Rinisha Sinha, profile picture
Uploaded byRinisha Sinha
27,029 views

Dental calculus

The document provides a comprehensive overview of dental calculus, including its definition as a mineralized plaque on teeth, classification based on various factors, and the complex process of its formation. It discusses historical perspectives on calculus, its microbial composition, and the pathological significance related to periodontal disease. The document also outlines diagnostic strategies and theories regarding the mechanisms of calculus formation and attachment.

Embed presentation

DR. RINISHASINHA MDS PARTI DEPARTMENT OF PERIODONTOLOGY DENTAL CALCULUS
CONTENTS • Introduction • Definition • Synonyms • History • Classification • Composition • Structure of Calculus • Formation of Calculus • Theories of Calculus Formation • Calculus Attachment • Attachment of Calculus on Implant • Microbiology of Dental Calculus • Prevalence • Assessment and Evaluation of Calculus • Advanced Diagnostic Aids • Etiological Significance of Calculus in Periodontal Disease • Conclusion • Reference
INTRODUCTION • Calculus is derived from GREEK words : Calcis – Limestone Tartar – white encrustations inside casks • Once a tooth erupts, various material gets accumulated on the tooth surface, frequently called tooth – accumulated deposits / materials. Soft Deposits Hard Deposits Acquired Pellicle Microbial Plaque Materia Alba Food Debris Calculus
DEFINITION • Calculus is a hard deposit that forms by mineralization of dental plaque on the surface of the natural teeth and dental prosthesis, and it is generally covered by a layer of unmineralized plaque. • Dental calculus is defined as mineralized dental plaque that is permeated with crystals of various calcium phosphates. • Dental calculus is essentially mineralized plaque covered on its external surface by vital, tightly adherent non-mineralized plaque. • Calculus is a hard concretion that forms on teeth or dental prosthesis through calcification of bacterial plaque. • Dental Calculus is a deposit of inorganic salts composed primarily of calcium carbonate and phosphate mixed with food debris bacteria and desquamated epithelial cells. Reference : Carranza’s Clinical Periodontology Reference : Schroeder - 1969; Perio 2000 vol 8 - 2009 Reference : Glossary of Periodontal terms (2001); 4th edition Reference : Mandel, 1988 Reference : Greene, 1967
SYNONYMS • Tartar • Disambiguation • Calcis • Odontolithiasis • Fossilized plaque Reference : Mandel et. Al; Calculus revisited : A Review - 2013
• Recognized as far as back in the 10th Century. • Hippocrates (460 – 337 BC) Found the association of dental deposits and oral disease. The deleterious effects of the teeth and gums of pituita (calculus). • Albucasis (936 – 1013 AD) Arabian physician and surgeon Explained relationship between calculus and disease. First to design a set of 14 scalers for the thorough cleaning of teeth. • Paracelsus (1535) Swiss German physician and alchemist Introduced term “tartar” as a designation for a variety of stony concretions that form in humans. Tartaric disease
• For nearly 5000 years, Calculus was considered to be the Prime Etiologic Agent in the Periodontal disease. • Microorganisms in Tartar were initially referred to as Animalcules. • There was a change in perception, that became most apparent in 1960’s, mainly as a response to two lines of investigation – Reference : Van Leeuwenhoek, 1967 Experimental and electron microscopic studies of developing plaque and calculus demonstrated that supra and subgingival calculus was mineralized plaque covered by an unmineralized bacterial layer. The experimental demonstration in humans that plaque, allowed to develop in the absence of oral hygiene, results in a gingivitis which is reversible on the resumption of tooth cleaning. Reference : Mandei et al – 1957; Muhleman and Schroeder – 1964; Oshrain et al - 1968 Reference : Loe et al – 1965
CLASSIFICATION According to Source of Mineralization Salivary calculus Serumal calculus Reference : Jenkins, Stewart – 1966Reference : Carranza’s Clinical Periodontology According to Location on the tooth surface as related to the adjacent Free Gingival Margin : Supragingival calculus Subgingival Calculus According to initiation and rate of accumulation, calculus formers are classified as : Non calculus formers Slight calculus formers Moderate calculus formers Heavy calculus formers Reference : Mandel JD et al - 1976 According to Surface Exogenous Endogenous Reference : Melz – 1950
SUPRAGINGIVAL CALCULUS SLIGHT MODERATE SEVERE SUBGINGIVAL CALCULUS
Features •Definition •Location •Source •Distribution •Color •Consistency •Composition •Other contents •Visibility •Attachment Supragingival Calculus Subgingival Calculus •Tightly adhering calculus deposit that forms on the crowns of the teeth coronal to the gingival margin •Forms coronal to the Gingival Margin •Derived from the Salivary Secretions : SALIVARY CALCULUS •Symmetrical arrangement, more on Facial surfaces of Maxillary Molars and Lingual surfaces of Mandibular Anterior teeth •It is white, tallow in color •Hard and clay like •More brushite and octa calcium phosphate. Less Magnesium whitlockite •Sodium content is less Salivary proteins are present •Clinically visible •Easily detached from the tooth •Calcified deposits that forms on the tooth surface below the free margin of gingiva •Deposits present apical to the crest of the Marginal Gingiva •Derived from the Gingival Exudate : SERUMINAL CALCULUS •Related to pocket depth, Heavier on Proximal Surfaces •Brown / Greenish Black in color •Hard and firm / flint or glass – like •Less brushite and octa calcium phosphate. More magnesium whitlockite •Sodium content increases with the depth of the pocket Salivary proteins are absent •Not visible on routine clinical examination •Firmly attached to the tooth surface
COMPOSITION Inorganic Content Organic Content Mature Supragingival Calculus 70 – 90 percent 20 - 30 percent Reference : Little et al – 1963; Lundberg et al – 1966; Schroeder – 1969 2/3 CRYSTALLINE
CRYSTAL FORMS Hydroxyapetite 58%Octa Calcium Phophate 21% Magnesium Whitelockite 12% Brushite 9% Hydroxyapetite Octa Calcium Phophate Magnesium Whitelockite Brushite Calcium 27 - 29 Phosphorous 16 - 18 Carbon Dioxide 1-3 Magnesium 0.6 - 0.8 Fluoride 0.003 – 0.04 PRINCIPLE ELEMENTS 75.9 % calcium phosphate Ca3(PO4) 2 3.1 % calcium carbonate CaCO3 Traces of magnesium phosphate Mg3(PO4) 2 Other metals Traces of Na, Zn, St, Cu, Br, Mg, Fe, Al, Si, Tg, Gold COMPONENTS Monetite and Calcite in small amounts
CO-RELATIVE ANALYSIS Supragingival Calculus : Hydroxyapatite + Octa Calcium Phosphate Subgingival Calculus : Large amount of Magnesium whitlockite Same Hydroxyapetite Presence of alkaline and anaerobic conditions and concomitant presence of magnesia (or Zn and CO3) Mandibular Anterior Region : Brushite (more common) Posterior Region : Magnesium whitlockite (more common) Reference : Sundberg & Friskopp 1985
ORGANIC CONTENT CALCULU S Desquamated epithelial cells Leukocytes Various Microorganisms Protein – polysaccharide complexes
STRUCTURE OF CALCULUS MINERAL CRYSTALS are deposited in an organic matrix composed of • degraded microorganisms, which are often filamentous, • embedded in a finely granular, fibrillar or amorphous ground substance and derived from organisms . The CALCULI are divided by incremental lines which tend to follow the tooth surface , • usually horizontal in supragingival calculus and • vertically in subgingival calculus. This stratification is considered to be indicative of calculus deposits growing by apposition of new layers of calcifying plaque.
• A number of different crystals types can be seen between and within the bacterial remnants, varying as identified by electron diffraction, as: • The matrix of subgingival calculus appears to be homogenous than that of supragingival calculus which frequently exhibit areas of non-decalcified material appearing at all levels. • Both types of deposits are covered by a layer of unmineralized plaque. • Recently Tan et al (2004), concluded that viable aerobic and anaerobic bacteria may be present in supragingival calculus, specifically within internal channels and lacunae. • Clinically this is important , since incomplete removal of calculus may expose these reservoirs of possible pathogenic bacteria and be a factor in recurrence of periodontal disease after treatment. STRUCTURE OF CALCULUS  Small needle shaped crystals : HYDROXYAPATITE  Long ribbon like crystals : OCTA CALCIUM PHOSPHATES (bundles and rosettes)  Large crystalline aggregates: BRUSHITE
• This is a Complex Process. • Calculus is a mineralized dental plaque. • Formation of calculus is complex and involves both biological, physical and chemical processes. • Initial stage • Biofilm of pellicle, bacteria and interbacterial matrix provides an environment within which mineralization may occur with the resultant formation of calculus. • Precipitation of salts starts between 1st and 14th day of plaque formation. • However calcification has been reported to occur as soon as 4 to 8 hours. • Calcifying plaques may become 50 % mineralized in 2 days and 60 to 90 % in 12 days. • All plaque does not necessarily undergo calcification. • Plaque that does not develop into calculus reaches a plateau of maximal mineral content within 2 days. FORMATION OF CALCULUS
• Plaque has the ability to concentrate calcium at 2 to 20 times its level in saliva. • Early plaque of heavy calculus formers contains more Ca, 3 times more Po4, and less potassium than that of non-calculus formers. • Abundant supply of urea from saliva and the high salivary film velocity promotes base formation in plaque and calcium phosphate precipitation • Begins along the inner surface of the supragingival plaque and in the attached component of subgingival plaque adjacent to the tooth. • Binding of calcium ions to the carbohydrate protein complexes followed by precipitation of crystalline Ca3(Po4)2 salts occurs. • Crystals form initially in the intercellular matrix. • Separate foci of calcification increase in size and coalesce to form solid masses of calculus. • As calcification progresses number of filamentous bacteria increases. Calcification
Most susceptible to calculus formation Lower anterior lingual and upper posterior buccal surfaces • Low sucrose concentration in saliva • High saliva film velocity • Promotes clearance of salivary sugar and acid from plaque • Higher resting plaque pH • Better access to salivary urea REASON Average daily increment of calculus formed is 0.10% to 0.15% of dry weight. As calcification progresses the number of filamentous bacteria increases and foci of calcification change from
FORMATION OF CALCULUS Introduction of the entire process in a Nutshell After tooth eruption / dental prophylaxis Acquired Pellicle Development of Biofilm Maturation of Biofilm by Microorganisms Development of Plaque Mineralizing Agent from Saliva and Gingival Crevicular Fluid enters the biofilm leading to Mineralization of Plaque Intercellular Matrix Chelation Carbohydrate ComplexProtein Complex Crystalline Calcium Phosphate Salts Precipitation CoalescenceofCalcifiedMass Reference : Sahithya RS; Essesntials of Periodontology
• Mineral appears to be deposited in layers. • Mineralization is phasic with periods of mineralization being interspersed with periods of salivary protein and bacteria accumulation on the surface. Crystalline Calcium Phosphate Salt Carbohydrate -protein complex Calcium ions Precipitation Early stages of mineralization Brushite Late stages of mineralization Octacalcium phosphate Final stages of mineralization Whitlockite Apatite Reference : Schroeder , 1969 Decline from maximal - Reversal phenomenon Mechanical wear from food and from the cheeks, lips and tongue Maximal level - 10 weeks and 6 months
Mineral Nucleating Proteolipids Inter Bacterial Substance M M M M M M M M M M M M M Mineralisation M M M M M M M
THEORIES OF CALCULUS FORMATION BOOSTER MECHANISM EPITACTIC CONCEPT INHIBITION THEORY TRANSFORMATION THEORY BACTERIAL THEORY ENZYMATIC THEORY
Precipitation of calcium salts from the saliva to form calculus is due to the loss of carbon dioxide from the saliva (increase in pH) Formation of calculus is due to the activity of the enzyme phosphatase Formation of calculus is due to a colloidal type of precipitation Formation of calculus is due to seeding agents inducing small foci of calcification Formation of calculus is due to the presence and activity of bacteria
BOOSTER MECHANISM MECHANISM 1 MECHANISM 2 Saliva – CO2 Tension = 54 – 65 mm Hg CO2 CO2Atmosphere CO2 Tension = 0.3 mm Hg Increase in Salivary pH Dissociation of Phosphoric Acid Phosphate ions Calcium Phosphate Crystal formation Dental Plaque Bacteria / Protein Precipitation Formation of Ammonia Loss of Carbon Dioxide Increased pH of the Saliva Lowered precipitation constant Precipitation of Calcium Phosphate salts Calculus Formation Presence of carbonic anhydrase was demonstrated in the saliva Reference : Rapp - 1946
• Liberated from dental plaque, desquamated epithelial cells, or bacteria • Precipitate Calcium phosphate by hydrolyzing organic phosphates in saliva • Increasing the concentration of free phosphate ions. ENZYME Hydrolysis of Organic phosphates (saliva) Produce Inorganic Phosphates Precipitated as CALCIUM – PHOSPHATE SALTS in calculus PHOSPHATASE Reference : Wasserman et al 1958
Colloidal substances in saliva became viscous and forms a matrix for precipitation of calculus. COLLOIDAL PRECIPITATION Reference : Prinz - 1921 Inanimate Nucleus Inanimate nucleus Ca Mg Ca MgLAMINATED APPEARANCE
The term “Epitactic” refers to crystal formation through Seeding by another compound (similar to hydroxyapatite crystals), leading to precipitation of Calcium salts from the metastable solution of Saliva. EPITACTIC CONCEPT Once, Initial Seed or Nucleus is formed Certain ions, like Calcium and Phosphate present in Saliva promote the growth of Hydroxyapatite crystals Seeding Agents, then, provoke the small foci of Calcification Coalescence and Enlargement occurs Initiated by a Carbohydrate / Protein complex Important role of Intercellular Matrix and Plaque Calcified Mass forms Reference : booskey et al - 1981
Poisons the Growth centers of the Crystal and prevents Initial Nucleus from growing This theory assumes about Calcification as occurring only at specific sites because of existence of an inhibiting mechanism at non-calcifying sites. INHIBITION THEORY Inhibited “Site of Calcification” Inhibitor is either Altered or Removed Inhibiting Enzyme : ALKALINE PYROPHOSPHATASE Pyrophosphate Phosphate Reference : Russell and Fleisch 1970 Inhibiting Substance : PYROPHOSPHATE HYDROLYSIS
Formation of supragingival calculus may be prevented or controlled by I. Reducing the amount of plaque available for mineralization using antimicrobial agents and enzymes, II. Modifying the attachment of plaque by antiadhesive agents and III. Inhibiting the process of mineralization by crystal growth inhibitors. INHIBITION THEORY Mineralization inhibitors Pyrophosphates, Diphosphonates and Zinc salts Crystal growth inhibitors Most effective and successful • Adsorb to the surface of crystals, thereby reducing the rate of crystal growth and phase transformations of calcium phosphate salts. • Retained within the plaque fluid to provide a reservoir that sustains activity between applications. Inhibit the growth of hydroxyapatite crystals Inhibits the plaque formationZINC
Most Noticeable Hypothesis Hydroxyapatite need not arise exclusively via Epistaxis or Nucleation. TRANSFORMATION THEORY Amorphous non – crystalline deposits and Brushite Octa Calcium Phosphate Hydroxyapatite Reference : Eanes et al - 1970 Controlling Mechanism : PYROPHOSPHATE Reference : Fleisch et al - 1968
BACTERIOLOGICAL THEORY Primary Cause of Calculus Formation Oral Microorganisms (A) Leptotrichia cells (Gram stain). (B) Leptotrichia cells (SEM). (C) Leptotrichia cells (SEM). (D) Leptotrichia colonies. Leptotrichia Actinomyces Non viable organisms calcify readily Reference : Ennever - 1967 Plaque bacteria actively participate in calculus mineralization by forming phosphates, by changing plaque pH or inducing mineralization Reference : Ennever – 1967; Mandel - 1960 The prevalent opinion is that bacteria are only passively involved. Reference : Gonzales and Rizzo et.al 1962 Occurrence of calculus in germ free animals supports this opinion. Reference : Gjmreo – 1974; Gustaffson and Krasee – 1962 Reference : Goodrich and Moseley – 1916 Reference : Naselund 1925 – 1926
ENZYMATIC THEORY PHOSPHATASES ORAL TISSUE ORAL MICROORGANISMS SALIVARY PHOSPHATE CONTAINING COMPLEX PHOSPHERIC ESTERS of the HEXOPHOSPHORIC Group Formation of CALCULUS occurs Reference : Sahithya, RS. Essentials of Periodontology – 1st Edition
CALCULUS ATTACHMENT Attachment by means of Organic Pellicle on Enamel Mechanical Interlocking in Cemental Resorption Lacunae Penetration of Calculus Bacteria in Cementum (Not acknowledged) Close adaptation of Calculus undersurface depressions to gently sloping mounds on the unaltered cementum surface Reference : Carranza’s Clinical Periodontology Reference : Zander - 1953
Shroff (1955) Type of calculus attachment depends on the length of time the calculus has been on the tooth. the organic matrix of the deposit adhered in some manner to the tooth, there may be changes in the cementum underlying the calculus that might change the type of attachment perhaps by bacterial or chemical means • Bacteria were important in the attachment of calculus.
• Calculus attachment : Less Intimate in Pure Titanium than to root surface structures • Smooth machined implants have LESS micro porosities for retention Calculus gets chipped off from implant without affecting it. ATTACHEMENT OF CALCULUS ON IMPLANT Reference : Matarasso et al; Clin Oral Implants Res – March 1996
MICROBIOLOGY OF DENTAL CALCULUS • Average microscopic count of Bacteria in Unmineralized Plaque = 2.1 × 10 mg wet weight. • Supragingival Calculus  Viable Aerobic and Anerobic Bacteria detected • Subgingival Calculus  Excellent environment for Microbial Adhesion and Growth • Periopathogens :  Aggregatibacter actinomycetemcomitans  Porphyromonas gingivalis  Treponema denticola • Bacteria are not essential for Calculus formation, but they enable its development. • Hence, high amount of Calculus indicates Poor Oral Hygiene for months or even years. Reference : Carranza’s Clinical Periodontology Reference : Zander et al. 1960, Schroeder 1969
PREVALENCE Calculus is prevalent in populations throughout the world.  Two national surveys by have provided data on the prevalence of calculus. The prevalence of supragingival calculus only and the mean proportion of teeth affected did not increase with age. In contrast, the prevalence of subgingival calculus, with or without supragingival calculus, showed a slight but consistent increase with age for both sexes. The prevalence of both types of calculus was approximately 3% higher in boys than girls. Approximately 8% of teeth had supragingival calculus only and 4% had subgingival deposits.
They studied two populations comprising A group of with no access to dental care and practicing no oral hygiene. A group of who performed twice-daily tooth brushing and received regular dental care. All Sri Lankans and most Norwegians (93%) had some calculus.  However, only 6% of teeth were calculus free in Sri Lankans compared with 74% in Norwegians. Less than 1% of Sri Lankans had only supragingival calculus compared with 56% of Norwegians. All Sri Lankans had subgingival calculus on almost all teeth, whereas only 36% of Norwegians had subgingival deposits involving an average of 9% of teeth. Anerud et al (1991)
National Health and Nutrition Examination Survey (NHANES Ι Ι Ι) They evaluated 9689 adults in United States between 1988 and 1994 out of which 91.8 % of subjects had detectable calculus and 55.1% had subgingival calculus.
ASSESSMENT AND EVALUATION OF CALCULUS SUPRAGINGIVAL CALCULUS • Usually by Direct Vision • Unstained small amount of calculus is invisible when they are wet with saliva. SUBGINGIVAL CALCULUS • Visually when the gingival margin is pushed open by Blowing Air down the Gingival Crevice or retracted by a dental instrument. • A brownish to black calcified hard mass with a rough surface may become visible at or beneath the gingival margin that shine from through the gingival margin ( due to its dark color ) Gentle air blast Transillumination Gingival tissue color change
DENTAL PROBE EXPLORER Stable modified pen grasp, held lightly to perceive the slightest vibration conducted through the shank. Method • A stable finger rest is established. • Instrument tip is inserted into the pocket depth. • On contact with the calculus, the tip of the probe is advanced more apically till the termination of the calculus is felt on the root surface. Interproximal calculus, a highly calcified deposit, is detected as radiopaque projections protruding into the interdental space. POOR DIAGNOSTIC METHOD Reference : Buchanan et al, 1987
ADVANCED DIAGNOSTIC AIDS Calculus Detection + Removal Systems Calculus Detection Systems Only
• Strong associations between calculus deposits and periodontitis have been demonstrated in experimental and epidemiologic studies. • It has to be realized that calculus is always covered by an unmineralized layer of viable bacterial plaque. • Calculus always has a layer of plaque on its outer surface and is difficult to separate the effects of these two on the periodontal disease. • It has been debated whether or not calculus may exert a detrimental effect on the soft tissues owing to its rough surface. • It has clearly been established that surface roughness alone does not initiate gingivitis. • It has been demonstrated that autoclaved calculus may be encapsulated in connective tissue without inducing marked inflammation or abscess formation. • These studies clearly exclude the possibility of dental calculus being a primary cause of periodontal diseases. • The effect of Calculus seems to be secondary by providing an ideal surface configuration conducive to further plaque accumulation and subsequent mineralization. • Calculus may amplify the effects of bacterial plaque by keeping the bacterial deposits in close contact with the tissue surface, thereby influencing both bacterial ecology and tissue response. ETIOLOGICAL SIGNIFICANCE OF CALCULUS IN PERIODONTAL DISEASE Reference : Wrhaug - 1952, 1955; Lovdal et al. - 1958 Reference : Wrhaug 1956 Reference : Allen & Kerr 1965 Reference : Friskopp & Hammarstrom 1980 Reference : Mandel - 1990
• Damage to the gingival margin is due to immunologic and enzymatic effects of plaque microorganisms. The process is however enhanced by supragingival calculus which provides further retention and plaque accumulation. • Calculus + plaque provokes a greater reaction than plaque alone. • Microscopically mineralized parts of supra and subgingival calculus are not in contact with the periodontal tissues and calculus is covered by plaque that is in contact with epithelial cells of gingival sulcus. • A study of daily use of chlorhexidine for 2 years found gingiva remained healthy even in presence of calculus. • Electronic microscopic study in monkeys treated with CHX revealed a normal junctional epithelium attached to subgingival calculus. • Autoclaved calculus may be encapsulated in connective tissue without causing marked inflammation. • These studies clearly exclude the possibility of dental calculus being a primary cause of periodontal diseases. by providing an ideal surface configuration conducive to further plaque accumulation and subsequent mineralization Reference : Schroeder - 1969 Reference : Mandel - 1986 Reference : Waerhaug – 1953 Reference : Loe et al – 1976 Reference : Listgarten and Ellegaro – 1973 Reference : Allen and Kerr - 1965 VARIOUS STUDIES
BUT THEN… Calculus may amplify the effects of bacterial plaque by keeping the bacterial deposits in close contact with the tissue surface, thereby influencing both bacterial ecology and tissue response. Reference : Friskopp and Hammarstrom – 1980 • Dental calculus represents mineralized bacterial plaque. • It is always covered by unmineralized viable bacterial plaque, and hence, does not directly come into contact with the gingival tissues. • Calculus, therefore, is a secondary etiologic factor for periodontitis. CONCLUDING
REFERENCES  Carranza’s Clinical Periodontology : 10th Edition  Periobasics : A textbook of Periodontics and Implantology  Journal of Pharmaceuticals and Scientific Innovation • Calculus revisited: A review • Mandel, Gaffar – 1986  Journal of Health Science and Research • A Comprehensive Review on Dental Calculus : Review Article • Aghanashini S et al - 2016  Periodontology 2000 • Supraginigival dental calculus • Stanley.P Hazen. - 1995 • The natural history and clinical course of calculus formation in man Ånerud, A., Lo¨e, H. & Boysen, H. - 1991 • Supragingival calculus and periodontal disease • M Robin et al - 1997
"Your tartar is your calcified hate. Not only the microflora in your oral cavity but also your muddled thoughts, your obstinate squinting backward, the way you regress when you mean to progress, in other words, the tendency of your diseased gums to form germ catching pockets, all that, the sum of dental picture and psyche, betrays you, it is stored up violence, full of murderous designs" Gunter Grass. THANK YOU

More Related Content

PPT
Dental Calculus
byAbhishek Gakhar
 
PPTX
Dental calculus
byPawan Kumar
 
PPTX
dental calculus ishu.pptx
byDr. ISHU SINGLA
 
PPTX
Dental Calculus ppt
byDr Fariya Ashraf
 
PPTX
2.calculus
bypunitnaidu07
 
PPTX
Dental calculus & other local contributing factors
byAl Rafidain University College / Dentistry Department
 
PPTX
Dental calculus
bydrSuriya2
 
PPTX
Gingival inflammation and features
byNavneet Randhawa
 
Dental Calculus
byAbhishek Gakhar
 
Dental calculus
byPawan Kumar
 
dental calculus ishu.pptx
byDr. ISHU SINGLA
 
Dental Calculus ppt
byDr Fariya Ashraf
 
2.calculus
bypunitnaidu07
 
Dental calculus & other local contributing factors
byAl Rafidain University College / Dentistry Department
 
Dental calculus
bydrSuriya2
 
Gingival inflammation and features
byNavneet Randhawa
 

What's hot

PPTX
Chemical Plaque Control
byMehul Shinde
 
PPTX
Clinical examination of gingiva
byDr. Mariyam Momin
 
PPTX
Dental Plaque
byDr. Anuj S Parihar
 
PPTX
Healing of extraction wound
byE- Dental
 
PPTX
Plaque control
byANIL KUMAR
 
PPTX
Dental plaque
byDr. Roshni Maurya
 
PPTX
Aggressive periodontitis
byBinaya Subedi
 
PPT
Gingivectomy
byParth Thakkar
 
PPTX
Mechanical plaque control
bynaseemashraf2
 
PPTX
Periodontal instruments
byAnkita Dadwal
 
PPTX
Plaque
byGanesh Nair
 
PPTX
Plaque hypothesis ppt
byPerio Files
 
PPTX
RAMPANT CARIES ITS MANAGEMENT AND PREVENTION.pptx
byMugilarasanMunisamy
 
PPTX
Biologic width
byDentalorg.com DR.DEBAISH
 
PPTX
Clinical reatures of gingivitis
byyasmin parvin ss
 
PPTX
Desquamative Gingivitis
byDandu Prasad Reddy
 
PPTX
Gingival Recession
byManishaSinha17
 
PPTX
Phase 1 periodontal therapy
byDr.Shraddha Kode
 
PPTX
Periodontal flap
byakshay shete
 
PDF
Gingivitis
byDr.Jaffar Raza BDS
 
Chemical Plaque Control
byMehul Shinde
 
Clinical examination of gingiva
byDr. Mariyam Momin
 
Dental Plaque
byDr. Anuj S Parihar
 
Healing of extraction wound
byE- Dental
 
Plaque control
byANIL KUMAR
 
Dental plaque
byDr. Roshni Maurya
 
Aggressive periodontitis
byBinaya Subedi
 
Gingivectomy
byParth Thakkar
 
Mechanical plaque control
bynaseemashraf2
 
Periodontal instruments
byAnkita Dadwal
 
Plaque
byGanesh Nair
 
Plaque hypothesis ppt
byPerio Files
 
RAMPANT CARIES ITS MANAGEMENT AND PREVENTION.pptx
byMugilarasanMunisamy
 
Biologic width
byDentalorg.com DR.DEBAISH
 
Clinical reatures of gingivitis
byyasmin parvin ss
 
Desquamative Gingivitis
byDandu Prasad Reddy
 
Gingival Recession
byManishaSinha17
 
Phase 1 periodontal therapy
byDr.Shraddha Kode
 
Periodontal flap
byakshay shete
 
Gingivitis
byDr.Jaffar Raza BDS
 

Similar to Dental calculus

PPTX
Dental Calculus.pptx
byDrDeepika10
 
PPTX
SEMINAR on the topic Dental calculus.pptx
byBHAVIKAJAIN79612
 
PPTX
Dental calculus PERIODONTICS HARD DEPOIST
byNeHaSahoo9
 
PPT
DENTAL CALCULUS complete power point presenattion
byaruna0611
 
PPTX
13.Calculus-and-Theories-of-calculus-formation-.pptx
byDailyTech3
 
PPT
16.Role of dental calculus.ppt
byDrNavyadidla
 
PPTX
DENTAL CALCULUS.pptx
byShilpaMathew23
 
PPTX
Dental Calculus - Formation, Pathogenesis and Removal
bydmathewspanickalwest
 
PDF
Dental calculus seminar
byNarendra Chauhan
 
PPT
calculus
byssardana1234
 
PDF
DENTISTRY: The Role of Dental Calculus.pdf
bysamsondoyin12
 
PPTX
LECT 4 DENTAL CALCULUS INCLUDING FORMATION AND CAUSES.pptx
bySamkeloKhumalo2
 
PPTX
Calculus- Calcification of the plaque maturation
bySaransh6292
 
PPTX
CALCULUS kinjal.pptx
byveena621629
 
PPTX
Calculus
byAysha Khatri
 
PPTX
Calculus (Classification, composition, microbiology etc.pptx
byDr. Faheem Ahmed
 
PPTX
DENTAL CALCULUS-3RD YEAR LECTURE-1.pptx
bymahalakshmiselvam1
 
PPTX
dental calculus and preventive measures DH
byvishveshvarvms
 
PDF
CALCULUS_OB2 (1).pdf
byDrCarlosIICapitan
 
PPTX
Dental calculus
byDr. Mansi Gandhi
 
Dental Calculus.pptx
byDrDeepika10
 
SEMINAR on the topic Dental calculus.pptx
byBHAVIKAJAIN79612
 
Dental calculus PERIODONTICS HARD DEPOIST
byNeHaSahoo9
 
DENTAL CALCULUS complete power point presenattion
byaruna0611
 
13.Calculus-and-Theories-of-calculus-formation-.pptx
byDailyTech3
 
16.Role of dental calculus.ppt
byDrNavyadidla
 
DENTAL CALCULUS.pptx
byShilpaMathew23
 
Dental Calculus - Formation, Pathogenesis and Removal
bydmathewspanickalwest
 
Dental calculus seminar
byNarendra Chauhan
 
calculus
byssardana1234
 
DENTISTRY: The Role of Dental Calculus.pdf
bysamsondoyin12
 
LECT 4 DENTAL CALCULUS INCLUDING FORMATION AND CAUSES.pptx
bySamkeloKhumalo2
 
Calculus- Calcification of the plaque maturation
bySaransh6292
 
CALCULUS kinjal.pptx
byveena621629
 
Calculus
byAysha Khatri
 
Calculus (Classification, composition, microbiology etc.pptx
byDr. Faheem Ahmed
 
DENTAL CALCULUS-3RD YEAR LECTURE-1.pptx
bymahalakshmiselvam1
 
dental calculus and preventive measures DH
byvishveshvarvms
 
CALCULUS_OB2 (1).pdf
byDrCarlosIICapitan
 
Dental calculus
byDr. Mansi Gandhi
 

More from Rinisha Sinha

PPTX
Crestal approach sinus lift.pptx
byRinisha Sinha
 
PPTX
Hard Tissue Augmentation.pptx
byRinisha Sinha
 
PPTX
Ridge Split Techniques.pptx
byRinisha Sinha
 
PPT
Tissue Engineering JC.ppt
byRinisha Sinha
 
PPTX
Acute Gingival Infections.pptx
byRinisha Sinha
 
PPTX
Attached Gingiva.pptx
byRinisha Sinha
 
PPTX
Controversies in Periodontal Dressing.pptx
byRinisha Sinha
 
PPTX
Treatment of Infrabony Pockets.pptx
byRinisha Sinha
 
PPTX
Papilla Preservation Techniques.pptx
byRinisha Sinha
 
PPTX
Wilckodontics.pptx
byRinisha Sinha
 
PPTX
Ridge Augmentation II.pptx
byRinisha Sinha
 
PPTX
Immediate Implant Placement.pptx
byRinisha Sinha
 
PPTX
Guided Tissue Regeneration
byRinisha Sinha
 
PPTX
Ridge augmentation
byRinisha Sinha
 
PPTX
CBCT in Periodontology
byRinisha Sinha
 
PPTX
Antibiotics in periodontics
byRinisha Sinha
 
PPTX
Aggressive periodontitis
byRinisha Sinha
 
PPTX
Periodontal flap
byRinisha Sinha
 
PPTX
Local Anesthesia
byRinisha Sinha
 
PPTX
Blood
byRinisha Sinha
 
Crestal approach sinus lift.pptx
byRinisha Sinha
 
Hard Tissue Augmentation.pptx
byRinisha Sinha
 
Ridge Split Techniques.pptx
byRinisha Sinha
 
Tissue Engineering JC.ppt
byRinisha Sinha
 
Acute Gingival Infections.pptx
byRinisha Sinha
 
Attached Gingiva.pptx
byRinisha Sinha
 
Controversies in Periodontal Dressing.pptx
byRinisha Sinha
 
Treatment of Infrabony Pockets.pptx
byRinisha Sinha
 
Papilla Preservation Techniques.pptx
byRinisha Sinha
 
Wilckodontics.pptx
byRinisha Sinha
 
Ridge Augmentation II.pptx
byRinisha Sinha
 
Immediate Implant Placement.pptx
byRinisha Sinha
 
Guided Tissue Regeneration
byRinisha Sinha
 
Ridge augmentation
byRinisha Sinha
 
CBCT in Periodontology
byRinisha Sinha
 
Antibiotics in periodontics
byRinisha Sinha
 
Aggressive periodontitis
byRinisha Sinha
 
Periodontal flap
byRinisha Sinha
 
Local Anesthesia
byRinisha Sinha
 
Blood
byRinisha Sinha
 

Recently uploaded

PPTX
NDIS Accommodation in Redbank Plains.pptx
bysuperiorqualitycare
 
PPTX
PCOS ,PCOS MANAGEMENT, WEIGHT LOSS,INFERTILITY IN PCOS
bymukeshkumar559904
 
PPTX
Scoliosis ppt- Dr Chandresh Choudhary resident
byDr Chandresh Choudhary
 
PPTX
Sliding Filament Theory | Muscle Physiology | KEMU
bymuhammadmoazzin7
 
PPTX
x-ray circuit x-ray circuit x-ray circuit x-ray circuit
bydivyashree1714
 
PPT
Anatomy of oesophagus physiology of the esophagus first attempt.ppt
byheadent
 
PPTX
HUMAN ANATOMY OF THE HEAD ( THE SKULL.ppt)
byClevinAswani
 
PPTX
2. Physical examination.pptx for nursing students
byDesalegn Emana
 
PDF
1150130-高雄地區第517次小兒科聯合病例討論會--高雄市醫師公會.pdf
byKs doctor
 
PDF
Ultrasound NT Scan: First Trimester Nuchal Translucency Screening Guide
byFelixRendon3
 
PDF
Vaccinations in the First Year: Timing, Myths, and Why They Matter
byDr. Allen Cherer
 
PPTX
nderstanding Male Sexual Health: Challenges and Solutions
bySujoy Dasgupta
 
PDF
The Basics of EHR - What Does EHR Stand For.pdf
byThinkitive Inc
 
PPTX
chronic bronchitis.pptx By gokulakrishnan
byGOKULAKRISHNAN JANARTHANAN
 
PPTX
Favus its etiology risk factor transmission and complication and treatment
bymugheeskhan4174
 
PPTX
Heat stroke General medicine Seminar .pptx
bypvmsiddharth
 
PPTX
Foot and ankle examination for ortho residents
bysibasishBrahma1
 
PPTX
opthalmology Red Eye - medicine and healthcare
byrenitanair2000
 
PPTX
GS - Tamaka Shwasa Chikitsa -Dr Manasa M .pptx
byDr Manasa Manjunath
 
PPTX
Hormonal IUS (Mirena®) Common Myths.pptx
byWafaa Benjamin
 
NDIS Accommodation in Redbank Plains.pptx
bysuperiorqualitycare
 
PCOS ,PCOS MANAGEMENT, WEIGHT LOSS,INFERTILITY IN PCOS
bymukeshkumar559904
 
Scoliosis ppt- Dr Chandresh Choudhary resident
byDr Chandresh Choudhary
 
Sliding Filament Theory | Muscle Physiology | KEMU
bymuhammadmoazzin7
 
x-ray circuit x-ray circuit x-ray circuit x-ray circuit
bydivyashree1714
 
Anatomy of oesophagus physiology of the esophagus first attempt.ppt
byheadent
 
HUMAN ANATOMY OF THE HEAD ( THE SKULL.ppt)
byClevinAswani
 
2. Physical examination.pptx for nursing students
byDesalegn Emana
 
1150130-高雄地區第517次小兒科聯合病例討論會--高雄市醫師公會.pdf
byKs doctor
 
Ultrasound NT Scan: First Trimester Nuchal Translucency Screening Guide
byFelixRendon3
 
Vaccinations in the First Year: Timing, Myths, and Why They Matter
byDr. Allen Cherer
 
nderstanding Male Sexual Health: Challenges and Solutions
bySujoy Dasgupta
 
The Basics of EHR - What Does EHR Stand For.pdf
byThinkitive Inc
 
chronic bronchitis.pptx By gokulakrishnan
byGOKULAKRISHNAN JANARTHANAN
 
Favus its etiology risk factor transmission and complication and treatment
bymugheeskhan4174
 
Heat stroke General medicine Seminar .pptx
bypvmsiddharth
 
Foot and ankle examination for ortho residents
bysibasishBrahma1
 
opthalmology Red Eye - medicine and healthcare
byrenitanair2000
 
GS - Tamaka Shwasa Chikitsa -Dr Manasa M .pptx
byDr Manasa Manjunath
 
Hormonal IUS (Mirena®) Common Myths.pptx
byWafaa Benjamin
 

Dental calculus

  • 1.
    DR. RINISHASINHA MDS PARTI DEPARTMENTOF PERIODONTOLOGY DENTAL CALCULUS
  • 2.
    CONTENTS • Introduction • Definition •Synonyms • History • Classification • Composition • Structure of Calculus • Formation of Calculus • Theories of Calculus Formation • Calculus Attachment • Attachment of Calculus on Implant • Microbiology of Dental Calculus • Prevalence • Assessment and Evaluation of Calculus • Advanced Diagnostic Aids • Etiological Significance of Calculus in Periodontal Disease • Conclusion • Reference
  • 3.
    INTRODUCTION • Calculus isderived from GREEK words : Calcis – Limestone Tartar – white encrustations inside casks • Once a tooth erupts, various material gets accumulated on the tooth surface, frequently called tooth – accumulated deposits / materials. Soft Deposits Hard Deposits Acquired Pellicle Microbial Plaque Materia Alba Food Debris Calculus
  • 4.
    DEFINITION • Calculus isa hard deposit that forms by mineralization of dental plaque on the surface of the natural teeth and dental prosthesis, and it is generally covered by a layer of unmineralized plaque. • Dental calculus is defined as mineralized dental plaque that is permeated with crystals of various calcium phosphates. • Dental calculus is essentially mineralized plaque covered on its external surface by vital, tightly adherent non-mineralized plaque. • Calculus is a hard concretion that forms on teeth or dental prosthesis through calcification of bacterial plaque. • Dental Calculus is a deposit of inorganic salts composed primarily of calcium carbonate and phosphate mixed with food debris bacteria and desquamated epithelial cells. Reference : Carranza’s Clinical Periodontology Reference : Schroeder - 1969; Perio 2000 vol 8 - 2009 Reference : Glossary of Periodontal terms (2001); 4th edition Reference : Mandel, 1988 Reference : Greene, 1967
  • 5.
    SYNONYMS • Tartar • Disambiguation •Calcis • Odontolithiasis • Fossilized plaque Reference : Mandel et. Al; Calculus revisited : A Review - 2013
  • 6.
    • Recognized asfar as back in the 10th Century. • Hippocrates (460 – 337 BC) Found the association of dental deposits and oral disease. The deleterious effects of the teeth and gums of pituita (calculus). • Albucasis (936 – 1013 AD) Arabian physician and surgeon Explained relationship between calculus and disease. First to design a set of 14 scalers for the thorough cleaning of teeth. • Paracelsus (1535) Swiss German physician and alchemist Introduced term “tartar” as a designation for a variety of stony concretions that form in humans. Tartaric disease
  • 7.
    • For nearly5000 years, Calculus was considered to be the Prime Etiologic Agent in the Periodontal disease. • Microorganisms in Tartar were initially referred to as Animalcules. • There was a change in perception, that became most apparent in 1960’s, mainly as a response to two lines of investigation – Reference : Van Leeuwenhoek, 1967 Experimental and electron microscopic studies of developing plaque and calculus demonstrated that supra and subgingival calculus was mineralized plaque covered by an unmineralized bacterial layer. The experimental demonstration in humans that plaque, allowed to develop in the absence of oral hygiene, results in a gingivitis which is reversible on the resumption of tooth cleaning. Reference : Mandei et al – 1957; Muhleman and Schroeder – 1964; Oshrain et al - 1968 Reference : Loe et al – 1965
  • 8.
    CLASSIFICATION According to Sourceof Mineralization Salivary calculus Serumal calculus Reference : Jenkins, Stewart – 1966Reference : Carranza’s Clinical Periodontology According to Location on the tooth surface as related to the adjacent Free Gingival Margin : Supragingival calculus Subgingival Calculus According to initiation and rate of accumulation, calculus formers are classified as : Non calculus formers Slight calculus formers Moderate calculus formers Heavy calculus formers Reference : Mandel JD et al - 1976 According to Surface Exogenous Endogenous Reference : Melz – 1950
  • 9.
  • 10.
    Features •Definition •Location •Source •Distribution •Color •Consistency •Composition •Other contents •Visibility •Attachment Supragingival Calculus SubgingivalCalculus •Tightly adhering calculus deposit that forms on the crowns of the teeth coronal to the gingival margin •Forms coronal to the Gingival Margin •Derived from the Salivary Secretions : SALIVARY CALCULUS •Symmetrical arrangement, more on Facial surfaces of Maxillary Molars and Lingual surfaces of Mandibular Anterior teeth •It is white, tallow in color •Hard and clay like •More brushite and octa calcium phosphate. Less Magnesium whitlockite •Sodium content is less Salivary proteins are present •Clinically visible •Easily detached from the tooth •Calcified deposits that forms on the tooth surface below the free margin of gingiva •Deposits present apical to the crest of the Marginal Gingiva •Derived from the Gingival Exudate : SERUMINAL CALCULUS •Related to pocket depth, Heavier on Proximal Surfaces •Brown / Greenish Black in color •Hard and firm / flint or glass – like •Less brushite and octa calcium phosphate. More magnesium whitlockite •Sodium content increases with the depth of the pocket Salivary proteins are absent •Not visible on routine clinical examination •Firmly attached to the tooth surface
  • 11.
    COMPOSITION Inorganic Content Organic Content Mature Supragingival Calculus 70 – 90 percent 20- 30 percent Reference : Little et al – 1963; Lundberg et al – 1966; Schroeder – 1969 2/3 CRYSTALLINE
  • 12.
    CRYSTAL FORMS Hydroxyapetite 58%Octa Calcium Phophate 21% Magnesium Whitelockite 12% Brushite 9% HydroxyapetiteOcta Calcium Phophate Magnesium Whitelockite Brushite Calcium 27 - 29 Phosphorous 16 - 18 Carbon Dioxide 1-3 Magnesium 0.6 - 0.8 Fluoride 0.003 – 0.04 PRINCIPLE ELEMENTS 75.9 % calcium phosphate Ca3(PO4) 2 3.1 % calcium carbonate CaCO3 Traces of magnesium phosphate Mg3(PO4) 2 Other metals Traces of Na, Zn, St, Cu, Br, Mg, Fe, Al, Si, Tg, Gold COMPONENTS Monetite and Calcite in small amounts
  • 13.
    CO-RELATIVE ANALYSIS Supragingival Calculus: Hydroxyapatite + Octa Calcium Phosphate Subgingival Calculus : Large amount of Magnesium whitlockite Same Hydroxyapetite Presence of alkaline and anaerobic conditions and concomitant presence of magnesia (or Zn and CO3) Mandibular Anterior Region : Brushite (more common) Posterior Region : Magnesium whitlockite (more common) Reference : Sundberg & Friskopp 1985
  • 14.
  • 15.
    STRUCTURE OF CALCULUS MINERALCRYSTALS are deposited in an organic matrix composed of • degraded microorganisms, which are often filamentous, • embedded in a finely granular, fibrillar or amorphous ground substance and derived from organisms . The CALCULI are divided by incremental lines which tend to follow the tooth surface , • usually horizontal in supragingival calculus and • vertically in subgingival calculus. This stratification is considered to be indicative of calculus deposits growing by apposition of new layers of calcifying plaque.
  • 16.
    • A numberof different crystals types can be seen between and within the bacterial remnants, varying as identified by electron diffraction, as: • The matrix of subgingival calculus appears to be homogenous than that of supragingival calculus which frequently exhibit areas of non-decalcified material appearing at all levels. • Both types of deposits are covered by a layer of unmineralized plaque. • Recently Tan et al (2004), concluded that viable aerobic and anaerobic bacteria may be present in supragingival calculus, specifically within internal channels and lacunae. • Clinically this is important , since incomplete removal of calculus may expose these reservoirs of possible pathogenic bacteria and be a factor in recurrence of periodontal disease after treatment. STRUCTURE OF CALCULUS  Small needle shaped crystals : HYDROXYAPATITE  Long ribbon like crystals : OCTA CALCIUM PHOSPHATES (bundles and rosettes)  Large crystalline aggregates: BRUSHITE
  • 17.
    • This isa Complex Process. • Calculus is a mineralized dental plaque. • Formation of calculus is complex and involves both biological, physical and chemical processes. • Initial stage • Biofilm of pellicle, bacteria and interbacterial matrix provides an environment within which mineralization may occur with the resultant formation of calculus. • Precipitation of salts starts between 1st and 14th day of plaque formation. • However calcification has been reported to occur as soon as 4 to 8 hours. • Calcifying plaques may become 50 % mineralized in 2 days and 60 to 90 % in 12 days. • All plaque does not necessarily undergo calcification. • Plaque that does not develop into calculus reaches a plateau of maximal mineral content within 2 days. FORMATION OF CALCULUS
  • 18.
    • Plaque hasthe ability to concentrate calcium at 2 to 20 times its level in saliva. • Early plaque of heavy calculus formers contains more Ca, 3 times more Po4, and less potassium than that of non-calculus formers. • Abundant supply of urea from saliva and the high salivary film velocity promotes base formation in plaque and calcium phosphate precipitation • Begins along the inner surface of the supragingival plaque and in the attached component of subgingival plaque adjacent to the tooth. • Binding of calcium ions to the carbohydrate protein complexes followed by precipitation of crystalline Ca3(Po4)2 salts occurs. • Crystals form initially in the intercellular matrix. • Separate foci of calcification increase in size and coalesce to form solid masses of calculus. • As calcification progresses number of filamentous bacteria increases. Calcification
  • 19.
    Most susceptible tocalculus formation Lower anterior lingual and upper posterior buccal surfaces • Low sucrose concentration in saliva • High saliva film velocity • Promotes clearance of salivary sugar and acid from plaque • Higher resting plaque pH • Better access to salivary urea REASON Average daily increment of calculus formed is 0.10% to 0.15% of dry weight. As calcification progresses the number of filamentous bacteria increases and foci of calcification change from
  • 20.
    FORMATION OF CALCULUS Introductionof the entire process in a Nutshell After tooth eruption / dental prophylaxis Acquired Pellicle Development of Biofilm Maturation of Biofilm by Microorganisms Development of Plaque Mineralizing Agent from Saliva and Gingival Crevicular Fluid enters the biofilm leading to Mineralization of Plaque Intercellular Matrix Chelation Carbohydrate ComplexProtein Complex Crystalline Calcium Phosphate Salts Precipitation CoalescenceofCalcifiedMass Reference : Sahithya RS; Essesntials of Periodontology
  • 21.
    • Mineral appearsto be deposited in layers. • Mineralization is phasic with periods of mineralization being interspersed with periods of salivary protein and bacteria accumulation on the surface. Crystalline Calcium Phosphate Salt Carbohydrate -protein complex Calcium ions Precipitation Early stages of mineralization Brushite Late stages of mineralization Octacalcium phosphate Final stages of mineralization Whitlockite Apatite Reference : Schroeder , 1969 Decline from maximal - Reversal phenomenon Mechanical wear from food and from the cheeks, lips and tongue Maximal level - 10 weeks and 6 months
  • 22.
  • 23.
    THEORIES OF CALCULUSFORMATION BOOSTER MECHANISM EPITACTIC CONCEPT INHIBITION THEORY TRANSFORMATION THEORY BACTERIAL THEORY ENZYMATIC THEORY
  • 24.
    Precipitation of calciumsalts from the saliva to form calculus is due to the loss of carbon dioxide from the saliva (increase in pH) Formation of calculus is due to the activity of the enzyme phosphatase Formation of calculus is due to a colloidal type of precipitation Formation of calculus is due to seeding agents inducing small foci of calcification Formation of calculus is due to the presence and activity of bacteria
  • 25.
    BOOSTER MECHANISM MECHANISM 1MECHANISM 2 Saliva – CO2 Tension = 54 – 65 mm Hg CO2 CO2Atmosphere CO2 Tension = 0.3 mm Hg Increase in Salivary pH Dissociation of Phosphoric Acid Phosphate ions Calcium Phosphate Crystal formation Dental Plaque Bacteria / Protein Precipitation Formation of Ammonia Loss of Carbon Dioxide Increased pH of the Saliva Lowered precipitation constant Precipitation of Calcium Phosphate salts Calculus Formation Presence of carbonic anhydrase was demonstrated in the saliva Reference : Rapp - 1946
  • 26.
    • Liberated fromdental plaque, desquamated epithelial cells, or bacteria • Precipitate Calcium phosphate by hydrolyzing organic phosphates in saliva • Increasing the concentration of free phosphate ions. ENZYME Hydrolysis of Organic phosphates (saliva) Produce Inorganic Phosphates Precipitated as CALCIUM – PHOSPHATE SALTS in calculus PHOSPHATASE Reference : Wasserman et al 1958
  • 27.
    Colloidal substances insaliva became viscous and forms a matrix for precipitation of calculus. COLLOIDAL PRECIPITATION Reference : Prinz - 1921 Inanimate Nucleus Inanimate nucleus Ca Mg Ca MgLAMINATED APPEARANCE
  • 28.
    The term “Epitactic”refers to crystal formation through Seeding by another compound (similar to hydroxyapatite crystals), leading to precipitation of Calcium salts from the metastable solution of Saliva. EPITACTIC CONCEPT Once, Initial Seed or Nucleus is formed Certain ions, like Calcium and Phosphate present in Saliva promote the growth of Hydroxyapatite crystals Seeding Agents, then, provoke the small foci of Calcification Coalescence and Enlargement occurs Initiated by a Carbohydrate / Protein complex Important role of Intercellular Matrix and Plaque Calcified Mass forms Reference : booskey et al - 1981
  • 29.
    Poisons the Growth centersof the Crystal and prevents Initial Nucleus from growing This theory assumes about Calcification as occurring only at specific sites because of existence of an inhibiting mechanism at non-calcifying sites. INHIBITION THEORY Inhibited “Site of Calcification” Inhibitor is either Altered or Removed Inhibiting Enzyme : ALKALINE PYROPHOSPHATASE Pyrophosphate Phosphate Reference : Russell and Fleisch 1970 Inhibiting Substance : PYROPHOSPHATE HYDROLYSIS
  • 30.
    Formation of supragingivalcalculus may be prevented or controlled by I. Reducing the amount of plaque available for mineralization using antimicrobial agents and enzymes, II. Modifying the attachment of plaque by antiadhesive agents and III. Inhibiting the process of mineralization by crystal growth inhibitors. INHIBITION THEORY Mineralization inhibitors Pyrophosphates, Diphosphonates and Zinc salts Crystal growth inhibitors Most effective and successful • Adsorb to the surface of crystals, thereby reducing the rate of crystal growth and phase transformations of calcium phosphate salts. • Retained within the plaque fluid to provide a reservoir that sustains activity between applications. Inhibit the growth of hydroxyapatite crystals Inhibits the plaque formationZINC
  • 31.
    Most Noticeable Hypothesis Hydroxyapatiteneed not arise exclusively via Epistaxis or Nucleation. TRANSFORMATION THEORY Amorphous non – crystalline deposits and Brushite Octa Calcium Phosphate Hydroxyapatite Reference : Eanes et al - 1970 Controlling Mechanism : PYROPHOSPHATE Reference : Fleisch et al - 1968
  • 32.
    BACTERIOLOGICAL THEORY Primary Causeof Calculus Formation Oral Microorganisms (A) Leptotrichia cells (Gram stain). (B) Leptotrichia cells (SEM). (C) Leptotrichia cells (SEM). (D) Leptotrichia colonies. Leptotrichia Actinomyces Non viable organisms calcify readily Reference : Ennever - 1967 Plaque bacteria actively participate in calculus mineralization by forming phosphates, by changing plaque pH or inducing mineralization Reference : Ennever – 1967; Mandel - 1960 The prevalent opinion is that bacteria are only passively involved. Reference : Gonzales and Rizzo et.al 1962 Occurrence of calculus in germ free animals supports this opinion. Reference : Gjmreo – 1974; Gustaffson and Krasee – 1962 Reference : Goodrich and Moseley – 1916 Reference : Naselund 1925 – 1926
  • 33.
    ENZYMATIC THEORY PHOSPHATASES ORAL TISSUE ORAL MICROORGANISMS SALIVARY PHOSPHATE CONTAINING COMPLEX PHOSPHERICESTERS of the HEXOPHOSPHORIC Group Formation of CALCULUS occurs Reference : Sahithya, RS. Essentials of Periodontology – 1st Edition
  • 34.
    CALCULUS ATTACHMENT Attachment bymeans of Organic Pellicle on Enamel Mechanical Interlocking in Cemental Resorption Lacunae Penetration of Calculus Bacteria in Cementum (Not acknowledged) Close adaptation of Calculus undersurface depressions to gently sloping mounds on the unaltered cementum surface Reference : Carranza’s Clinical Periodontology Reference : Zander - 1953
  • 35.
    Shroff (1955) Type ofcalculus attachment depends on the length of time the calculus has been on the tooth. the organic matrix of the deposit adhered in some manner to the tooth, there may be changes in the cementum underlying the calculus that might change the type of attachment perhaps by bacterial or chemical means • Bacteria were important in the attachment of calculus.
  • 36.
    • Calculus attachment: Less Intimate in Pure Titanium than to root surface structures • Smooth machined implants have LESS micro porosities for retention Calculus gets chipped off from implant without affecting it. ATTACHEMENT OF CALCULUS ON IMPLANT Reference : Matarasso et al; Clin Oral Implants Res – March 1996
  • 37.
    MICROBIOLOGY OF DENTALCALCULUS • Average microscopic count of Bacteria in Unmineralized Plaque = 2.1 × 10 mg wet weight. • Supragingival Calculus  Viable Aerobic and Anerobic Bacteria detected • Subgingival Calculus  Excellent environment for Microbial Adhesion and Growth • Periopathogens :  Aggregatibacter actinomycetemcomitans  Porphyromonas gingivalis  Treponema denticola • Bacteria are not essential for Calculus formation, but they enable its development. • Hence, high amount of Calculus indicates Poor Oral Hygiene for months or even years. Reference : Carranza’s Clinical Periodontology Reference : Zander et al. 1960, Schroeder 1969
  • 38.
    PREVALENCE Calculus is prevalentin populations throughout the world.  Two national surveys by have provided data on the prevalence of calculus. The prevalence of supragingival calculus only and the mean proportion of teeth affected did not increase with age. In contrast, the prevalence of subgingival calculus, with or without supragingival calculus, showed a slight but consistent increase with age for both sexes. The prevalence of both types of calculus was approximately 3% higher in boys than girls. Approximately 8% of teeth had supragingival calculus only and 4% had subgingival deposits.
  • 39.
    They studied twopopulations comprising A group of with no access to dental care and practicing no oral hygiene. A group of who performed twice-daily tooth brushing and received regular dental care. All Sri Lankans and most Norwegians (93%) had some calculus.  However, only 6% of teeth were calculus free in Sri Lankans compared with 74% in Norwegians. Less than 1% of Sri Lankans had only supragingival calculus compared with 56% of Norwegians. All Sri Lankans had subgingival calculus on almost all teeth, whereas only 36% of Norwegians had subgingival deposits involving an average of 9% of teeth. Anerud et al (1991)
  • 40.
    National Health andNutrition Examination Survey (NHANES Ι Ι Ι) They evaluated 9689 adults in United States between 1988 and 1994 out of which 91.8 % of subjects had detectable calculus and 55.1% had subgingival calculus.
  • 41.
    ASSESSMENT AND EVALUATIONOF CALCULUS SUPRAGINGIVAL CALCULUS • Usually by Direct Vision • Unstained small amount of calculus is invisible when they are wet with saliva. SUBGINGIVAL CALCULUS • Visually when the gingival margin is pushed open by Blowing Air down the Gingival Crevice or retracted by a dental instrument. • A brownish to black calcified hard mass with a rough surface may become visible at or beneath the gingival margin that shine from through the gingival margin ( due to its dark color ) Gentle air blast Transillumination Gingival tissue color change
  • 42.
    DENTAL PROBE EXPLORER Stable modifiedpen grasp, held lightly to perceive the slightest vibration conducted through the shank. Method • A stable finger rest is established. • Instrument tip is inserted into the pocket depth. • On contact with the calculus, the tip of the probe is advanced more apically till the termination of the calculus is felt on the root surface. Interproximal calculus, a highly calcified deposit, is detected as radiopaque projections protruding into the interdental space. POOR DIAGNOSTIC METHOD Reference : Buchanan et al, 1987
  • 43.
    ADVANCED DIAGNOSTIC AIDS CalculusDetection + Removal Systems Calculus Detection Systems Only
  • 44.
    • Strong associationsbetween calculus deposits and periodontitis have been demonstrated in experimental and epidemiologic studies. • It has to be realized that calculus is always covered by an unmineralized layer of viable bacterial plaque. • Calculus always has a layer of plaque on its outer surface and is difficult to separate the effects of these two on the periodontal disease. • It has been debated whether or not calculus may exert a detrimental effect on the soft tissues owing to its rough surface. • It has clearly been established that surface roughness alone does not initiate gingivitis. • It has been demonstrated that autoclaved calculus may be encapsulated in connective tissue without inducing marked inflammation or abscess formation. • These studies clearly exclude the possibility of dental calculus being a primary cause of periodontal diseases. • The effect of Calculus seems to be secondary by providing an ideal surface configuration conducive to further plaque accumulation and subsequent mineralization. • Calculus may amplify the effects of bacterial plaque by keeping the bacterial deposits in close contact with the tissue surface, thereby influencing both bacterial ecology and tissue response. ETIOLOGICAL SIGNIFICANCE OF CALCULUS IN PERIODONTAL DISEASE Reference : Wrhaug - 1952, 1955; Lovdal et al. - 1958 Reference : Wrhaug 1956 Reference : Allen & Kerr 1965 Reference : Friskopp & Hammarstrom 1980 Reference : Mandel - 1990
  • 45.
    • Damage tothe gingival margin is due to immunologic and enzymatic effects of plaque microorganisms. The process is however enhanced by supragingival calculus which provides further retention and plaque accumulation. • Calculus + plaque provokes a greater reaction than plaque alone. • Microscopically mineralized parts of supra and subgingival calculus are not in contact with the periodontal tissues and calculus is covered by plaque that is in contact with epithelial cells of gingival sulcus. • A study of daily use of chlorhexidine for 2 years found gingiva remained healthy even in presence of calculus. • Electronic microscopic study in monkeys treated with CHX revealed a normal junctional epithelium attached to subgingival calculus. • Autoclaved calculus may be encapsulated in connective tissue without causing marked inflammation. • These studies clearly exclude the possibility of dental calculus being a primary cause of periodontal diseases. by providing an ideal surface configuration conducive to further plaque accumulation and subsequent mineralization Reference : Schroeder - 1969 Reference : Mandel - 1986 Reference : Waerhaug – 1953 Reference : Loe et al – 1976 Reference : Listgarten and Ellegaro – 1973 Reference : Allen and Kerr - 1965 VARIOUS STUDIES
  • 46.
    BUT THEN… Calculus mayamplify the effects of bacterial plaque by keeping the bacterial deposits in close contact with the tissue surface, thereby influencing both bacterial ecology and tissue response. Reference : Friskopp and Hammarstrom – 1980 • Dental calculus represents mineralized bacterial plaque. • It is always covered by unmineralized viable bacterial plaque, and hence, does not directly come into contact with the gingival tissues. • Calculus, therefore, is a secondary etiologic factor for periodontitis. CONCLUDING
  • 47.
    REFERENCES  Carranza’s Clinical Periodontology: 10th Edition  Periobasics : A textbook of Periodontics and Implantology  Journal of Pharmaceuticals and Scientific Innovation • Calculus revisited: A review • Mandel, Gaffar – 1986  Journal of Health Science and Research • A Comprehensive Review on Dental Calculus : Review Article • Aghanashini S et al - 2016  Periodontology 2000 • Supraginigival dental calculus • Stanley.P Hazen. - 1995 • The natural history and clinical course of calculus formation in man Ånerud, A., Lo¨e, H. & Boysen, H. - 1991 • Supragingival calculus and periodontal disease • M Robin et al - 1997
  • 48.
    "Your tartar isyour calcified hate. Not only the microflora in your oral cavity but also your muddled thoughts, your obstinate squinting backward, the way you regress when you mean to progress, in other words, the tendency of your diseased gums to form germ catching pockets, all that, the sum of dental picture and psyche, betrays you, it is stored up violence, full of murderous designs" Gunter Grass. THANK YOU