pH in solution drops (the concentration of hydrogen ions increases), OH- and (PO4)3 - tend to be removed by H+ by forming water and more acidic forms of phosphate, respectively

71. Salivary flow rate – increased salivary flow rate decreases the calculus formation. Salivary flow rate affects calcium phosphate saturation. Salivary calcium concentration - Elevated salivary calcium concentration, increases the rate of calculus formation. Higher total salivary lipid levels – is associated with increased calculus formation Emotional status - increased calculus formation has been associated with disturbed emotional status.

72. DETECTION OF CALCULUS (A) VISUAL Transillumination Airblast Color change 72

73. (B) Tactile Probe explorer (C) Radiographs 73

74. LATEST METHOD OF DETECTION OF CALCULUS Fiberooptic endoscopy-based technology Spectro - optical technology Auto fluorescence based technology Ultrasonic oscillating system Laser based technology DETECTION ONLY COMBINED CALCULUS DETECTION AND REMOVAL 74

75. FIBEROOPTIC BASED TECHNOLOGY Perioscopy involves a modified medical endoscope exclusively for periodontal purpose. Fiberoptic system permits visualization of the subgingival root surface, tooth structure and calculus in real time on a display monitor. 75

76. SPECTRO OPTICAL BASED TECHNOLOGY Uses a light emitting diode and fiberoptic technology. The characteristic spectral signature of subgingival calculus which is caused by absorption, reflection and diffraction when irradiated by red light is sensed by an optical fiber and converted into an electrical signal that is analysed by a computer processed algorithm 76

77. AUTO FLUORESCENCE BASED TECHNOLOGY The ability of calculus to emit light following irradication with light of certain wavelength enables the detection of calculus. 77

78. ULTRASONIC TECHNOLOGY Ultrasonic calculus detection technology is based on a conventional piezo – driven ultrasonic scaleand is similar to the way one might tr ap on the rim of a glass with a spoon to identify cracks acoustically. The ultrasonic device currently available ( Perioscan ) provides a detection mode to discriminate between calculus deposits and clean roots, along with a treatment mode that allows conventional ultrasonic treatment at different power levels. 78

79. LASER BASED TECHNOLOGY Key laser 3 combines calculus detection and treatment in a feedback controlled manner for selective removal calculus . The device is based on a 655 nm InGaAs diode laser for autoflourescence based calculus detection whereas a 2940 nm ER:YAG LASER is used for treatment. 79

80. Significance of removal of calculus MOMBELLI et al showed that pocket depth reduction w/o calculus removal altered clinical course of periodontitis BIAGINI et al demonstrated growth of periodontal ligament fibroblast on cementum that had attached calculus. LISTGARTEN and ELLGARD as early as 1973 noted gingival epithelial reattachment to calculus depoisits sterlized by 2% chlorhexidine 80

81. PREVENTIVE ASPECTS There are several methods for coping with the problem of calculus. The patient must understand the importance of individual daily removal & how professional maintenance appointments on a regular basis can supplement the personal care . 81

82. PERSONAL PLAQUE CONTROL Removal of plaque appropriately by selected brushing, flossing and various supplementary methods is major factor in the control of dental calculus formation 82

83. ANTI CALCULUS AGENT 83

84. CLASSIFICATION 84

85. 85

86. Prophylatic tooth paste Triclosan with pvm /ma copolymer Pyrophate and pvm /ma copolymer Zinc ions 86

87. 87

88. 88  Potassium pyrophosphate, sodium pyrophosphate in a combined concentration of 5%. Also sodium fluoride 0.24% equivalent to 900 ppm Zinc citrate in 0.454 % SnF 2  multi-benefit The polypyrophosphate   sodium hexametaphosphate   - targets plaque calcification and has shown anti-calculus benefits in a dentifrice as high as 55% greater versus a regular dentifrice in clinical investigations .

89. 89

90. Calculus inhibitors CALCIFICATION NUCLEATION INHIBITORS 90 MAGNESIUM blocks apatite crystallization stabilzes calcium phosphate as amorphous material DIPHOSPHONATES Inhibit both apatite and crystal growth Clinically not used

91. CRYSTAL GROWTH INHIBITORS IN SALIVA Salivary proteins inhibitory action on crystal growth Proline rich protien PRPS M argolis et al 1982 STATHERIN CYSTATINS 91

92. Promoters of calculus formation Urea Fluorides Silicon 92

93. Calcification promoters – Urea is a product from the metabolism of nitrogen -containing substances. Urea can be secreted in normal saliva at concentrations of between 5 and 10 mmol /L but can be as high as 30 mmol /L in patients with renal disease Gingival crevicular fluid contains up to 60mmol/L urea. Urease is responsible for bacterial urea hydrolysis. At a neutral pH, urea is hydrolyzed by urease to NH 4 + and bicarbonate.

94. Fluoride - anti – bacterial action Inhibit the acid production by the bacteria Potential to increase plaque PH – formation of calculus Sodium fluoride – inhibit bacterail enzymes that known to cause calculus formation Silicon – found in drinking water , silicic acid – monoand poly salicylic acids – strong promotors – calcium phosphates and silica . A study done in indonesian and norwegian population – more calculus formation – consumption of large amount of rice – enriched in silicon . 94

95. SCALING AND ROOT PLANING 95

96. LASER 96

97. CLINICAL MEASUREMENT Oral calculus index (Greene and Vermilion 1964) Calculus Index ( Ramfjord , 1959) Calculus surface severity index( Ennener et al 1961 ) Calculus rating (Volpe and Manhold , 1962) Marginal line calculus index ( Muhlanann and Villa1967) 97

98. CONCLUSION Calculus plays an important role in maintaining and accentuating periodontal disease by keeping plaque in close contact with the gingival tissues and creating areas where plaque removal is impossible. Therefore the clinician must not only possess the clinical skills to remove the calculus and other irritants that attach to teeth . 98

99. REFERENCES Periodontology 2000; volume 55 Mandel ID, Gaffar A. Calculus revisited- A review. J Clin Periodontol1986;13: 249-257 Newmann , Takei, Klokkevold , Carranza: Clinical periodontology. 10th Edition. Noida: Elsevier; 2009. Glossary of periodontal terms (2001). 4th edn . Chicago: The American academy of periodontology. Greene JC. The Oral Hygiene Index—Development and uses. Journal of Periodontology. 1967;38( Suppl ): 37 Periobasics . 99