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Dental calculus

This document discusses dental calculus, including its definition, classification, prevalence, formation, and clinical significance. It covers several key points: - Calculus is mineralized dental plaque that forms on tooth surfaces. It consists primarily of hydroxyapatite and other calcium phosphate minerals. - Calculus formation starts within days as plaque mineralizes. By age 30, most people have calculus covering all tooth surfaces. - Calculus promotes further plaque buildup and can harbor bacteria. It is detected using visual, tactile, radiographic, and newer optical methods. - Removing calculus through scaling disrupts the bacterial matrix and is an important part of periodontal therapy. Various chemical and enzymatic

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DENTAL CALCULUS AND ROLE OF IATROGENIC FACTORS Presented by Mansi Gandhi
Definitions History Classification Supragingival calculus Subgingival calculus Prevalance Rate of formation Attachment of calculus Diagnosis Formation of calculus Theories of mineralization Clinical significance Anticalculus agents Indices Future research CONCLUSION REFERENCES
DEFINITION:  Calculus is a hard deposit that is formed by mineralization of dental plaque on the surfaces of natural teeth and dental prosthesis, generally covered by a layer of unmineralized plaque. ( carranza ) Schroder ( 1969) defined calculus as mineralised plaque that is permeated with crystals of various calcium phosphates.
DISTRIBUTION
Muhler and Enever,1962)
Proteins5.9-8.2% Salivaryproteins Lipids0.2% Neutralfats Freefattyacids Cholesterol Phospholipids Carbohydrates1.9-9.1% Galactose Glucose Rhamnose Galactosamin Glucosamine Gluconate (Little, 1964)
are detectedHydroxyapatite and Octacalcium phosphate frequently in supragingival calculus. (97-100%) Brushite - mandibular anterior region; present only in the early-stage supragingival calculus (Rowles, 1964). When supragingival calculus ages- Brushite HAP,OCP&WHT (Shroeder,1967) Magnesium whitlockite - in the posterior areas
D i s t r i b u t i o n o f c a l c i u m p h o s p h a t e c o m p o u n d s OCP - detected near the superficial layer always in contact with saliva HA was the main component - Middle layer of the calculus. WL - adjacent to the gingival and subgingivalcalculus. Brushite - very rare ; adjacent to the gingiva.
Location Colour Textureand consistency
calculus except that it has higherSimilar to supragingival concentration of-Ca,Mg,Fl. Ca:P ratio is higher Na content increases with depth of periodontal pocket Salivary proteins are absent. Supragingival & subgingival calculus contains 37% & 58% mineral content by volume respectively
Whitlockite – mainly found Same HAP, more WL, less Brushite and OCP as compared to supragingival calculus WL to HAP ratio ishigher
calculus - interproximal surface ; least- buccalSubgingival surfaces. Maxillary incisors and bicuspids - least involved. Supragingival calculus starts forming with 6 years of eruption age while Subgingival at 8 yrs of age ; Subgingival calculus is least before 20 yrs of age. Deposition of supragingival calculus - maximal scores around 25 to 30 yrs. of age; By age 45 only a few teeth ,typically the premolars were without calculus By age 30 - all surfaces of all teeth had subgingival calculus without any pattern of predilection.
Plaque mineralization begins within 24-72 hrs and takes an average of 12 days to mature. Soft plaque is hardened by mineralization between 1st and 14th days of plaque formation. Calcification is reported to occur in as little as 4-8 hrs. (Tibetts 1970) Calcifying plaque may become 50% mineralized in 2 days and 60% to 90%mineralization in 12 days
Calculus is formed in layers which are often separated by a thin cuticle that becomes embedded in calculus as calcification progresses. Plaque has the ability to concentrate calcium at 2 to 20 times its level in saliva.
• vary from person to person for different teeth and at different times of same person According to this they are classified as heavy, moderate or slight calculus former (MuhlerandEnnever1962) slight moderate heavy
Early plaque of heavy calculus former - more calcium, three times more phosphorous and less potassium than that of non- calculus former The average daily increment in calculus former- 0.10% to 0.15% of dry weight The time required by calculus to reach the maximal level has been reported as 10 weeks(Conroy 1968) and 6 months.(Volpe 1969)
Attachmentby meansoforganic pellicleonenamel Mechanical interlockingin cementalresorption lacunae Closeadaptationof calculus undersurface depressionsto gentlysloping moundsonthe unaltered cementumsurface. Penetration of calculus bacteria in cementum. But this modeofattachment was not acknowledged Modes of attachment of calculus
ATTACHMENT OF CALCULUS ON IMPLANT Attachmenttopuretitaniumislessintimatethantorootsurfacesstructure. Smoothmachinedimplantshavelessmicroporositiesforretention. (Thiswouldmeanthatcalculusmaybechippedofffromimplantswithoutaffectingit) Matarrasoetal1996
ROLE OF MICRO-ORGANISMS IN MINERALIZATION Mineralization of plaque starts both extracellulary & intracellulary by gram +ve and –ve microorganisms. Filamentous organisms,diptheroids,bacterionema and vellionella species have the ability to form intracellular apatite crystals. Bacterial plaque may actively participate in the mineralization of calculus by forming phosphates, which changes the Ph of plaque and induces mineralization.
 Two principal categories are  Mineral precipitation theory - resultsfromlocalriseinthe degreeofsaturationof CaandPhosphate ions which maybe dueto  1.risein phofsaliva.  2.colloidalproteins.  3.phosphatase liberatedfrom dentalplaque  Epitactic concept or hetrogenous nucleation or Seeding theory – seeding agents induce small foci of calcification that enlarge and coalesce to form a calcified mass.
FEW PROPOSED THEORIESARE: 1. Booster mechanism 2. Epitactic concept 3. Inhibition theory 4. Transformation theory 5. Bacterial theory 6. Enzymatic theory
Calcification will occur in a particular locus when local pH + calcium and phosphorous concentrations  precipitation of a calcium phosphate salt. Factors such as 1. loss of CO2 & production of ammonia could account for an elevation in pH; 2. Acid or alkaline phosphatase activity could result in a higher phosphate concentration; 3. Liberation of bound or complexed calcium from the salivary proteins would produce higher calciumlevels.
Saliva– CO2tension=54-65mmHg AtmosphereCO2tension=0.3 mmHg CO2 CO2 CO2 IncreaseinsalivarypH Dissociationofphosphoric acid Phosphateions Calciumphosphatecrystal formation
UREA AMMONIA INCREASEINpH PRECIPITATIONOFCALCIUMPHOSPHATE Mandel and thompson 1967- Rapid calculus producers have a higher than average urea concentrationsin salivawhichincreasesammonialevelsin plaque
 Seeding agents induce small foci of calcification that enlarge and coalesce to form a calcified mass.  Carbohydrate protein complexes initiates the calcification by removing calcium from saliva by chelation and binds with the nuclei that induce subsequent deposition of minerals.
Calcification at specific sites - because of inhibiting mechanism at non-calcifying sites. The sites where calcification occurs , the inhibitor is apparently altered or removed. Possible inhibiting substance- pyrophosphate & other polyphosphates. Among controlling mechanisms is the enzyme pyrophosphatase - hydrolyze the pyrophosphate  alkaline phosphate (Russell and Fleisch 1970). Pyrophosphate inhibits calcification - prevents the initial nucleus from growing, possibly by poisoning the growth centers of thecrystals
Hypothesis - hydroxyapatite need not arise exclusivelyvia epitaxis or nucleation. Amorphous non-crystalline deposits and brushite can be transformed into octacalcium phosphate and then to hydroxyapatite (Eanes et al 1970). It has been suggested that controlling mechanism in transformation mechanism can be pyrophosphate (Fleisch et al 1968).
Oral microorganisms are the primary cause of calculus, and that they are invovled in its attachment to the tooth surface. Leptotrichia and Actinomyces have been considered most often as the causative microorganism.
Calculus formation resultant of the derived is the from either oral tissues action of or oral on some salivary phosphate containing phosphatases microorganism complex,most probably phospheric esters of the hexophosphoric group.(Adamson.KT1929)
Visualexamination Gentleairblast Transillumination Gingivaltissuecolorchange Tactileexamination Probe Explorer Radiographs
 CALCULUS DETECTION SYSTEMS  1. Perioscopy - perioscopy is a minimally invasive approach that was introduced in the year 2000. - Perioscope is a miniature periodontal endoscope.
 When inserted into the periodontal pocket, it images the subgingival root surface, tooth surface, and calculus.  Components of the perioscope include fiber-optic bundles bound by multiple illumination fibers, a light source, and an irrigation system.  Not widely used, owing to its high cost and the need for a rigorous training period prior to use. 2. Optical spectrometry  The Detec-Tar (Dentsply Professional, York, PA, USA) calculus detection device utilizes light-emitting diode and fiber-optic technologies.  An optical fiber in the device recognizes the characteristic spectral signals of calculus caused by the absorption, reflection, and diffraction of red light (Kasaj et al., 2008).  Advantages of the device include its portability and emission of audible and luminous signals upon calculus detection.
3. Autofluorescence-based technology  Diagnodent is a commercially available calculus detection device (Meissner and Kocher, 2011).  The InGaAsP-based red laser diode used in Diagnodent emits a wavelength of 655 nm through an optical fiber, causing fluorescence of calculus (Hibst et al., 2001)
Highly calcified interproximal calculus deposits - detectable as radioopaque projections However, the sensitivity level of calculus detection by radiographs is low. The location of calculus does not indicate the bottom of the periodontal pocket because the most apical plaque is not sufficiently calcified to be visible on radiographs.
• Brings plaque bacteria close to supporting tissues. • Provides fixed nidus for plaque accumulation. • Interferes with local self cleansing mechanisms. • Reservoir for substances like endotoxins, antigenic materials and bone resorbing factors because of its permeability and porous nature.
 Calculus inhibition influences  (1) calculus adhesion, (2) the microbial matrix and (3) crystal formation.  Two methods of theoretically inhibiting calculus are discussed:  1. Combating the colonization and adhesion of microorganisms, their multiplication, their extracellular products and their metabolic activity. Inhibitors directed against certain types of microorganisms which form a large portion of the calculus matrix (intermicrobial polysaccharides) would be required to achieve significant change in microbial composition or activity.  2. Combating initial nucleation of crystals which would play only a subordinate role in the interphase reactions between oral fluid and tooth substances..
TOOTHBRUSHING Toothpaste abrasives may interfere with supragingival calculus formation, either by removal of the matrix for the deposition of salts or removal of the calculus in the early stages of calcification. Using a quantitative scoring procedure, Villa in 1968 was able to demonstrate that thorough brushing alone could reduce calculus formation by as much as 50 percent on the lingual surfaces of the lower anterior teeth.
It is the most commonly practiced therapeutic intervention for calculus formation. Scaling and root planing is done to remove plaque and calculus from crowns and root surface of teeth. Sickles, curettes and ultrasonic and sonic instruments are most commonly used for the removal of calculus.
Laser most commonly used in periodontal therapy include 1. Semiconductor diode laser(gallium,arsenide,alluminium) 2. Solid state laser such as Nd:YAG(neodenium doped-yttrium aluminium garnet),Er:YAG & Er,Cr:YSGG(yttrium,scandilium,garnet,galium) 3. Carbon dioxide laser Among all lasers - Er:YAG laser is most suitable for the non surgical periodontal debridement.
First GENERATION: 1)DISSOLUTION • ChelatingAgents Ethylene diamine tetra acetate Sodium Hexa Metaphosphate • Acids –Aromatic sulphuric acid Nitro-muriatic Acid 20% TrichloroaceticAcid • Spring Salts • Sodium Ricinolate • Alkalies 2)ALTERING PLAQUE ATTACHMENTS Silicones Ion exchange resins.
3)PLAQUE INHIBITION Antibiotics Antiseptics Example : Niddamycin Example : Chloramines 4)MATRIX DISRUPTION Enzymes Example :Mucinase Dehydrated Pancreas Trypsin, chymotrypsin Carboxypeptidase, lipase, amylase 30% UREA( solvent action on protein)
2nd GENERATION Inhibition of crystal growth VitaminC (By crystal poisoning mechanism ) Pyrophosphatase Pyrophosphatase + Sodium fluoride Zincsalts Biphosphonates Polymers & CoPolymers
Earliest techniques - wooden stick + aromatic sulphuric acid & introduced into a periodontal pocket to dissolvecalculus(Barker 1872). Niles (1881) - the nitro muriatic acid. Other acids included - 20% trichloroacetic acid, bifluoride of mercury and 10% sulphuric acid. Disadvantages: i. Caustic to soft tissues ii. Decalcify tooth structure. (Stones (1939) and grossman (1954) so their use was discontinued
Badanes (1929) argued that it was the action of the mild alkalis contained in the waters that dissolved the principal organic constituents of salivary calculus. These findings agreed with those of Prinz (1921), but the ideafailed to find support.
Thesechemicals removecalcium from solution. • Sodium hexametaphosphate was found to remove supragingival calculus from extracted teeth in 10 to 15 days (Kerr & Field 1944). • Warren et al. (1964) exposed extracted teeth to a saturated solution of sodium hexametaphosphate for 24 h and found a large reduction in the hardness of the cementum and the decalcification of the calculus was less than that of cementum. Because of this nonspecific demineralization effect, the use of chelating agents in anticalculus dentifrices ceased.
EDTA gelJabro et al. (1992) found that application of (SofscaleTM) resulted in ease of calculus removal. However, subsequent studies by Maynar et al. (1994), Smith et al. (1994), Harding et al.(1996) and Nagy et al. (1998) have failed to confirm this effect. Smith et al. (1994) noted that sufficient time has to be allowed for the gel to penetrate the bulk of the calculus deposit and this may negate the reason for using it.
Mode of action – 1.To break down plaque matrix OR 2. To affect the binding of the calculus to the tooth. The first enzyme to be tested- mucinase (Stewart 1952)Calculus formation reduced & calculus formed was softer and more easily removed (Stewart 1952). Aleece & Forscher (1954) - introduced mylase. Enzyme with high proteolytic and low amylase activity- most effective inhibitor of calculus formation. Draus et al. (1963) Dehydrated pancreas (Viokase) - tested on the basis of a high proteolytic enzyme activity - reduce calculus formation by 60% (Jensen 1959). Enzymes of fungal origin have also been tested.
The anticalculus effect - ability to dissolve the mucoproteinaceous material within which the calcium salts are deposited and/or by increasing the solubility of calcium saltsin saliva. It was found that increasing the concentration of urea resulted in progressive inhibition of calcium deposition. A maximum inhibition of 70% was reached at a concentration of 30% urea. greater than 30% led to a progressiveUrea concentrations decrease in inhibition.
Then came into research, the concept of inhibiting urease activity. Ethanehydroxydiphosphonate (EHDP) or acetohydroxamic acid (AHA) were tested for their anti calculus potential
Results demonstrated a significant reduction formation in both the EHDP and AHAgroups. not significant in humans. ( SonBut such changes were &Muhlemann 1971) This finding together with the observation that AHA had been shown to increase caries (Regolati & Muhlemann 1971) led to a decline in interest in AHA as an anticalculusagent.
Attempts have been made to prevent calculus deposition by coating the teeth with adhesive to alter the binding of the calculus to the tooth. Dimethylpolysiloxane and cyanoacrylate monomer adhesive,- no effect Silicones- no effect Lactone- effective but caused de-mineralisation of teeth. Sulphonated polystyrene membrane – effective but temporary
Sodium ricinoleate - interferes with the attachment of microorganisms to teeth. (Dossenbach & Muhlemann (1961) The results showed almost total absence of microorganisms,and calculus formation was almost totally inhibited. Unfortunately, sodium ricinoleate had a particularly unacceptable taste and needed to be applied at high concentrations.
The magnetic water was thought to bring Ca2 and PO4 ions closer together, consequently reducing attachment. The group using a magnetic water irrigator had 44% greater reduction in calculus volume and a 42% greater reduction in calculus area when compared with the group using an irrigator with no magnetic water.
Schaeken et al. (1990) investigated a 5% calcium lactate solution on calcium and phosphate levels in saliva. The group using the dentifrices with calcium lactate had a 44% reduction in calculus and those using the calcium lactate with sodium lauryl sulphate had a 47% reduction in calculus with respect to the control group. The authors concluded that calcium lactate probably did not act asan inhibitor of crystal growth but may offset secretion and activity of salivary phosphoproteins.
Penicillin- no effect Cetylpyridinium chloride- no effect Chlorhexidine Chlorhexidine is a cationic bis-biguanide which acts by being adsorbed onto the bacterial cell wall, leading to damage of the permeability barriers. At higher concentrations, precipitation and coagulation of the cytoplasmic contents occurs (Hennessey 1977). Many studies have confirmed that chlorhexidine is an excellent antiplaque agent (Lo¨ e & Schiott 1970, Hamp et al. 1973, Tepeet al.1983)
Strong activity toward a variety of gram positive organisms; enterococci, corynebacteria, bacilli and certainstreptococci, protozoas. No known medical uses; not significantly absorbed orally or systemically, and no in vivo bacterial resistance had been reported (Stallard et al.1969). Research into the use of Niddamycin as an anticalculus agent was discontinued - concern over the development of bacterial cross resistance to other antimicrobials.
Triclosan ( trivial name of 2,4,4-trichloro-2-hydroxydiphenyl ether) a non-ionic antibacterial agent with a wide spectrum of activity against bacteria, fungi and yeasts. When delivered from a dentifrice- seems to bind to oral mucous membranes and tooth surfaces, and is particularly well retained in plaque. Triclosan is predominantly used in combination with other anti- calculus
PVM/MA Copolymer is a copolymer of methyl vinyl ether and maleic anhydride and is used as a binder. Promotes uptake of triclosan by enamel and buccal epithelial cells (Nabi et al., 1989). Composed of two groups: an attachment group and a solubilizing group. The solubilizing group retains triclosan in surfactant micelles so that the attachment group can have enough time to react with tooth surfaces via calcium in the liquid adherent layer.
Metals Use of heavy metals - suggested by Hanke (1940) - in solution, these metals suffered from having a disagreeable metallic taste, or caused an unsightly discoloration of the teeth. Mechanisms by which they can affect calculus formation: i. Firstly, they inhibit plaque growth. ii. Secondly, metal salts are potent inhibitors of mineralization (Bachra & van Harskamp 1970, Thomas 1982). Metal ions can bind to hydroxyapatite although this binding is reversible.
ZINC ions 1. Reduce plaque acidogenicity (Opperman 1980) 2. Plaque growth (Saxton 1986) It inhibits crystal growth by binding to the surface of solid CaP (Gilbert 1988) Zn at a conc of 0.1mmol/L inhibits the formation of DCPD,OCP and amorphous Ca P but at a higher conc of0.5-2 mmol/L promotes the formation of amorphousCaP.
Bisphosphonates are a group of synthetic pyrophosphate analogues thought to prevent calculus deposition by inhibiting crystal growth. BISPHOSPHONATES
Vitamin C is a surface active organophosphorus compound that has been shown to be effective in inhibiting the in vitro crystallization of calcium phosphate on to smears of supragingival calculus (Turesky et al. 1965). crystal growth by a crystal poisoningVitamin C inhibits mechanism.
Pyrophosphate could prevent calcification by 1. Interrupting the conversion of amorphous calcium phosphate to hydroxyapatite (Fleisch & Bisaz 1962 2. Inhibiting crystal growth 3. Reduce acquired pellicle formation. Lower concentrations of pyrophosphate were noted in the parotid saliva of calculus formers than in saliva of non-formers (Vogel & Amdur 1967). The concentration of pyrophosphate in the plaque of low calculus formers was also significantly greater than that in heavy calculus formers (Edgar & Jenkins 1972).
Pyrophosphate undergo rapid hydrolysis in the oral cavityby bacterial and host phosphatases (Gaffar et al 1986) The addition of co polymer PVM/MA is believed toprevent this hydrolysis
Two indices – quantitating calculus deposits calculus component of OHI calculus component of PI Calculus surface index (Ennever 1961) Marginal line calculus index (Muhlem1967) Volpe – manhold index (1965) Calculus surface severity index
 Role of iatrogenic factors
a. Proximal contact relation: The integrity and location of the proximal contacts prevent interproximal food impaction. Food impaction is the forceful wedging of food into the periodontium by occlusal forces.
• They appear as narrow wedge-shaped extensions of enamel pointing from the cementoenamel junction (CEJ) toward the furcation area. The clinical significance of CEPs is that they are plaque retentive and can predispose to furcation involvement.
• The palatogingival groove often begins at the cingulum and extends apically for a variable distance. • Deep pocketing of maxillary incisors, especially isolated, should prompt an examination for this plaque – retentive root anomaly. • If the palatogingival groove is associated with bone loss and attachment loss, the clinician may attempt to remove the groove through odontoplasty or to reduce its depth to minimize plaque retention .
• Inadequate dental procedures that contribute to the deterioration of the periodontal tissues are referred to as iatrogenic factors.
• The improper use of rubber dam clamps, matrix bands and burs can lacerate the gingiva resulting in varying degree of mechanical trauma and inflammation. • Restorations can do more harm than good to the patient’s oral health if performed improperly. Overhanging margins of restorations and crowns accumulate additional plaque by limiting the patient’s access.
• Overcontoured crowns and restorations tend to accumulate plaque and possibly prevent the self- cleaning mechanisms of the adjacent cheek, lips, and tongue. Restorations that fail to reestablish adequate interproximal embrasure spaces are associated with papillary inflammation. • Overhanging margins: (1)changing the ecologic balance of the gingival sulcus to an area that favors the growth of disease- associated organisms (predominately gram- negative anaerobic species) at the expense of the health-associated organisms (predominately gram- positive facultative species) and (2)inhibiting the patient's access to remove accumulated plaque.
• Gross iatrogenic irritants such as poorly designed clasps, prosthesis saddles and pontics exert a direct traumatic influence upon periodontal tissues.
• Orthodontic therapy may affect the periodontium by brackets favoring plaque retention, by directly injuring the gingiva as a result of overextended bands, chemical irritation by exposed cement and by creating excessive, unfavorable forces, or both.
• The extraction of impacted third molars often results in the creation of vertical bone defects distal to the second molars. • Careless use of elevators or forceps during extraction results in crushing of alveolar bone.
• Crowded or malaligned teeth can be more difficult to clean than properly aligned teeth. • In deepbite, maxillary incisors impinge on the mandibular labial gingiva or mandibular incisors on the palatal gingiva, causing gingival and periodontal inflammation.
• The tooth surface, usually the root surface, can be abraded away by improper toothbrushing technique, especially with a hard toothbrush. • The abrasives in toothpaste may contribute significantly to this process. The defect usually manifests as V- shaped notches at the level of the CEJ. Tooth brush trauma
• Flossing & tooth picks can also cause damage to dental hard and soft tissues. • Flossing clefts may be produced when floss is forcefully snapped through the contact point so that it cuts into the gingiva. Also, anaggressive up and down cleaning motion can produce a similar injury.
• Mouth breathing can dehydrate the gingival tissues and increase susceptibility to inflammation. • These patients may or may not have increased levels of dental plaque. In some cases, gingival enlargement may also occur. • Excellent plaque control and professional cleaning should be recommended, although these measures may not completely resolve the gingival inflammation.
• is often associated with an anterior open bite. • During swallowing the tongue is thrust forward against the teeth instead of being placed against the palate. • When the amount of pressure against the teeth is great, it can lead to tooth mobility and cause increased spacing of the anterior teeth. • This problem is difficult to treat but must be recognized in the diagnostic phase as a potentially destructive contributing factor.
• Smoking is one of the most significant risk factors currently available to predict the development and progression of periodontitis.
• Self-inflicted or factitial injuries can be difficult to diagnose because their presentation is often unusual. These injuries are produced in a variety of ways including pricking the gingiva with a fingernail , with knives, hair pins and by using toothpicks or other oral hygiene devices.
While the bacterial plaque that coats the teeth is the main etiologic factor in the development of periodontal disease, the removal of subgingival plaque and calculus constitute the cornerstone of periodontal therapy. Calculus plays an important role in maintaining and accentuating periodontal disease by keeping plaque in close contact with the gingival tissue and creating areas where plaque removal is impossible. Therefore the clinician must possess the clinical skill to remove the calculus and other irritants as a basis for adequate periodontal and prophylactic therapy.
CARRANZA–CLINICALPERIODONTOLOGY10THED JANLINDHE– CLINICALPERIODONTOLOGYANDIMPLANTOLOGY4THED SUPRAGINGIVALCALCULUS:FORMATIONANDCONTROL(YEJIN) SUPRAGINGIVALCALCULUSANDPERIODONTALDISEASE,PERIO2000(ROBINM .DAVIESR,OGERP.ELLWOODA,NTHONYR.VOLPE&MARGAREET.P ETRONE) CALCULUSREVISITED:Areview ,MandeiIDandGaffar249-257PeriodontolJ9S6; ANTICALCULUSAGENTS (FairbrotherKJ,HeasmanPA:Anticalculusagents.JClinPeriodontol2000;27:285– 301.CMunksgaard, 2000.)
SUBGINGIVALCALCULUS:WHEREAREWENOW?ACOMPARATIVEREVIEW (E.A.Roberts-Harry*,V.Clerehugh) CALCULUS-DETECTIONTECHNOLOGIESANDTHEIRCLINICALAPPLICATION (GritMeissner&ThomasKocher)PERIO2000 CALCULUSREMOVALANDTHEPREVENTIONOFITSFORMATION (SørenJepsen,JamesDeschner,AndreasBraun,FrankSchwarz&Jo¨ Rg Eberhard) PERIO2000. WHITEDJ:DENTEDCALCULUS:RECENTINSIGHTSINTOOCCURRENCE, FORMATION,PREVENTION,REMOVALANDORALHEALTHEFFECTSOF SUPRAGINGIVALANDSUBGINGIVALDEPOSITS (.EurJOralSci1997:105:508-522.©Munksgaard,1997)
Dental calculus

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Dental calculus

  • 1.
    DENTAL CALCULUS ANDROLE OF IATROGENIC FACTORS Presented by Mansi Gandhi
  • 2.
    Definitions History Classification Supragingival calculus Subgingival calculus Prevalance Rateof formation Attachment of calculus Diagnosis Formation of calculus Theories of mineralization Clinical significance Anticalculus agents Indices Future research CONCLUSION REFERENCES
  • 3.
    DEFINITION:  Calculus isa hard deposit that is formed by mineralization of dental plaque on the surfaces of natural teeth and dental prosthesis, generally covered by a layer of unmineralized plaque. ( carranza ) Schroder ( 1969) defined calculus as mineralised plaque that is permeated with crystals of various calcium phosphates.
  • 5.
  • 6.
  • 7.
  • 8.
    are detectedHydroxyapatite andOctacalcium phosphate frequently in supragingival calculus. (97-100%) Brushite - mandibular anterior region; present only in the early-stage supragingival calculus (Rowles, 1964). When supragingival calculus ages- Brushite HAP,OCP&WHT (Shroeder,1967) Magnesium whitlockite - in the posterior areas
  • 11.
    D i st r i b u t i o n o f c a l c i u m p h o s p h a t e c o m p o u n d s OCP - detected near the superficial layer always in contact with saliva HA was the main component - Middle layer of the calculus. WL - adjacent to the gingival and subgingivalcalculus. Brushite - very rare ; adjacent to the gingiva.
  • 12.
  • 13.
    calculus except thatit has higherSimilar to supragingival concentration of-Ca,Mg,Fl. Ca:P ratio is higher Na content increases with depth of periodontal pocket Salivary proteins are absent. Supragingival & subgingival calculus contains 37% & 58% mineral content by volume respectively
  • 14.
    Whitlockite – mainlyfound Same HAP, more WL, less Brushite and OCP as compared to supragingival calculus WL to HAP ratio ishigher
  • 15.
    calculus - interproximalsurface ; least- buccalSubgingival surfaces. Maxillary incisors and bicuspids - least involved. Supragingival calculus starts forming with 6 years of eruption age while Subgingival at 8 yrs of age ; Subgingival calculus is least before 20 yrs of age. Deposition of supragingival calculus - maximal scores around 25 to 30 yrs. of age; By age 45 only a few teeth ,typically the premolars were without calculus By age 30 - all surfaces of all teeth had subgingival calculus without any pattern of predilection.
  • 16.
    Plaque mineralization beginswithin 24-72 hrs and takes an average of 12 days to mature. Soft plaque is hardened by mineralization between 1st and 14th days of plaque formation. Calcification is reported to occur in as little as 4-8 hrs. (Tibetts 1970) Calcifying plaque may become 50% mineralized in 2 days and 60% to 90%mineralization in 12 days
  • 17.
    Calculus is formedin layers which are often separated by a thin cuticle that becomes embedded in calculus as calcification progresses. Plaque has the ability to concentrate calcium at 2 to 20 times its level in saliva.
  • 18.
    • vary fromperson to person for different teeth and at different times of same person According to this they are classified as heavy, moderate or slight calculus former (MuhlerandEnnever1962) slight moderate heavy
  • 19.
    Early plaque ofheavy calculus former - more calcium, three times more phosphorous and less potassium than that of non- calculus former The average daily increment in calculus former- 0.10% to 0.15% of dry weight The time required by calculus to reach the maximal level has been reported as 10 weeks(Conroy 1968) and 6 months.(Volpe 1969)
  • 20.
  • 21.
    ATTACHMENT OF CALCULUSON IMPLANT Attachmenttopuretitaniumislessintimatethantorootsurfacesstructure. Smoothmachinedimplantshavelessmicroporositiesforretention. (Thiswouldmeanthatcalculusmaybechippedofffromimplantswithoutaffectingit) Matarrasoetal1996
  • 22.
    ROLE OF MICRO-ORGANISMSIN MINERALIZATION Mineralization of plaque starts both extracellulary & intracellulary by gram +ve and –ve microorganisms. Filamentous organisms,diptheroids,bacterionema and vellionella species have the ability to form intracellular apatite crystals. Bacterial plaque may actively participate in the mineralization of calculus by forming phosphates, which changes the Ph of plaque and induces mineralization.
  • 23.
     Two principalcategories are  Mineral precipitation theory - resultsfromlocalriseinthe degreeofsaturationof CaandPhosphate ions which maybe dueto  1.risein phofsaliva.  2.colloidalproteins.  3.phosphatase liberatedfrom dentalplaque  Epitactic concept or hetrogenous nucleation or Seeding theory – seeding agents induce small foci of calcification that enlarge and coalesce to form a calcified mass.
  • 25.
    FEW PROPOSED THEORIESARE: 1.Booster mechanism 2. Epitactic concept 3. Inhibition theory 4. Transformation theory 5. Bacterial theory 6. Enzymatic theory
  • 26.
    Calcification will occurin a particular locus when local pH + calcium and phosphorous concentrations  precipitation of a calcium phosphate salt. Factors such as 1. loss of CO2 & production of ammonia could account for an elevation in pH; 2. Acid or alkaline phosphatase activity could result in a higher phosphate concentration; 3. Liberation of bound or complexed calcium from the salivary proteins would produce higher calciumlevels.
  • 27.
  • 28.
    UREA AMMONIA INCREASEINpH PRECIPITATIONOFCALCIUMPHOSPHATE Mandel and thompson1967- Rapid calculus producers have a higher than average urea concentrationsin salivawhichincreasesammonialevelsin plaque
  • 29.
     Seeding agentsinduce small foci of calcification that enlarge and coalesce to form a calcified mass.  Carbohydrate protein complexes initiates the calcification by removing calcium from saliva by chelation and binds with the nuclei that induce subsequent deposition of minerals.
  • 30.
    Calcification at specificsites - because of inhibiting mechanism at non-calcifying sites. The sites where calcification occurs , the inhibitor is apparently altered or removed. Possible inhibiting substance- pyrophosphate & other polyphosphates. Among controlling mechanisms is the enzyme pyrophosphatase - hydrolyze the pyrophosphate  alkaline phosphate (Russell and Fleisch 1970). Pyrophosphate inhibits calcification - prevents the initial nucleus from growing, possibly by poisoning the growth centers of thecrystals
  • 31.
    Hypothesis - hydroxyapatiteneed not arise exclusivelyvia epitaxis or nucleation. Amorphous non-crystalline deposits and brushite can be transformed into octacalcium phosphate and then to hydroxyapatite (Eanes et al 1970). It has been suggested that controlling mechanism in transformation mechanism can be pyrophosphate (Fleisch et al 1968).
  • 32.
    Oral microorganisms arethe primary cause of calculus, and that they are invovled in its attachment to the tooth surface. Leptotrichia and Actinomyces have been considered most often as the causative microorganism.
  • 33.
    Calculus formation resultantof the derived is the from either oral tissues action of or oral on some salivary phosphate containing phosphatases microorganism complex,most probably phospheric esters of the hexophosphoric group.(Adamson.KT1929)
  • 34.
  • 35.
     CALCULUS DETECTIONSYSTEMS  1. Perioscopy - perioscopy is a minimally invasive approach that was introduced in the year 2000. - Perioscope is a miniature periodontal endoscope.
  • 36.
     When insertedinto the periodontal pocket, it images the subgingival root surface, tooth surface, and calculus.  Components of the perioscope include fiber-optic bundles bound by multiple illumination fibers, a light source, and an irrigation system.  Not widely used, owing to its high cost and the need for a rigorous training period prior to use. 2. Optical spectrometry  The Detec-Tar (Dentsply Professional, York, PA, USA) calculus detection device utilizes light-emitting diode and fiber-optic technologies.  An optical fiber in the device recognizes the characteristic spectral signals of calculus caused by the absorption, reflection, and diffraction of red light (Kasaj et al., 2008).  Advantages of the device include its portability and emission of audible and luminous signals upon calculus detection.
  • 37.
    3. Autofluorescence-based technology Diagnodent is a commercially available calculus detection device (Meissner and Kocher, 2011).  The InGaAsP-based red laser diode used in Diagnodent emits a wavelength of 655 nm through an optical fiber, causing fluorescence of calculus (Hibst et al., 2001)
  • 39.
    Highly calcified interproximalcalculus deposits - detectable as radioopaque projections However, the sensitivity level of calculus detection by radiographs is low. The location of calculus does not indicate the bottom of the periodontal pocket because the most apical plaque is not sufficiently calcified to be visible on radiographs.
  • 40.
    • Brings plaquebacteria close to supporting tissues. • Provides fixed nidus for plaque accumulation. • Interferes with local self cleansing mechanisms. • Reservoir for substances like endotoxins, antigenic materials and bone resorbing factors because of its permeability and porous nature.
  • 41.
     Calculus inhibitioninfluences  (1) calculus adhesion, (2) the microbial matrix and (3) crystal formation.  Two methods of theoretically inhibiting calculus are discussed:  1. Combating the colonization and adhesion of microorganisms, their multiplication, their extracellular products and their metabolic activity. Inhibitors directed against certain types of microorganisms which form a large portion of the calculus matrix (intermicrobial polysaccharides) would be required to achieve significant change in microbial composition or activity.  2. Combating initial nucleation of crystals which would play only a subordinate role in the interphase reactions between oral fluid and tooth substances..
  • 42.
    TOOTHBRUSHING Toothpaste abrasives mayinterfere with supragingival calculus formation, either by removal of the matrix for the deposition of salts or removal of the calculus in the early stages of calcification. Using a quantitative scoring procedure, Villa in 1968 was able to demonstrate that thorough brushing alone could reduce calculus formation by as much as 50 percent on the lingual surfaces of the lower anterior teeth.
  • 43.
    It is themost commonly practiced therapeutic intervention for calculus formation. Scaling and root planing is done to remove plaque and calculus from crowns and root surface of teeth. Sickles, curettes and ultrasonic and sonic instruments are most commonly used for the removal of calculus.
  • 44.
    Laser most commonlyused in periodontal therapy include 1. Semiconductor diode laser(gallium,arsenide,alluminium) 2. Solid state laser such as Nd:YAG(neodenium doped-yttrium aluminium garnet),Er:YAG & Er,Cr:YSGG(yttrium,scandilium,garnet,galium) 3. Carbon dioxide laser Among all lasers - Er:YAG laser is most suitable for the non surgical periodontal debridement.
  • 46.
    First GENERATION: 1)DISSOLUTION • ChelatingAgents Ethylenediamine tetra acetate Sodium Hexa Metaphosphate • Acids –Aromatic sulphuric acid Nitro-muriatic Acid 20% TrichloroaceticAcid • Spring Salts • Sodium Ricinolate • Alkalies 2)ALTERING PLAQUE ATTACHMENTS Silicones Ion exchange resins.
  • 47.
    3)PLAQUE INHIBITION Antibiotics Antiseptics Example :Niddamycin Example : Chloramines 4)MATRIX DISRUPTION Enzymes Example :Mucinase Dehydrated Pancreas Trypsin, chymotrypsin Carboxypeptidase, lipase, amylase 30% UREA( solvent action on protein)
  • 48.
    2nd GENERATION Inhibition ofcrystal growth VitaminC (By crystal poisoning mechanism ) Pyrophosphatase Pyrophosphatase + Sodium fluoride Zincsalts Biphosphonates Polymers & CoPolymers
  • 49.
    Earliest techniques -wooden stick + aromatic sulphuric acid & introduced into a periodontal pocket to dissolvecalculus(Barker 1872). Niles (1881) - the nitro muriatic acid. Other acids included - 20% trichloroacetic acid, bifluoride of mercury and 10% sulphuric acid. Disadvantages: i. Caustic to soft tissues ii. Decalcify tooth structure. (Stones (1939) and grossman (1954) so their use was discontinued
  • 50.
    Badanes (1929) arguedthat it was the action of the mild alkalis contained in the waters that dissolved the principal organic constituents of salivary calculus. These findings agreed with those of Prinz (1921), but the ideafailed to find support.
  • 51.
    Thesechemicals removecalcium fromsolution. • Sodium hexametaphosphate was found to remove supragingival calculus from extracted teeth in 10 to 15 days (Kerr & Field 1944). • Warren et al. (1964) exposed extracted teeth to a saturated solution of sodium hexametaphosphate for 24 h and found a large reduction in the hardness of the cementum and the decalcification of the calculus was less than that of cementum. Because of this nonspecific demineralization effect, the use of chelating agents in anticalculus dentifrices ceased.
  • 52.
    EDTA gelJabro etal. (1992) found that application of (SofscaleTM) resulted in ease of calculus removal. However, subsequent studies by Maynar et al. (1994), Smith et al. (1994), Harding et al.(1996) and Nagy et al. (1998) have failed to confirm this effect. Smith et al. (1994) noted that sufficient time has to be allowed for the gel to penetrate the bulk of the calculus deposit and this may negate the reason for using it.
  • 53.
    Mode of action– 1.To break down plaque matrix OR 2. To affect the binding of the calculus to the tooth. The first enzyme to be tested- mucinase (Stewart 1952)Calculus formation reduced & calculus formed was softer and more easily removed (Stewart 1952). Aleece & Forscher (1954) - introduced mylase. Enzyme with high proteolytic and low amylase activity- most effective inhibitor of calculus formation. Draus et al. (1963) Dehydrated pancreas (Viokase) - tested on the basis of a high proteolytic enzyme activity - reduce calculus formation by 60% (Jensen 1959). Enzymes of fungal origin have also been tested.
  • 54.
    The anticalculus effect- ability to dissolve the mucoproteinaceous material within which the calcium salts are deposited and/or by increasing the solubility of calcium saltsin saliva. It was found that increasing the concentration of urea resulted in progressive inhibition of calcium deposition. A maximum inhibition of 70% was reached at a concentration of 30% urea. greater than 30% led to a progressiveUrea concentrations decrease in inhibition.
  • 55.
    Then came intoresearch, the concept of inhibiting urease activity. Ethanehydroxydiphosphonate (EHDP) or acetohydroxamic acid (AHA) were tested for their anti calculus potential
  • 56.
    Results demonstrated asignificant reduction formation in both the EHDP and AHAgroups. not significant in humans. ( SonBut such changes were &Muhlemann 1971) This finding together with the observation that AHA had been shown to increase caries (Regolati & Muhlemann 1971) led to a decline in interest in AHA as an anticalculusagent.
  • 57.
    Attempts have beenmade to prevent calculus deposition by coating the teeth with adhesive to alter the binding of the calculus to the tooth. Dimethylpolysiloxane and cyanoacrylate monomer adhesive,- no effect Silicones- no effect Lactone- effective but caused de-mineralisation of teeth. Sulphonated polystyrene membrane – effective but temporary
  • 58.
    Sodium ricinoleate -interferes with the attachment of microorganisms to teeth. (Dossenbach & Muhlemann (1961) The results showed almost total absence of microorganisms,and calculus formation was almost totally inhibited. Unfortunately, sodium ricinoleate had a particularly unacceptable taste and needed to be applied at high concentrations.
  • 59.
    The magnetic waterwas thought to bring Ca2 and PO4 ions closer together, consequently reducing attachment. The group using a magnetic water irrigator had 44% greater reduction in calculus volume and a 42% greater reduction in calculus area when compared with the group using an irrigator with no magnetic water.
  • 60.
    Schaeken et al.(1990) investigated a 5% calcium lactate solution on calcium and phosphate levels in saliva. The group using the dentifrices with calcium lactate had a 44% reduction in calculus and those using the calcium lactate with sodium lauryl sulphate had a 47% reduction in calculus with respect to the control group. The authors concluded that calcium lactate probably did not act asan inhibitor of crystal growth but may offset secretion and activity of salivary phosphoproteins.
  • 61.
    Penicillin- no effect Cetylpyridiniumchloride- no effect Chlorhexidine Chlorhexidine is a cationic bis-biguanide which acts by being adsorbed onto the bacterial cell wall, leading to damage of the permeability barriers. At higher concentrations, precipitation and coagulation of the cytoplasmic contents occurs (Hennessey 1977). Many studies have confirmed that chlorhexidine is an excellent antiplaque agent (Lo¨ e & Schiott 1970, Hamp et al. 1973, Tepeet al.1983)
  • 62.
    Strong activity towarda variety of gram positive organisms; enterococci, corynebacteria, bacilli and certainstreptococci, protozoas. No known medical uses; not significantly absorbed orally or systemically, and no in vivo bacterial resistance had been reported (Stallard et al.1969). Research into the use of Niddamycin as an anticalculus agent was discontinued - concern over the development of bacterial cross resistance to other antimicrobials.
  • 63.
    Triclosan ( trivialname of 2,4,4-trichloro-2-hydroxydiphenyl ether) a non-ionic antibacterial agent with a wide spectrum of activity against bacteria, fungi and yeasts. When delivered from a dentifrice- seems to bind to oral mucous membranes and tooth surfaces, and is particularly well retained in plaque. Triclosan is predominantly used in combination with other anti- calculus
  • 64.
    PVM/MA Copolymer isa copolymer of methyl vinyl ether and maleic anhydride and is used as a binder. Promotes uptake of triclosan by enamel and buccal epithelial cells (Nabi et al., 1989). Composed of two groups: an attachment group and a solubilizing group. The solubilizing group retains triclosan in surfactant micelles so that the attachment group can have enough time to react with tooth surfaces via calcium in the liquid adherent layer.
  • 65.
    Metals Use of heavymetals - suggested by Hanke (1940) - in solution, these metals suffered from having a disagreeable metallic taste, or caused an unsightly discoloration of the teeth. Mechanisms by which they can affect calculus formation: i. Firstly, they inhibit plaque growth. ii. Secondly, metal salts are potent inhibitors of mineralization (Bachra & van Harskamp 1970, Thomas 1982). Metal ions can bind to hydroxyapatite although this binding is reversible.
  • 66.
    ZINC ions 1. Reduceplaque acidogenicity (Opperman 1980) 2. Plaque growth (Saxton 1986) It inhibits crystal growth by binding to the surface of solid CaP (Gilbert 1988) Zn at a conc of 0.1mmol/L inhibits the formation of DCPD,OCP and amorphous Ca P but at a higher conc of0.5-2 mmol/L promotes the formation of amorphousCaP.
  • 67.
    Bisphosphonates are agroup of synthetic pyrophosphate analogues thought to prevent calculus deposition by inhibiting crystal growth. BISPHOSPHONATES
  • 68.
    Vitamin C isa surface active organophosphorus compound that has been shown to be effective in inhibiting the in vitro crystallization of calcium phosphate on to smears of supragingival calculus (Turesky et al. 1965). crystal growth by a crystal poisoningVitamin C inhibits mechanism.
  • 69.
    Pyrophosphate could preventcalcification by 1. Interrupting the conversion of amorphous calcium phosphate to hydroxyapatite (Fleisch & Bisaz 1962 2. Inhibiting crystal growth 3. Reduce acquired pellicle formation. Lower concentrations of pyrophosphate were noted in the parotid saliva of calculus formers than in saliva of non-formers (Vogel & Amdur 1967). The concentration of pyrophosphate in the plaque of low calculus formers was also significantly greater than that in heavy calculus formers (Edgar & Jenkins 1972).
  • 70.
    Pyrophosphate undergo rapidhydrolysis in the oral cavityby bacterial and host phosphatases (Gaffar et al 1986) The addition of co polymer PVM/MA is believed toprevent this hydrolysis
  • 71.
    Two indices –quantitating calculus deposits calculus component of OHI calculus component of PI Calculus surface index (Ennever 1961) Marginal line calculus index (Muhlem1967) Volpe – manhold index (1965) Calculus surface severity index
  • 72.
     Role ofiatrogenic factors
  • 73.
    a. Proximal contactrelation: The integrity and location of the proximal contacts prevent interproximal food impaction. Food impaction is the forceful wedging of food into the periodontium by occlusal forces.
  • 74.
    • They appearas narrow wedge-shaped extensions of enamel pointing from the cementoenamel junction (CEJ) toward the furcation area. The clinical significance of CEPs is that they are plaque retentive and can predispose to furcation involvement.
  • 75.
    • The palatogingivalgroove often begins at the cingulum and extends apically for a variable distance. • Deep pocketing of maxillary incisors, especially isolated, should prompt an examination for this plaque – retentive root anomaly. • If the palatogingival groove is associated with bone loss and attachment loss, the clinician may attempt to remove the groove through odontoplasty or to reduce its depth to minimize plaque retention .
  • 76.
    • Inadequate dentalprocedures that contribute to the deterioration of the periodontal tissues are referred to as iatrogenic factors.
  • 77.
    • The improperuse of rubber dam clamps, matrix bands and burs can lacerate the gingiva resulting in varying degree of mechanical trauma and inflammation. • Restorations can do more harm than good to the patient’s oral health if performed improperly. Overhanging margins of restorations and crowns accumulate additional plaque by limiting the patient’s access.
  • 78.
    • Overcontoured crownsand restorations tend to accumulate plaque and possibly prevent the self- cleaning mechanisms of the adjacent cheek, lips, and tongue. Restorations that fail to reestablish adequate interproximal embrasure spaces are associated with papillary inflammation. • Overhanging margins: (1)changing the ecologic balance of the gingival sulcus to an area that favors the growth of disease- associated organisms (predominately gram- negative anaerobic species) at the expense of the health-associated organisms (predominately gram- positive facultative species) and (2)inhibiting the patient's access to remove accumulated plaque.
  • 79.
    • Gross iatrogenicirritants such as poorly designed clasps, prosthesis saddles and pontics exert a direct traumatic influence upon periodontal tissues.
  • 80.
    • Orthodontic therapymay affect the periodontium by brackets favoring plaque retention, by directly injuring the gingiva as a result of overextended bands, chemical irritation by exposed cement and by creating excessive, unfavorable forces, or both.
  • 81.
    • The extractionof impacted third molars often results in the creation of vertical bone defects distal to the second molars. • Careless use of elevators or forceps during extraction results in crushing of alveolar bone.
  • 82.
    • Crowded ormalaligned teeth can be more difficult to clean than properly aligned teeth. • In deepbite, maxillary incisors impinge on the mandibular labial gingiva or mandibular incisors on the palatal gingiva, causing gingival and periodontal inflammation.
  • 84.
    • The toothsurface, usually the root surface, can be abraded away by improper toothbrushing technique, especially with a hard toothbrush. • The abrasives in toothpaste may contribute significantly to this process. The defect usually manifests as V- shaped notches at the level of the CEJ. Tooth brush trauma
  • 85.
    • Flossing &tooth picks can also cause damage to dental hard and soft tissues. • Flossing clefts may be produced when floss is forcefully snapped through the contact point so that it cuts into the gingiva. Also, anaggressive up and down cleaning motion can produce a similar injury.
  • 86.
    • Mouth breathingcan dehydrate the gingival tissues and increase susceptibility to inflammation. • These patients may or may not have increased levels of dental plaque. In some cases, gingival enlargement may also occur. • Excellent plaque control and professional cleaning should be recommended, although these measures may not completely resolve the gingival inflammation.
  • 87.
    • is oftenassociated with an anterior open bite. • During swallowing the tongue is thrust forward against the teeth instead of being placed against the palate. • When the amount of pressure against the teeth is great, it can lead to tooth mobility and cause increased spacing of the anterior teeth. • This problem is difficult to treat but must be recognized in the diagnostic phase as a potentially destructive contributing factor.
  • 88.
    • Smoking isone of the most significant risk factors currently available to predict the development and progression of periodontitis.
  • 89.
    • Self-inflicted orfactitial injuries can be difficult to diagnose because their presentation is often unusual. These injuries are produced in a variety of ways including pricking the gingiva with a fingernail , with knives, hair pins and by using toothpicks or other oral hygiene devices.
  • 90.
    While the bacterialplaque that coats the teeth is the main etiologic factor in the development of periodontal disease, the removal of subgingival plaque and calculus constitute the cornerstone of periodontal therapy. Calculus plays an important role in maintaining and accentuating periodontal disease by keeping plaque in close contact with the gingival tissue and creating areas where plaque removal is impossible. Therefore the clinician must possess the clinical skill to remove the calculus and other irritants as a basis for adequate periodontal and prophylactic therapy.
  • 91.
  • 92.