Dental Plaque

Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976

Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003

1. 1 GOOD MORNING

2. DENTAL PLAQUE 2

3. DR. ANUJ SINGH PARIHAR Senior Lecturer Dept. of Periodontics 3

4. CONTENTS INTRODUCTION HISTORY DEFINITION OF TERMS CLASSIFICATION OF DENTAL PLAQUE COMPOSITION OF DENTAL PLAQUE FORMATION OF DENTAL PLAQUE MICROBIAL COMPLEXES DENTAL PLAQUE AS BIOFILM MICROBIAL SPECIFICITY OF PERIODONTAL DISEASE CRITERIAS OF IDENTIFICATION OF PATHOGENS PLAQUE CONTROL CONCLUSION 4

5. 5 DENTAL PLAQUE A BIOFILM MICRO-ORGANISMS PERIODONTITIS DENTAL CARIES

6. DEFINITIONS Dental Plaque Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations” Bowen , 1976 Bacterial aggregations on the teeth or other solid oral structures L indhe, 2003 6

7. DEFINITIONS 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.” WHO-1961 7

8. Dental Calculus is a an adherent calcified or calcifying mass that forms on the surface of natural teeth & prosthesis. MATERIA ALBA is a deposit composed of aggregate of microorganisms, leucocytes & dead exfoliated epithelial cells , randomly organized & loosely adherent to the surfaces of the teeth, plaque & gingiva. 8

9. HISTORY J Leon Williams (1897) – described dental plaque GV Black (1899) – coined term “gelatinous dental plaque” Waerhaug (1950) described the importance of bacterial plaque in the etiology of periodontal disease 9

10. HISTORY 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 diseaes . W.Loesche (1976) Modern theories of specificity PD Marsh (1994) Ecological plaque hypothesis 10

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12. CLASSIFICATION 12

13. SUPRA- GINGIVAL PLAQUE Supragingival plaque is found at or above the gingival margin . Supragingival plaque in direct contact with the gingival margin is referred to as marginal plaque 13

14. SUBGINGIVAL PLAQUE Sub gingival plaque is found below the gingival margin, between the tooth and gingival sulcular tissue. 14

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16. 16 Tooth attached Unattached Tissue Attached Gram positive – rods and cocci , Gram negative rods, filaments, spirochetes Gram variable Does not extend to JE Extend to JE Extend to JE Calculus formation, root caries Gingivitis Gingivitis, periodontitis May penetrate cementum - May penetrate epithelium and connective tissue

17. COMPOSITION OF DENTAL PLAQUE 17

18. COMPOSITION OF DENTAL PLAQUE Dental plaque is composed primarily of microorganisms. These organisms exist within an intercellular matrix. 18

19. BIOFILM The term biofilm describes the relatively indefinable microbial community associated with a tooth surface or any other hard, non-shedding material . (Wilderer & Charaklis 1989) 19

20. Biofilm consists of one or more communities of micro-organisms embedded in glycocalyx , that are attached to solid surfaces. (Costerton et al 1994) 20

21. INTERCELLULAR MATRIX This contains a few host cells such as epithelial cells , macrophages & leukocytes. Forms 20%-30 % of plaque mass. 21

22. ORGANIC MATERIAL Polysaccharides ( 30% ) produced by bacteria. Dextran Protein (30%) –Albumin (originating from GCF) Glycoproteins from saliva. Lipid (15%) consists of debris from disrupted bacteria, host cells & food debris 22

23. INORGANIC MATERIAL Predominantly – calcium, sodium, phosphorous, potassium & fluorides (in traces) Source of inorganic material in supragingival plaque is primarily saliva source of inorganic material in sub gingival plaque is GCF 23

24. EXOPOLYSACCHARIDES – the backbone of the biofilm The bulk of the biofilm consists of the matrix, composed predominantly of water and aqueous solutes . 24

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26. One gram of plaque contains approximately 2 X 10 11 bacteria. (Socransky SS,1953), (Schroeder, De Boever-1970) 26

27. NON BACTERIAL ORGANISMS IN PLAQUE 27

28. FORMATION OF DENTAL PLAQUE 28

29. Dental plaque may be readily visualized on teeth after 1-2 days of no oral hygiene. 29

30. FORMATION OF DENTAL PELLICLE Acquired pellicle may be defined as a homogenous, membranous, acellular film that covers the tooth surface and frequently form the interface between the tooth ,the dental plaque and calculus . (SCHLUGER) `A fully established pellicle is found within 30 min. Within 24 hr, the pellicle is around 0.1-0.8 µm in diameter. Derived from components of saliva and crevicular fluid as well as bacterial and host tissue cell products and food debris. 30

31. Consists of numerous components, including glycoprotein (mucins), proline-rich proteins, phosphoproteins (e.g., statherin), histidine-rich proteins, enzymes (e.g., α-amylase), and other molecules that can function as adhesion sites for bacterial receptors. 31

32. FUNCTIONS OF DENTAL PELLICLE 32

33. INITIAL ADHESION & ATTACHMENT OF BACTERIA We cannot conclude a single mechanism that dictates the adhesiveness of micro-organisms . 33 SCHEIE ( 1994)

34. A) TRANSPORT TO SURFACE The first stage involves the initial transport of the bacterium to the tooth surface. Random contacts may occur Brownian motion (average displacement of 40 µm/hour) Sedimentation of microorganisms, Liquid flow Active bacterial movement (chemotactic activity). 34

35. B) INITIAL ADHESION There is an initial, reversible adhesion of the bacterium. It is initiated by the interaction between the bacterium and the surface, from a certain distance (50 nm), through long-range and short-range forces , including van der Waals attractive forces and electrostatic repulsive forces. The total interaction energy, also called the total Gibbs energy (G TOT ). (G TOT = GA + GE) 35

36. INITIAL ADHESION For most bacteria, G TOT consists of a Secondary minimum (where a reversible binding takes place: 5-20 nm from the surface) A positive maximum (an energy barrier B) to adhesion A steep primary minimum (located at <2 nm away from the surface), where an irreversible adhesion is established. 36

37. C) ATTACHMENT After initial adhesion, a firm anchorage between bacterium and surface will be established by specific interactions (covalent, ionic, or hydrogen bonding). The bonding between the bacteria & pellicle is mediated by specific extracellular components of organisms & complementary receptors on pellicle surface. 37

38. ATTACHMENT OF BACTERIA The attachment to tooth surface is the essential first step in the development of a biofilm. Many bacterial species possess surface structures such as FIMBRIAE and FIBRILS that aid in their attachment to different surfaces. 38

39. The fimbriae of A. naeslundii are the best characterized of the gram-positive oral bacteria. 39

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42. COLONIZATION & PLAQUE MATURATION The early colonizers (e.g., streptococci and Actinomyces species) use oxygen and lower the reduction-oxidation potential of the environment, which then favors the growth of anaerobic species. 42

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44. Secondary colonizers are the microorganisms that do not initially colonize clean tooth surfaces, including Prevotella intermedia , Prevotella loescheii , Capnocytophaga spp ., Fusobacterium nucleatum , and Porphyromonas gingivalis . 44

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46. COAGGREGATION Coaggregation is referred to as cell-to cell recognition of genetically distinct partner cell types. Occurs primarily through the highly specific stereo chemical interaction of protein and carbohydrate molecules located on the bacterial cell surfaces. Also by the less specific interactions resulting from hydrophobic, electrostatic, and van der Waals forces. 46

47. COAGGREGATION 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. 47

48. COAGGREGATION BRIDGES A co-aggregation bridge is formed when the common partner bears two or more types of coaggregation mediators. These mediators can be various types of polysaccharides or various adhesin or combination of two 48

49. Thus most coaggregation among strains of different genera are mediated by lectin-like adhesin & can be inhibited by lactose & other glycosides. 49

50. CORN COB formation – streptococci adhere to filaments of Bacterionema.matruchotti or F.nucleatum. 50 CORNCOB STRUCTURE TEST TUBE BRUSH

51. MICROBIAL COMPLEXES Socransky et al. in 1998 examined over 13,000 subgingival plaque samples from 185 adult subjects and DNA hybridization methodology described the presence of specific complexes of periodontal microorganisms. 51

52. 52 ACTINOMYCES SPECIES V. Parvula A.odontolyticus S.Mitis S.Oralis S.Sanguis Streptococcus sp. S.gordonii S.intermedius PRIMARY COLONIZERS

53. 53 P.Intermedia P.Nigrescens P.Micros F.nucleatum C.rectus E.nodatum C.showae E.Corrodens Capnocyptophaga spp A.actinomycetemcomitans P.Gingivalis B.Forsythus T.denticola SECONDARY COLONIZERS

54. ACTINOBACILLUS ACTINOMYCETEMCOMITANS It is non motile & gram negative. This bacteria is small, short ,straight or curved with rounded ends. AGGREGAGIBACTER. ACTINOMYCETUMCOMITANS ( LAURITSON & KILION,2006) 54

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56. VIRULENCE FACTORS OF A. ACTINOMYCETEMCOMITANS FACTOR EFFECT LIPOPOLYSACCHARIDE Release of endotoxin LEUKOTOXIN forms pores in the membranes of Pmns, monocytes and lymphocytes causing osmotic imbalance leading to cell death COLLAGENASE reduce collagen density PROTEASE Able to cleave Ig G 56

57. PORPHYROMONAS GINGIVALIS It is a gram negative , non-motile & obligate anaerobe. 57

58. VIRULENCE FACTORS OF PORPHYROMONAS GINGIVALIS FACTOR EFFECT FIMBRIAE attach to epithelial cells, fibroblasts, hemoglobin PROTEINASES provide nutrients for bacterial growth degrade type I and IV collagen and extracellular matrix proteins FIMBRILLIN bind to proline rich proteins PROTEASE Able to cleave Ig G HAEMOLYSIN & COLLAGENASE 58

59. GINGIPAIN Trypsine like protinases 59 ARGININE LYSINE GINGIPAINS

60. BACTERIODS FORSYTHUS It is a non-motile , spindle shaped & gram negative obligate anaerobe. TANNERELLA.FORSYTHENSIS ( SAKA MOTO et al ,2002) TANNERELLA.FORSYTHIA (MAIDEN et al,2003) 60

61. VIRULENCE FACTORS OF TANNERELLA FORSYTHIA FACTOR EFFECT LIPOPROTEINS bind to other bacteria and host cells PROTEINASES degrades benzoyl arginine naphthylamide, activity of which appears related to sites of periodontal infection ENVELOPE LIPOPROTEIN activate gingival fibroblasts to produce elevated levels of IL-6 and TN F α 61

62. TREPONEMA.DENTICOLA This is a classified species of SPIROCHAETES. These organisms are gram negative spiral , motile organisms It is difficult to grow these organisms on culture media , as these require strict anaerobic conditions. PATHOGENIC CHARACTER Ability to travel in viscous environment & penetrate both epithelium and connective tissue. These can degrade collagen & dentine . Produce proteolytic enzymes that destroys immunoglobulins. 62

63. CHARACTERSTICS OF BIOFILM 63

64. PHYSIOLOGICAL HETEROGENECITY WITHIN BIOFILM Cells of same microbial species can exhibit extremely different physiological states in a biofilm though separated by little distance of 10 micrometer. pH can vary quite remarkably over short distances within a biofilm . Bacteria in biofilm several enzymes Beta- lactamase, Superoxide dismutase, Elastases, Cellulases. 64

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66. QUORUM SENSING Quorum sensing in bacteria , ‘‘involves the regulation of expression of specific genes through the accumulation of signaling compounds that mediate intercellular communication.” (Prosser 1999) This is a method of intercellular communication. Quorum sensing depends on cell density. Once signaling compounds reach a threshold level, gene expression is activated. 66

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68. Quorum sensing may give biofilms their distinct properties: 68

69. ANTIBIOTIC RESISTANCE: Resistance of bacteria to antibiotics, or preservatives is affected by their - position of bacteria - growth rate - temperature & PH 69

70. PROPERTIES OF BIOFILM Cooperating community of various types of micro-organisms. Micro-organisms are arranged in microcolonies. Micro-organisms are surrounded by protective matrix. There is differing environment within micro-colonies which impact the property of PHYSIOLOGICAL HETEROGENICITY. Micro-organisms have antibiotic resistance mainly due to phenomenon of QUORUM SENSING . 70

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72. EXPERIMENTAL GINGIVITIS MODEL ( SAYED, LOESCHE, 1978) 72

73. TOPOGRAPHY OF SUPRA GINGIVAL PLAQUE 73

74. PLAQUE RETENTIVE FACTORS 74

75. VARIATIONS IN DENTITION 75

76. MICROBIAL SPECIFICITY OF PERIODONTAL DISEASES 76

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78. NON SPECIFIC PLAQUE HYPOTHESIS Non specific plaque hypothesis was proposed by WALTER LOESCHE(1976). In the mid-1900s, periodontal disease was believed to result from an accumulation of plaque over time in conjunction with a diminished host response and increased host susceptibility with age. This thinking is referred as “ NON-SPECIFIC PLAQUE HYPOTHESIS” 78

79. The nonspecific plaque hypothesis maintains that periodontal disease results from the “ elaboration of noxious products by the entire plaque flora .” Thus it lead to concept that control of periodontal disease depends on control of the amount of plaque accumulation. Treatment of periodontitis by debridement (nonsurgical or surgical) and oral hygiene measures focuses on the removal of plaque and its products 79

80. SPECIFIC PLAQUE HYPOTHESIS Specific plaque hypothesis states that only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms. NEWMAN MG , SOCRANSKY SS (1977),ADI et al ,(1978 ) Plaque harboring specific bacterial pathogens results in periodontal disease. A. actinomycetemcomitans as a pathogen in localized aggressive periodontitis. 80

81. TISSUE INVASIVE PROPERTY 81

82. ECOLOGICAL PLAQUE HYPOTHESIS A change in a key environmental factor (or factors) will trigger a shift in the balance of the resident plaque microflora, and this might predispose a site to disease. ( PD Marsh 1994) This hypothesis is based on the theory that the unique local microenvironment influences the composition of the oral microflora. 82

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84. This hypothesis postulated dynamic relationship between environmental cause & ecological shifts within the biofilm. It also introduced the concept that the disease can be prevented not only by inhibiting the putative pathogens, but also interfering with the environmental factors driving the selection & enrichment of these bacteria. 84

85. CRITERIA FOR IDENTIFICATION OF PERIODONTAL PATHOGENS In the 1870s, Robert Koch postulated the criteria by which an organism can be judged to be causative agent in human infections 85

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88. SIGMUND SOCRANSKY (1992) proposed criteria by which periodontal microorganisms may be judged to be potential pathogens. 88

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90. PLAQUE CONTROL

91. DETECTION OF PLAQUE 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 . THE AGENTS THAT ARE USED AS DISCLOSING AGENTS ARE: Iodine preparation B ismark brown Erythrosine Fast green Basic fuschin

92. 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.

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

94. INTER DENTAL AIDS DENTAL FLOSS

95. INTER DENTAL AIDS INTER DENTAL BRUSH

96. INTER DENTAL AIDS UNITUFTED BRUSHED

97. 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

98. POVIDONE IODINE ADVANTAGE 1. no staining of teeth seen 2. reduces inflammation DISADVANTAGE reduced substantivity

99. DELMOPINOL This is a morpholinoethanol derivative. Inhibits plaque growth & reduces inflammation. But has less substantivity in comparison to others

100. CONCLUSION

101. 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, 135–187 104

102. 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, 12–55 105

103. 106 THANKYOU