plaque and calculus malti periodoto.pptx

perio

1. Dental plaque and calculus PRESENTED BY- DR MALTI GUIDED BY- DR DEEPAK GROVER PRESENTED TO- DR. VINITI GOEL(HOD&PROFF.) DR. DEEPAK GROVER (PROF.) . SARVANI CHANDEL & DR. VIKRAM (3RD YEAR) DR. SONAM (2ND YEAR) DR. SANTUSHTI & DR. ANURAG (1ST YEAR) 1

2. CONTENTS Introduction History Definition Biofilm Structure of Biofilm Characteristics of biofilm Dental plaque as biofilm Classification of dental plaque Composition of dental plaque Formation of dental plaque Pathogenesies - Plaque hypothesis Role of plaque in periodontal disesase Classification of calculus Composition of calculus 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 plaque and Calculus in Periodontal Disease Conclusion References PLAQUE and calculus 2

3. INTRODUCTION - DENTAL PLAQUE & calculus Dental plaque is a complex community of micro- organisms that forms on the surfaces of teeth and restorations. It has been implicated as the primary etiological factor in the development of periodontal disease. Periodontal disease are the result of complex interactions between the host and the bacteria and prevalence of certain bacteria increases at the sites where active periodontal destruction is taking place. Dental calculus is calcified dental plaque, composed primarily of calcium phosphate mineral salts deposited between and within remnants of formerly viable microorganisms. A viable dental plaque covers mineralized calculus deposits. Dental calculus is a hardest deposit of the dental plaque on the surface of the natural teeth or prosthesis. The word calculus derived from the Greek word CALCIS which means “lime stone” 3

4. Classification of soft deposits and hard deposits MATERIAL ALBA FOOD DEBRIS A non-cellular thin film An organized transparent deposit which is primarily composed of bacteria and their products Soft, whitish deposit with no specific architecture, which can be removed by water spray. Retained food which is usually removed by saliva and oral muscular action. Schwartz et al 1969 ACQUIRED PELLICLE DENTAL PLAQUE Mineralized plaque Calculus Stains Pigmented deposits 4

5. HISTORICAL PERSPECTIVE 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 and explained the need for the removal of deposits. Albucasis described the way to remove calculus from teeth. Paracelsus (1493-1541) swiss physician developed an interesting theory called as doctrine of calculus. He understood that pathologic calcification occurred in a variety of organs, and he considered these disease conditions to result from a metabolic disturbance.He Introduced term "tartar" as a designation for a variety of stony concretions that form in humans and Tartaric disease. In 1683, van leeuwenhoek described microorganism in tartar, he called them “ANIMALCULES” he first described oral bacteria, related lack of oral hygiene to an increase in the quantity of these organisms. He also recommended oral hygiene procedures to keep the gums healthy (use of salt, and toothpicks). 5

6. HISTORICAL PERSPECTIVE Adolph Witzel (1882) – Identified bacteria as cause of periodontal disease. WD Miller (1890) – first true oral microbiologist, periodontal disease was a mixed infection of non-specific oral flora (non-specific plaque theory) persisted largely unchallenged for almost 6 decades. J leon Williams (1897) – described dental plaque. GV black (1899) – coined term “gelatinous dental plaque”. W D Miller (1902) - Bacterial plaque Younger (1905 ) - first prominent clinicians to recognize periodontal disease as a bacterial infection . 6

7. HISTORICAL PERSPECTIVE Wild (1941) - Shortened Black’s terminology to the term ‘Plaque’ Waerhaug (1950 ) Described the importance of bacterial plaque in the etiology of periodontal disease . Until the 1960s, the prevalent thinking in dentistry was that dental calculus was the cause of periodontal diseases; that by its roughness it was irritating and that bacteria then had a secondary influence. However, a series of classic studies on experimental gingivitis published from 1965 to 1968 clearly demonstrated the causative relation between dental plaque and gingivitis 1970s, the first studies of ancient dental calculus took place on archaeological samples of cattle, sheep, and horse teeth ( Armitage, 1975) and revealed the presence of numerous oral phytoliths (silica content of some plant cells). Current thinking is that dental plaque is the precursor of calculus, which is mineralized plaque & Calculus is invariably covered with plaque on its surface. Schei (1959), Russel (1967) - Epidemiological studies- Positive correlation between the amount of bacterial plaque and the severity of gingivitis. Loe et al (1965), Landmark study on plaque , saying that plaque is main etiological agent in periodontal disease 7

8. W.Loesche (1976) - Modern theories of specificity – “Specific plaque hypothesis” Newman et al. (1976, 1977) ; Slots (1976 ) - demonstrated that the microbial composition of subgingival plaque taken from diseased sites differed substantially from the samples taken from healthy sites in subjects with localized juvenile periodontitis. Socransky 1979 - Modern Version of Specific Plaque Hypothesis Thelaide 1986 - Unified Theory PD Marsh & Martin (1999 ) - Ecological plaque hypothesis Costerton (1999) - defined Biofilm Hajishengallis et al 2012 - Keystone Pathogenic Hypothesis, Recent model for periodontal disease etiology and progression. Page and kornman non linear model 1997 Biological system model by Offenbacher 2008 PSD MODEL 2015 –Polymicrobial synergistic model Based on keystone pathogen hypothesis . 8

9. definitions Davies et al (1963) defined plaque as a soft concentrated mass containing mainly of large variety of bacteria together with certain amount of cellular debris which develops within a short time after tooth brushing. According to Schwartz & Massler (1969) – Plaque is a dense microbial Layer consisting of coherent mass of filamentous, rod like and coccoidal microorganisms embedded in an inter microbial matrix which accumulates on tooth surface Bowen W.H. (1976) defined dental plaque clinically as a structured, resilient,yellow -grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations 9

10. According to WHO (1961) DENTAL PLAQUE “ is a specific but highly variable structural entity, resulting from sequential colonization of microorganisms on tooth surfaces, restorations & other parts of oral cavity, composed of salivary components like mucin, desquamated epithelial cells, debris & microorganisms, all embedded in extracellular gelatinous matrix.” According to the GPT, 4th Edition An organized mass, consisting mainly of microorganisms, that adheres to teeth, prostheses, and oral surfaces and is found in the gingival crevice and periodontal pockets. Other components include an organic, polysaccharide-protein matrix consisting of bacterial by-products such as enzymes, food debris, desquamated cells, and inorganic components such as calcium and phosphate According to Carranza, 11th Edition Dental plaque is defined clinically as a structured, resilient yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations. Lindhe – bacterial aggregations on the teeth or other solid oral structures. 10

11. Calculus- definitions 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. Carranza clinical periodontology Dental Calculus is a deposit of inorganic salts composed primarily of calcium carbonate and phosphate mixed with food debris bacteria and desquamated epithelial cells. Greene- 1967 .Dental calculus is defined as mineralized dental plaque that is permeated with crystals of various calcium phosphates. Schroeder-1969 Dental calculus is essentially mineralized plaque covered on its external surface by vital, tightly adherent non-mineralized plaque. Mandel 1988 . Calculus is a hard concretion that forms on teeth or dental prosthesis through calcification of bacterial plaque. GPT 2001-4 TH EDITION 11

12. Definitions Calculus consists of mineralized bacterial plaque that forms on the surface of natural teeth and dental prosthesis, covered on its external surface by vital. tightly adherent, non mineralized plaque Genco When dental plaque calcifies the resulting deposit is called calculus Grant 12

13. BIOFILM Matrix enclosed bacterial populations adherent to each other and/or to surfaces or interfaces (Costerton et al, 1994) Gilbert : Bio-films are functional consortia of microbial cells enveloped within sometimes – extensive matrices of extra-cellular polymers ( glyco calyx) and concentrated products of their own metabolism together with ions and nutrients sequestrated from the environment Biofilm grow virtually everywhere in almost any environment where there is a combination of moisture, nutrient supply and surfac e. They are characterized by: Surface attachment & Extracellular matrix Structural heterogenicity & Genetic diversity Complex community interactions 13 A biofilm is defined as a community of microorganisms attached to an inert or living surface by a self-produced polymeric matrix or an assemblage of microbial cells associated with a surface and enclosed in a matrix of primarily polysaccharide material.

14. A microbial biofilm is considered a community that meets the following four basic criteria: 2/45 14

15. BASIC STRUCTURE OF BIOFILM Micro colonies of bacterial cells-15- 20% Matrix or glycocalyx-75-80% Water channels ( Sockransky 2003) The structures can be of various types based on the resource concentration ( Wimpenny & Colasanti 1997) Simple stalked/irregular branching Mushroom/tulip shaped structures penetrated by large & small pores. More or less flat homogenous structures. e.g : Human mouth 15

16. Schematic representation of the types of interaction that occur in a microbial community, such as dental plaque BENEFITS OF MICROBIAL COMMUNIY LIFESTYLE 3/45 16

17. BENEFITS OF MICROBIAL COMMUNIY LIFESTYLE OF BIOFILM 17

18. Briefly, these stages are: Reversible and irreversible adherence of cells to a conditioned surface Rapid division and growth of adherent cells A plateau of accumulation. Superimposed on accumulation of biofilm cells there is loss of cells through the action of shear forces and the shedding of daughter cells . STAGES IN THE DEVELOPMENT OF BIOFILMS: The development of biofilms follows a series of stages : (Costerton et al 1987; Characklis 1990; Gilbert et al 1993) 18

19. PROPERTIES OF BIOFILM 19

20. 1. STRUCTURE OF A BIOFILM  Biofilms are composed of microcolonies of bacterial cells (15–20% by volume) that are non-randomly distributed in a matrix or glycocalyx (75–80% volume). The bacterial vitality varies throughout the biofilm, with the most viable bacteria present in the central part of plaque. ( Auschill et al 2001) 20

21. The biofilm matrix is penetrated by fluid channels that conduct the flow of nutrients, waste products, enzymes, metabolites, and oxygen.  Structure of the Biofilm depends on environmental parameters under which they are formed. These include: • Surface and interface properties • Nutrient availability • Composition of the microbial community • Hydrodynamics 21

22. The bacteria in a biofilm use a communication system termed quorum sensing that involves sending out chemical signals .  These chemical signals trigger the bacteria to produce potentially harmful proteins and enzymes, virulence factors that help the intraoral biofilm bypass host defense systems 22

23. EXOPOLYSACCHARIDES – the backbone of the biofilm The bulk of the biofilm consists of the matrix or glycocalyx and is composed predominantly of water and aqueous solutes The “dry” material is a mixture of exopolysaccharides, proteins, salts, and cell material. Exopolysaccharides (EPS), which are produced by the bacteria in the biofilm, are the major components of the biofilm making up 50–95% of the dry weight. 23

24. 2. ATTACHMENT OF BACTERIA   The key characteristic of a biofilm - the microcolonies within the biofilm attach to a solid surface. Many bacterial species possess surface structures such as fimbriae and fibrils that aid in their attachment to different surfaces. Fimbriae have been detected on a number of oral species including P. gingivalis , A. actinomycetemcomitans and some strains of streptococci. Oral species that possess fibrils include S. salivarius , the S. mitis group, Pr. intermedia, Pr. nigrescens , and Streptococcus mutans . Sigmund S. Socransky & Anne D. Haffajee . Dental Biofilms: Difficult Therapeutic Targets Periodontology 2000 2001;28:12–55. 24

25. Selected Bacterial Adhesins & Target Substrates ATTACHMENT SURFACE SUBSTRATE BACTERIAL SPECIES ADHESIN SUBSTRATE RECEPTOR Tooth Saliva coated surfaces A.Viscsus S.Mitis F.Nucleatum Fimbriae Proline rich proteins. Saliva treated hydroxyapatite Tissue Epithelial cells Fibroblasts PMN`S Connective tissue P.Gingivalis A.Viscosus T.Denticola A.Viscosus A.Naeslundii P.Gingivalis P.intermedia Fimbriae Fimbriae Surface protein Fimbriae Membrane protein Galactosyl residues Galactosyl / Mannose residues Fibrinogen/ fibronectin Pre existing plaque mass S.Sanguis A.Naeslundii A.Israelii S.Sanguis A.Israelii P.Gingivalis C.Ochracea P.Loescheii F.Nucleatum Heat sensitive protein Fimbrial protein Outer membrane protein Rhamnose / fucose / N-acetyl neura acid Galactosyl residues 25

26. 3. PHYSIOLOGICAL HETEROGENEITY Cells of the same microbial species can exhibit extremely different physiologic states in a biofilm even though separated by as little as 10 μm . Clinical Periodontology and Implant Dentistry by Jan Lindhe , 5 th Edition. Studies to date indicate that sessile cells growing in mixed biofilms can exist in an almost infinite range of chemical and physical microhabitats within microbial communities. 26

27. The residents in the microbial community display extensive interactions while forming biofilm structures, carrying out physiological functions, and inducing microbial pathogenesis. These interactions, include Competition between bacteria for nutrients Synergistic interactions which may stimulate the growth or survival of one or more residents Production of an antagonist by one resident which inhibits the growth of another Neutralization of a virulence factor produced by one organism by another resident Interference in the growth-dependent signaling mechanisms of one organism by another. 4. MICROBIAL INTERACTIONS 27

28. Metabolic interactions among different bacterial species found in plaque , and between the host and plaque bacteria. These interactions are likely to be important for the survival of bacteria in the periodontal environment. 28

29. GENERAL METABOLIC PRODUCTS WHICH INFLUENCE BIOFILM RESIDENT INTERACTIONS Antagonistic effect - S. sanguinis group are producers of H 2 O 2 , a nonspecific antimicrobial agent - an antagonistic effect on other coresidents , such as S. mutans . Synergistic effect - lactic acid produced by S. mutans can be readily metabolized by members of the Veillonella family. Co-operative metabolic interactions - 29

30. Bacterial co-aggregation influences localization within biofilms Well characterized interaction include the coaggregation of: Fusobacterium nucleatum S. sanguis , Prevotella loescheii A. viscosus Capnocytophaga ochraceus A. viscosus Streptococci show intrageneric co-aggregation  bind to the nascent monolayer of already bound streptococci. Later stages – coaggregation between different Gram negative species seen – F. nucleatum & P. gingivalis or T. denticola 30 Fusobacterium nucleatum , can co-adhere with almost all other bacteria found in dental plaque, and is considered to be a key bridging organism between early and later colonisers Co-aggregation is the interaction between planktonic micro-organisms of a different strain or species Co-adhesion is the interaction between a sessile, already adhering organism and planktonic micro- oganisms of a different strain or species

31. BACTERIOCINS Proteinaceous bactericidal substances produced by bacteria to inhibit the growth of closely related bacterial species or strains (Hojo et al 2009) Regulated by genetic and environmental factors Enable bacteria to select their neighbours , promote the establishment of a community with specific bacterial species. Inhibition of growth of P.gingivalis , T.forsythia , S.salivarius , S.sanguinis by bacteriocin produced by L.paracaesi Nigrescin , produced by P.nigrescens display bactericidal effect against P.gingivalis , P.intermedia , T.forsythia , Actinomyces spp. Bacteriocin production also reported by P.intermedia , A.a , C.ochracea , F.nucleatum , E.corrodens , H.influenzae 31

32. 5. QUORUM SENSING It is defined as the cell density dependent regulation of gene expression in response to soluble signals called autoinducers ( Bassler 1999) It has been defined by Miller (2001) as “the regulation of gene expression in response to fluctuations in cell population density”. Quorum sensing can occur within a single bacterial  species   as well as b/w diverse species. 32

33. Quorum sensing has been described in both G+ve & G- ve bacteria. Cell-cell communication may occur b/w and within bacterial species (Miller, 2001) Quorum sensing-controlled behaviors are those that only occur when bacteria are at high cell population densities. 33

34. Three types of molecules : Acyl- homoserine lactones (AHLs) - signaling molecules used by many G- ve bacteria, it synthesized by Lux-I family protiens . Autoinducer peptides (AIPs) - signaling molecules used by G + ve bacteria Autoinducer-2 (AI-2) - used by both G- ve & G+ve bacteria, chemically it is furanosyl borate diester . Synthsized by protein Lux-S. Schauder , S. and B. L. Bassler (2001). "The languages of bacteria." QUORUM SENSING MOLECULES 34

35. 35

36. 36

37. This communication controls various functions reflecting the needs of a specific bacterial species to inhabit a particular niche such as the production of virulence factors, or by the transmission and acquisition of the generic information needed to produce virulence factors from other species in the biofilm development ( Passador et al ., 1993; Reading et al ., 2006). Several strains of P. intermedia, T. forsythia, F. nucleatum and P. gingivalis were found to produce quorum sensing signal molecules (Frias et al ., 2001; Sharma et al., 2005). 37

38. 6. ANTIBIOTIC RESISTANCE Bacteria growing in a biofilm are highly resistant to antibiotics, up to 1,000-1,500 times more resistant than the same bacteria not growing in a biofilm. MIC of chlorhexidine and amine fluoride was 300 and 75 times greater respectively, when S.sobrinus was grown in biofilm compared to planktonic cells Biofilms of P.gingivalis tolerated 160 times the MIC of metronidazole than planktonic cells 38

39. 39

40. 40

41. . 41

42. 7. EXCHANGE OF GENETIC INFORMATION Conjugation, transformation and transduction have all been shown to occur in naturally occurring mixed species biofilms. Clinical Periodontology and Implant Dentistry by Jan Lindhe , 5th Edition . 42

43. Detachment Can be Movement of Individual cells or Biofilm en masse Brading et al have emphasized the importance of physical forces in detachment, stating that the three main processes for detachment are (JADA 1996) erosion or shearing (continuous removal of small portions of the biofilm) sloughing (rapid and massive removal), and abrasion (detachment due to collision of particles from the bulk fluid with the biofilm) 43

44. Individual Cell Transfer Erosion - detachment of single cells in a continuous predictable fashion Sloughing - sporadic detachment of large groups of cells or Intermediate process whereby large pieces of biofilm are shed from the biofilm in a predictable manner, resulting in detached clusters consisting of about 104 cells. This possibility has been demonstrated in vitro studies of mixed biofilm that showed movement of intact biofilm structures across solid surfaces while remaining attached to them. Advantage - formation of the biofilm is not reliant on planktonic cells, which are known to be more susceptible to antimicrobial agents Stoodley 1991 En masse transfer 44

45. Factors affecting biofilm development and behavior ROLE OF SALIVA Saliva contains – mixture of glycoproteins – mucin. Bacteria – enzymes ( glycosidases ) – split off carb. – utilized as nutrients. Remaining protein – contributes to plaque matrix Neuraminidase – separates sialic acid from salivary glycoprotein. Loss of sialic acid - ↓ salivary viscosity - Formation of precipitate – factor in plaque formation 45

46. 2. ROLE OF INGESTED NUTRIENTS Most readily utilized nutrients – diffuse easily into plaque – sucrose, glucose, fructose, maltose & less amt. of lactose. Dextran – greater quantity, adhesive properties , relative insolubility & resistance to destruction by bacteria. Levan – Used as carbohydrate nutrient by plaque bacteria in absence of exogenous sources. 3. DIET AND PLAQUE FORMATION Consistency affects the rate of plaque formation : Forms rapidly on soft diets, hard chewy food retard it. Dietary supplements of sucrose ↑ plaque formation and affect its bacterial composition. i.e ECM Plaque formation occurs on high protein fat diets and carbohydrate - free diets but in smaller amounts. 46

47. PERIO 2000 VOLUME- 55 47

48. CLASSIFICATION 48

49. Characteristics Supragingival Subgingival Location Above the gingival margin Below the margins of gingiva Color White, yellow in color Brown or greenish-black in color Gram Reaction +/- Dominated by - Composition More brushite and octacalcium phosphate and less magnesium whitlockite Conversely less brushite and octacalcium phosphate and more magnesium whitlockite Morphological Types Cocci, branching rods, filaments, spirochetes dominated by rods and spirochetes Energy metabolism Facultative with some anaerobes Dominated by anaerobes Energy source Derived from salivary secretions. Generally ferment carbohydrates. Formed from gingival exudate Motility Firmly adherent to plaque matrix Adherence less pronounced with many motile forms Causes Can cause caries and gingivitis Can cause gingivitis and periodontitis 49

50. COMPOSITION OF DENTAL PLAQUE Sterp . Mutans Strep. Sanguis A. Viscosus T. Denticola 50

51. Derived from- saliva, gingival crevicular fluid and bacterial products 51

52. STRUCTURE AND COMPOSITION Microscopic structure: Supragingival plaque : Stratified organization of a multilayered accumulation of bacteria. Gm + ve cocci & short rods predominate at the tooth surface. Gm – ve rods, filaments & spirochetes predominate in outer surface of the mature plaque mass. 52

53. Supragingival plaque -Calculus formation -Caries Marginal plaque -Gingivitis Microcolonies of plaque bacteria extending perpendicularly away from tooth surfaces. Developed supragingival plaque showing overfilamentous nature and microcolonies extending away from the tooth surface. Saliva plaque interface(S) is also seen . 53

54. Subgingival plaque: Tooth associated : characterized by gram-positive rods and cocci , including Streptococcus mitis , S. sanguis , A. viscosus , Actinomyces naeslundii , and Eubacterium spp - In deeper parts of pocket filamentous organisms become fewer - The apical border is separated from the junctional epithelium by a layer of host leukocytes, and the bacteria show an increased concentration of gram-negative rods 54

55. Topography of Supragingival Plaque Early plaque formation on teeth initiates from the gingival margin and interdental space. Later further extension in the coronal direction occurs. This pattern changes when the tooth surface contains irregularities that offer a favorable growth path. 55

56. Plaque formation can also start from grooves, cracks, perikymata , or pits. In surface irregularities bacterias can escape from shear forces which allows them time to change from reversible to irreversible binding. 56

57. 57

58. DEVELOPMENT OF DENTAL PLAQUE 58

59. S.mitis S.oralis S.sanguis Streptococcus sps S.gorondi , S.intermedius EARLY COLON I ZERS V.parvula A.odontolyticus P.intermedia P.nigrescens P.micros F.nucleatum C.rectus E.nodatum C.showae E.corrodens Capnocytophaga sps A.actinomycetocomitans P.gingivalis T.forsythus T.denticola CLOSELY ASSOCIATED COMPLEXES IN THE ORAL CAVITY LATE COLONIZERS Socransky et al (1998) 59

60. 60

61. The first stage in pellicle formation involves adsorption of salivary proteins to tooth surfaces. The mechanism of selective adsorption includes ELECTROSTATIC FORCES between negatively charged hydroxyapatite and positively charged salivary glycoproteins A. Formation of an organic Pellicle B. Bacterial adherence During initial adherence, interactions occur mainly between specific bacteria and pellicle. They include: BACTERIAL ATTACHMENT VIA ELECTROSTATIC INTERACTIONS BACTERIAL ATTACHMENT VIA HYDROPHOBIC INTERACTIONS BACTERIAL ATTACHMENT VIA SPECIFIC LECTIN-LIKE SUBSTANCES 61

62. Transport To The Surface : Random contacts may occur: 1. Brownian motion 2. Sedimentation of microorganisms 3. Liquid flow 4. Active bacterial movement Initial Adhesion : Initial, reversible adhesion of bacterium takes place through long range and short range forces. 62 C) Attachment : The bonding between bacteria and pellicle is mediated by specific extracellular components and complementary receptors on pellicle surface. Many bacterial species posses FIMBRIAE and FIBRILS that aid in attachment.

63. FUCTIONS OF DENTAL PELLICLE 63

64. C. Colonization and Plaque maturation The early colonizers ( Streptococci and Actinomyces species) use oxygen and lower the reduction-oxidation potential of the environment. Secondary colonizers do not initially colonize the tooth surfaces. They adhere to the bacteria already adherent on the tooth. This is termed as COAGGREGATION Factors that include plaque maturation include: OXYGEN LEVELS, NUTRITIONAL SOURCES and INTERBACTERIAL RELATIONS 64

65. ATTACHMENT OF BACTERIA The key characteristic of a biofilm - the microcolonies within the biofilm attach to a solid surface. Many bacterial species possess surface structures such as fimbriae and fibrils that aid in their attachment to different surfaces. Fimbriae have been detected on a number of oral species including P. gingivalis , A. actinomycetemcomitans and some strains of streptococci. Oral species that possess fibrils include S. salivarius , the S. mitis group , Pr. intermedia , Pr. nigrescens , and Streptococcus mutans. The association of bacteria within mixed biofilms is not random. It has been shown that there are specific associations among bacteria in dental biofilms. Socransky et al. (1998) COAGGREGATION/CO-ADHESION of bacteria 65

66. Test tube brush : Composed of a central axis of a filamentous bacterium with perpendicularly associated short filaments. Commonly seen in the subgingival plaque of teeth associated with periodontitis Detected between filaments of bacteria to which gram – ve rods adhere. Corncob formation : Feature of plaque present on teeth associated with gingivitis . R od-shaped bacterial cells eg. Bacterionema matruchotii or Actinomyces sp. that forms inner core of the structure and coccal cells eg . Streptococci or P. gingivalis that attach along the surface of the rod shaped cells. Described by Gibbsons and Nygaard 66

67. PLAQUE HYPOTHESIS; 67

68. HYPOTHESIS DESCRIPTION ETIOLOGY TREATMENT Non Specific Plaque Hypothesis Miller Early 1 9 3 ’ s Periodontal disease results from the elaboration of noxious products by the entire plaque flora. All plaque are equally pathogenic. All bacteria Eliminate plaque NSPT/ SRP Surgical debridement Specific Plaque Hypothesis Loesc h e 1976 Only certain plaque is pathogenic and its pathogenicity depends on the presence of or increase in specific microorganisms these microorganism exogenic in nature Specific bacteria Plaque control antibiotics Modern Version of Specific Plaque Hyp o thesis S o cra n sky 1979 6-12 bacterial species may be responsible for majority of destructive periodontitis and additional species may be responsible for small number of other cases. All bacteria,virulence factor Plaque control, virulence factor target 68

69. Unified Theory Thel a ide 1986 All bacterial plaque may contribute to pathogenic potential of subgingival flora to greater or lesser extent based on ecological or environmental conditions. So all plaque is pathogenic but not equally. All bacteria to greater or lesser extent depending on ability to colonize and evade host defence Plaque control Ecological Plaque Hyp o thesis PD Marsh & Martin 1994 Any change in nutrient status of pocket are primary cause for overgrowth of pathogens. Homeostasis to dysbiosis Enrichment of specific bacteria in an ecological system. Plaque control, host-microbial environment Host modulation Antibiotics Habit recession Lifestyle change Keystone Pathoge n ic Hypothesis Haji s henga llis et al 2012 Certain low-abundance microbial pathogens can orchestrate inflammatory disease by remodelling a normally benign microbiota into a dysbiotic one. Specific bacteria- P.gingivalis dependent on remaining bacteria. Reduction in keystone and accessory pathogen load- dysbiosis to symbiosis 69

70. Ecological plaque hypothesis 70

71. Keystone pathogen hypothesis 71 TLR 4 response manipulation IL-8 SUBVERSION SERINE PHOSPHATE LOCAL CHEMOKINE PARALYSIS CURRUPTION OF COMPLEMENT INCREASE TLR2

72. Drawback of above hypothesis Non Specific Plaque Hypothesis-Some individuals with good amount of plaque and calculus develop gingivitis, but never develop destructive periodontitis. Some individuals with periodontitis demonstrate site specificity in the pattern of disease. Some sites in mouth are unaffected, whereas deep pockets are found in adjacent sites Specific Plaque Hypothesis- Loesc h e 1976- Studies showed that periodontitis occurred even in absence of pathogens like red/green complex .Sometime these pathogens were found to be present in absence of disease. Modern Version of Specific Plaque Hyp o thesis S o cra n sky 1979- cannot answer why In some people, gingivitis never progress to periodontitis, whereas some people rapidly develop periodontitis. 72

73. Ecological Plaque Hyp o thesis PD Marsh & Martin 1999 - Like the other hypotheses, it does not address the role of host genetic factors that contribute to the composition of plaque and to susceptibility of periodontitis; as gingivitis don ’ t lead to periodontitis in every case and genetic factors can be responsible in addition to environmental factors Keystone Pathoge n ic Hypothesis Haji s henga llis et al 2012- Like the other hypotheses, it does not address the role of host genetic factors that contribute to the composition of plaque and to susceptibility of periodontitis Also this hypothesis has yet to be proved in humans. 73

74. Page and kornman non linear model 1997 74 1960s Linear model; (b) Circa 1980s model; (c) Classical model (1997). PMNs – Polymorphonuclear leukocytes (Reprinted from Kornman ).

75. Biological system model by Offenbacher 2008 75 The clinical phenotype can be broken down into respective subclinical components The outermost component represents the unique exposures of the individual at a subject level, including the characteristics of the biofilm (e.g., the type of bacterial challenge) as well as the presence of other health conditions (e.g., diabetes) and environmental influences (e.g., smoking). The subject-level component interacts with the genetic background (gene polymorphisms that affect the host response), which potentially shapes the biologic phenotype (cellular and molecular processes including inflammatory biomarkers) which, in turn, determines the final clinical phenotype.

76. MICROBIAL SHIFT/DYSBIOSIS 76 polymicrobial synergy and dysbiotic model for periodontal disease etiology The polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology (HAJISHENGALLIS 2012).

77. 77

78. MICROBIAL SHIFT LEADING TO PERIODONTITIS GRAM +VE AEROBES GRAM -VE ANAEROBES Gradually changes the symbiotic host–microbe relationship to a pathogenic one. Prevotella intermedia Fusobacterium nucleatum P. Gingivalis Tannerella forsythia Treponema denticola 78

79. METHODS OF DETECTION OF DENTAL PLAQUE 79

80. 1. DIRECT VISION : - Thin plaque – may be translucent & therefore not visible Stained plaque – may be acquired e.g - tobacco stained Thick plaque – tooth may appear dull & dirty 2. USE OF EXPLORER : - Tactile Examination – when calcification has started it appears slightly rough, otherwise it may feel slippery due to coating of soft , slimy plaque Removal Of Plaque – when no plaque is visible , an explorer can be passed over the tooth surface & when plaque is present it will adhere to explorer tip.this technique is used when evaluating plaque index. This can be done by running the explorer or probe along the gingival 3 rd of the tooth 80

81. 3. Disclosing Agents: It is a preparation in liquid , tablet or lozenge which contains a dye or other colouring agent. A disclosing agent is used for identification of dental plaque which is otherwise not visible to naked eye . Two tone Erythrosine Bismark Basic Fuschin Disclosing Tablets – Dental Mart, oral B 81

82. Plaque control It is defined as the removal of microbial plaque & prevention of its accumulation on the teeth & adjacent gingival tissue. It also deals with prevention of calculus formation. MECHANICAL CHEMICAL Dental plaque biofilm cannot be eliminated permanently. However, the pathogenic nature of the dental plaque biofilm can be reduced by reducing the bioburden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing,flossing and rinsing with antimicrobial mouthrinses. This can result in the prevention or management of the associated sequelae, including the development of periodontal diseases and possibly the impact of periodontal diseases on specific systemic disorders. 82

83. MANUAL TOOTH BRUSH IONIC TOOTH BRUSH SONIC TOOTHBRUSH POWERED TOOTH BRUSH 83

84. INTER DENTAL AIDS INTER DENTAL BRUSH DENTAL FLOSS 84

85. INTER DENTAL AIDS UNITUFTED BRUSHED 85

86. CHLORHEXIDINE GLUCONATE ADVANTAGE 1. anti plaque & anti bacterial properties 2. property of SUBSTANTIVITY DISADVANTAGE brownish staining of teeth MECHANISM 1. prevent pellicle formation. 2. prevent plaque maturation 86

87. DELMOPINOL This is a morpholinoethanol derivative Amine alcohol. Plaque matrix inhibitor Inhibits plaque growth & reduces inflammation. But has less substantivity in comparison to others 87 It causes weak binding of plaque to the tooth surface, thus aiding in easy removal of plaque by mechanical procedures. It is therefore indicated as a prebrushing mouthrinse.

88. If not removed, plaque will turn into calculus after around 2 weeks. 88

89. Prevalence: According to the national health and nutritional examination survey(NHANES)-conducted in1988-1994 was found that 91.8% of the population was having supragingival calculus and 54.1% of the population was having subgingival calculus. A second study on the CPITN by Anerudh and loe on two groups those were academician group of Norway and tea workers from srilanka,so it but obvious that academicians from Norway were educated & they were privileged to have all the dental care facilities where as that wasn’t the case in tea workers of the srilanka now when these people were studied it was in that in case of tea workers from srilanka there was a constant calculus was deposited that took place and it was seen that at the age of 40 most of the teeth except premolars was covered by calculus in case of tea workers where as in case of Norwegian academicians was seen that at the age of 40-45 years of age about 70 % of the population is calculus free so the interproximal areas are free of calculus Basically this study emphasized the role of dental care prevent the accumulation of the calculus. 89

90. Classification of dental calculus : it is classified under three modalities: 1.based on the location: Supragingival calculus Supramarginal Calculus Coronal Calculus Extragingival Calculus Subgingival calculus Submarginal Calculus Hematogenetic Calculus The calculus which is coronal to the gingival margin Visible Colour is either whitish or yellowish and it also imparts the colour of the food Hard and clay like consistency Composition: high quantity of brushite and octa calcium phosphate The calculus which is apical to the gingival margin Cannot be seen should be examined with periodontal probe or explorer Greenish or brownish Hard and flint like consistency Composition: high amount of magnesium whitlokite crystals where as low in the brushite and octa calcium phosphate. 90

91. 91

92. The various forms of submarginal and subgingival calculus are • Spicules : Small isolated pieces of calculus. These are frequently located at line angles and interdental areas. • Ledge : A larger deposit that forms on a section of the tooth and is approximately parallel to the cementoenamel junction (CEJ). • Ring form : A ledge like deposit that encircles the tooth, forming a ring of calculus. In addition to calculus, roughness on the tooth surface may be caused by rough restorations, carious lesion, or necrotic cementum. 92

93. 2.Based on the mineralisation: Salivary calculus Serumnial calculus (Jenkins, Stewart 1966) The supragingival calculus which is exposed to the saliva and mineralises by the saliva so it is called as salivary calculus The subgingival area is not exposed to saliva but it is exposed by the gingival exudates such as GCF and other components so it mineralises by the gingival exudates so it is called as ceremonial calculus 93

94. 3.Based upon the rate of accumulation or formation of the dental calculus: Non calculus formers Slight calculus formers Moderate calculus formers Heavy calculus formers 94

95. Composition: In organic (70-90%) Organic (10%) 1.ELEMENTS: Calcium(39%) Phosphorous(19%) Sodium, zinc, aluminium, magnesium ..etc (traces). 2.COMPONENTS/MOLECULES: Calcium phosphate(70%) Calcium carbonate(3%) Magnesium phosphate(traces) 3.CRYSTALS: Hydroxyapatite crystals(58%) Octa calcium(21%)- seen majority in supragingival calculus Mg with loci (12%)-seen majority in subgingival calculus Brucite(9% )-seen majority in supragingival calculus 1.CARBOHYDRATES(9.1%) Glucose Fructose Mannose 2.AMINOACIDS(8.2%) 3.Lipids(0.2%) 95

96. Microbiology of dental calculus The percentage of gram positive and gram- negative filamentous organisms is greater within calculus than in the remainder of oral cavity. The microorganisms at the periphery are predominantly gram-negative rods and cocci. Most of the organisms within the calculus is nonviable. Friskopp & Hammarstrom (1980) With TEM & SEM found differences in the nature of the microbial coverings. On supragingival calculus filamentous organisms,oriented at right angles to the surface dominated. Subgingival calculus was covered by cocci, rods and filaments with no distinct pattern of orientation. 96

97. PELLICLE FORM A TION PLAQUE FORM A TI O N MINERA L IZ A TI O N 97

98. All surfaces of the oral cavity are coated with a pellicle. Following tooth eruption or a dental prophylaxis, a thin, saliva- derived layer, called the acquired pellicle, covers the tooth surface Initial adhesion and attachment of bacteria Transport to the surface – involves the initial transport of the bacterium to the tooth surface. Initial adhesion – reversible adhesion of the bacterium, initiated by the interaction between the bacterium and the surface , through long-range and short-range forces Attachment – a firm anchorage between bacterium and surface will be established by specific interactions. Pellicle formation 98

99. When the firmly attached microorganisms start growing and the newly formed bacterial clusters remain attached, microcolonies or a biofilm can develop. Gram- positive coccoidal organisms are the first settlers to adhere to the formed enamel pellicle, and subsequently, filamentous bacteria gradually dominate the maturing plaque biofilm (Scheie, 1994). Colonization and Plaque Maturation MINERALIZATION Rate of formation and accumulation Formation of plaque consist of amorphous and/ or finely granular organic matrix containing mass of variety of gram positive and gram negative coccoid bacteria and filamentous form. The matrix is a form of mucopolysaccride derived from either saliva or bacteria or both. 99

100. Soft plaque is hardened by precipitation of mineral salts which usually starts between the first and the fourteen day of plaque formation. Calcification has been reported to occur as soon as 4 to 8 hours . Calcifying plaque may become 50% mineralized within 2 days and 60% to 90% mineralized in 12 days. Early plaque contains a small amount of i n or g a n ic mat e ri a l w h i ch i n cre a ses as a p l a q ue develops into calculus. 7 day: coccoid bacteria is still present but the surface and central portions contains mass of filamentous organisms 12 Day: plaque composed entirely of gram variable filamentous bacteria in a fairly granular or amorphous ground substance. 14 Day: the starting time of calcification area in different individuals and in different teeth in same individual 100

101. C A L CIUM IONS C A R B OHY D R A TE PROTEIN COMPLEX C R Y S T ALL I NE CALCIUM PHOSPHATE SALT Calculus is formed by the precipitation of mineral salts which can start between 1st to14th day of plaque formation Calcification is reported to occur in as little as 4-8 hrs. ( Tibetts 1970) 101

102. soft plaque is hardened by the precipitation of mineral salts, which usually starts between the 1 st and 14 th days of plaque formation calcification has been reported to occur in as little as 4 to 8 hours Microorganisms are not always essential in calculus formation Calcification entails the binding of calcium ions to the carbohydrate – protein complexes of the organic matrix and the precipitation of crystalline. Mineralization consists of crystal formation, namely hydroxyapatite, octacalcium phosphate, magnesium whitlockite , and brushite each with a characteristic developmental pattern. . calculus characterstics 102

103. The crystal forms in the intercellular matrix, on the surface of bacteria and finally within the bacteria. Formation of calculus difference in person to persons, It may be classified as heavy, moderate, or slight calculus formers or as noncalculus formers. Heavy calculus formers have higher salivary levels of calcium and phosphorus than do light calculus formers. Light calculus formers have higher levels of parotid pyrophosphate. Pyrophosphate is an inhibitor of calcification. 103

104. MODES OF ATTACHMENT OF CALCULUS TO THE TOOTH SURFACE AND IMPLANT Helmut A. Zander in 1952 described four types of calculus attachment 1. Attachment by means of an organic pellicle. 2. Mechanical locking into surface irregularities such as resorption lacunae and caries. This type of attachment make the removal of calculus difficult as calculus embedded beneath the cementum surface penetrates into the dentin. 104

105. 3. Penetration of calculus bacteria into cementum. 4. Close adaptation of calculus undersurface depressions to the gently sloping mounds of the unaltered cementum surface. Shroff later theorized that the type of calculus attachment probably depends on the length of time the calculus has been on the tooth. The attachment of calculus to pure titanium implant is less intimate than to root surface. 105

106. Theories of formation of calculus: Booster mechanism Bacteriological mechanism Epitactic theory Inhibition theory Transformation theory Enzymatic theory 106

107. Booster mechanism: In the booster mechanism there are some agents which boosts the plaque and further leads to the calcification Booster mechanism was further divided into three mechanisms : Booster mechanism which is associated with co2. Booster mechanism which is associated with colloidal proteins of saliva. Booster mechanism which is associated with the proteins produced by the bacteria. 107

108. 1.Booster mechanism which is associated with the carbon dioxide: 1.Co2 produced by the salivary ducts in the oral cavity is around 55-65mmhg pressure and the atmospheric co2 is nearly 0.3mmhg pressure which causes co2 tension and leads to dissipation of co2 from saliva to the atmosphere (55-65mmhg)Co2(saliva)======(0.3mmhg)co2(atmosphere) 2. Ph of the saliva increases which means saliva becomes alkaline in nature. 3.Which leads to the further dissociation of acids in the saliva especially the phosphoric acid which dissociates and produces secondary and tertiary phosphate ions H3PO4= 2°&3° phosphate ions (acts as booster mechanism) 4.Precipitated Calcium and phosphate crystals ( ca&p crystals) 5.These ca and p crystals directly precipitates on the surface of the teeth and undergoes calcification of plaque and produces calculus. 108

109. 2.Booster mechanism associated with colloidal proteins of the saliva Saliva containing the colloidal proteins has the tendency to bind with the ca and phosphate ions present in saliva Colloidal proteins + Ca & P ions = supersaturated solution Precipitation of Ca & P ions and settle down the surface of teeth And undergoes calcification of the plaque and produces calculus 109

110. Booster mechanism associated with proteins produced by the bacteria: Proteins present in the plaque breaks down Amino acids Left over amino acids breakdown into ammonia This ammonia will increase the ph of the saliva (alkaline in nature) Causes the precipitation of ca and p ions Calcification of dental plaque Formation of dental calculus 110

111. 2.Bacteriological theory: Certain bacteria in the dental plaque such as provotella intermedia and fusobacterium nucleatum themselves produces Ammonia This ammonia increases the ph of saliva Precipitation of calcium and phosphate ions Calcification of plaque and leads to formation of dental calculus. This theory is not well accepted theory because there is a formation of calculus seen in the germ free organisms also. 111

112. 3.*Epitactic theory: The word epitactic means crystal growth or mineral deposition. Saliva contains ca and p crystals where as on the tooth surface the plaque contains proteins and carbohydrate complex According to the epitactic theory the calcium and phosphate crystals present in the saliva are not enough to precipitates the proteins and carbohydrates on the dental plaque so they promote the growth of hydroxyapatite crystals to precipitate the proteins and carbohydrates present on the dental plaque, so here the carbohydrates and proteins on the plaque acts as seedling agent. This hydroxyapatite crystals first form the small foci of the calcification later they enlarge & coalesce with each other and form large masses of the calcification this process is called heterogenous calcification ***points to remember: 1.The proteins and the carbohydrates present in the plaque on the surface of the tooth acts as seedling agent 2.The hydroxyapatatite crystals form the calcification masses through heterogenous calcification. 112

113. 4.Tansformation theory: According to this theory there are the presence of some non crystal deposits inside the saliva further gets transformed into octa calcium phosphate and hydroxyapatite crystals which leads to the calcification of dental plaque Non crystal growth deposits in saliva (transformed) Octacalcium+hydroxy apatite crystals Calcification of dental plaque 113 calculus

114. 5.Inhibition theory: Calculus formation on teeth is not uniform it differs from area to area or tooth to tooth it is because of the inhibition theory according to this theory the area where the calculus formation is high, in that area the inhibitory agents are removed or altered. The inhibitory agents are pyrophosphates in the saliva What are this pyrophosphates will do? This will chelates calcium(means removes calcium Prevents the crystallisation leads to the less formation of calculus inhibitory agents are removed or altered leads to the more deposition of calculus 114

115. 6.Enzymatic theory: According this theory the enzymes are the important factors to cause calcification of plaque bacterias esterases host ( macrophages,epi cells) Capable of Hydrolysing the fatty acids Free fatty acids Soap Ca and mg Ca and mg crysatls ( has the capability of precipitation on the tooth surface and cause the calcification) 115

116. Role of dental calculus in gingival inflammation and periodontal destruction: The dental plaque is a primary etiological factor in gingival inflammation and periodontal destruction. The dental calculus is a contributing factor in gingival inflammation and periodontal destruction. Why how? 116

117. Acquired pellicle-- plaque-- gingival inflammation, salivary flow increase Minerals get deposited Dental calculus Again plaque forms on the dental calculus Hence calculus is considered as a contributing factor* 117

118. Detection methods of dental calculus: As we know dental calculus is supragingival and subgingival and supragingival calculus is visible and subgingival calculus is unseen So how to detect subgingival calculus ???? Conventional techniques Advanced techniques 1.By inserting any type of probe or explorer 2.Radiographs 3.compressed air 118

119. Advanced techniques Detect only dental calculus Detect calculus and removes 1.Peioscope-uses endoscopy technique 1.perio scan – uses ultrasonic tech. 2.Detectar-specto optical technique 2. keylaser -laser technology 3.Diagnodent-Auto fluorescence tech.. 119

120. Conventional techniques: By using probe or explorer : by inserting probe or any explorer into the periodontal pocket and tactile sensation should be used to detect the subgingival calculus Radiographs : the radio opaque projections on the radiograph detect the subgingival calculus but we cannot relay on the radiographs entirely because there are some disadvantages Disadv : - it cannot detect facial and lingual subgingival calculus -if the subgingival calculus present deep inside the alveolar bone we cannot differentiate between the bone and subgingival calculus. 3. Compressed air : some amounts of calculus is unnoticeable if it is wet , when we use the compressed air in the wetty area the calculus become dry and chalky and can be visible and it is easy to detect and remove Since all these are conventional techniques ,these are associated with major drawbacks so we moved on to the advanced techniques for the detection of subgingival calculus. 120

121. Advanced techniques: A . Detect only dental calculus: 1.Perioscope: This perioscope uses the endoscopic technique, it has 3 important features Fibro optic bundle Light source helps to maintain Irrigation system clean field The fibro optic bundle will pickup the image to a screen in magnified manner Subgingival calculus is magnified in 24X46 , so that it can magnified and visible clearly. 121

122. 122

123. 2.Detec Tars: OPTIC –AUDIO AID This instruments available as a portable instruments It consist of a periodontal probe at the end of tip of instrument which consists of millimetre markings which helps in measuring the periodontal pocket It also consists of light emitting diode and optical fibre Detec Tars fibre-optic probe reads light reflected off tooth structure and transmits internal computer for analysis It sounds a tone when it detects the unique spectral signature of subgingival calculus. 123

124. 3. Diagnodent pen: It uses autofluorescence technology to detect the subgingival calculus The calculus usually covers with the plaque which consist of micro organisms and their by-products These micro organisms present in the plaque has the flourophores , this fluorophores' contains the chemical substance which emits light when they are excited or activated When we place this diagnodent pen in the periodontal pocket it projects a light into the pocket with the wavelength 400-420nm, in return to this the fluorophore's in the pocket gets activates and emits a light with the wavelength of 570-730nm Now this light is captured by the optical fibre present in the diagnodent pen According to the manufacturers there are some measurement values present on the screen of a pen if the value is > 40 - there is a presence of heavy mineralized deposits 5-40 - there is a small deposits of calcified calculus <5 - the surface of the root is absolutely clean . 124

125. 125

126. B. instruments which detect both calculus and removes the calculus: 1.perioscan: Perio scan is nothing but of ultrasonic scaler which detects the subgingival calculus by generating a particular impulse which is different from the impulse generated by a clean root surface . This impulse is picked up a convers into a light signalling in a perioscan When it emits a green light there is a presence of cementum or clean root surface and blue light represents the presence of dental calculus on the root surface Later we can shift the mode into treatment by a switch present on the perio scan Lower power for plaque Higher power for calculus 126

127. 127

128. 2.keylaser: It uses the laser technology Key laser contains two types of laser technologies detection treatment Indium gallium arsenium diode laser er;yag laser at a wavelength of 2940nm to to remove dental calculus With 655nm wavelength for detection after detection 128

129. 129

130. ROLE OF CALCULUS IN PERIODONTAL DISEASE Calculus may be harmful both physically and chemically to adjacent gingiva. Calculus is permeable and thus, may absorb and adsorb toxic products. Calculus is rough and porous which facilitates the retention of dental plaque. Calculus is always covered with unmineralized plaque which provides further retention and promotes new plaque accumulation and thus, causes periodontal destruction in the following manner: Calculus brings bacterial overlay closer to the supporting tissues Interfere with local self-cleansing mechanism Provide nidus for continuous plaque accumulation. Make plaque removal more difficult. 130

131. Anticalculus agent ANTICALCULUS AGENT:- FIRST GENERATION AGENTS: • DISSOLUTION AGENTS(1950): • ACIDS • SPRING SALTS • SODIUM RICINOLEATE • PLAQUE ATTACHMENT INHIBITORS : • SILICONS • ION EXCHANGE RESINS PLAQUE INHIBITON AGENTS : • ANTIBIOTICS (NIDDAMYCIN) • ANTISEPTICS (CHLORAMINE-T) • MATRIX DISRUPTION AGENTS: • ENZYMES (MUCINASE) • ASCORBIC ACID • SODIUM PERCARBONATE • COPPER SULPHITE • 30% UREA SECOND GENERATION AGENTS :- • INHIBITORS OF CRYSTAL GROWTH(1970): • VITAMIN C • PYROPHOSPHATE • DIPHOSPHONATE • ZINC SALT • CALCIUM LACTATE • SODIUM FLOURIDE SODIUM CITERATE COMMERCIAL ANTICALCULUS PRODUCT  MOUTHWASH • CHLORHEXIDINE GLUCONATE (0.2%) IS THE RECOMMENDED BY THE WORLD HEALTH ORGANISATION. • IT IS A CATIONIC BISBIGUANIDE. • EXHIBIT ANTIPLAQUE AND ANTI BACTERIAL PROPERTY. • EFFECTIVE AGAINST GRAM +VE AND GRAM –VE ORGANISMS. 131

132. 132

133. CONCLUSION Calculus plays an important role in maintaining and accentuating periodontal disease by keeping plaque in close contact with the gingival tissues and creating areas where plaque removal is impossible. Therefore the clinician must not only possess the clinical skills to remove the calculus and other irritants that attach to teeth . 133 The nature of biofilm helps explain why periodontal diseases are difficult to prevent and treat. In general, once established, the microbial composition of the biofilm at a site remains stable over time, unless a major perturbation. Such perturbations can drive shifts in the balance of the microbiota, which can increase the risk of disease. Dental plaque biofilm cannot be eliminated permanently. However, the pathogenic nature of the dental plaque biofilm can be reduced by reducing the bioburden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing, flossing and rinsing with anti-microbial rinses.

134. REFERENCES Clinical Periodontology - Carranza (9th & 10th edn ) Clinical Periodontology- Jan Lindhe , Thorklid Karring , Niklaus P Lang Clinical Periodontology : Listgarten Periodontal microbial ecology - Perio 2000,Vol. 38, 2005, 135–187 Are dental diseases examples of ecological catastrophes? - P. D. Marsh - Microbiology (2003), 149, 279–294 Dental biofilms: difficult therapeutic targets - Periodontology 2000, Vol. 28, 2002, 12–55 Dental biofilms: difficult therapeutic targets - Periodontology 2000, Vol. 28, 2002, 12–55 Socransky SS, Haffajee AD. Periodontal microbial ecology. Periodontol 2000 2005: 38: 135–187. Teles RP, Haffajee AD, Socransky SS. Microbiological goals of periodontal therapy. Periodontol 2000 2006: 42: 180–218. 134

135. Clinical Periodontology- Jan Lindhe, Thorklid Karring , Niklaus P Lang Periodontal microbial ecology - Perio 2000,Vol. 38, 2005, 135–187 Glickman; Clinical periodontology 4th edition: Saunders Carranza, Newman ;Clinical Periodontology, 8th edition: Saunders Newman, Takei, Klokkevold , Carranza; Clinical Periodontology; 10th Edition: Elseveir Jan Lindhe , Niklaus P. Lang, Thorkildkarring ; Clinical Periodontology And Implant Dentistry: 5th Edition: Blackwell Socransky SS, Haffajee AD. Dental biofilms: difficult therapeutic targets. Peridntol 2000 2002 : 28; 12-55. Marsh PD, Moter A, Devine DA. Dental plaque biofilms: commuinties , conflict and control. Periodontol 2000 2011; 55: 16-35 Max A. Listgarten , The structure of dental plaque, Periodontology 2000, Vol. 5, 1994, 52-65 Interspecies Interactions within Oral Microbial Communities Howard K. et al Microbiology And Molecular Biology Reviews, Dec. 2007, P. 653–670 135