Dental plaque formation

Dental plaque formation , What Makes Dental plaque Pathogenic ? , Microorganisms associated with periodontal diseases

1. Dental Plaque Formation Under the supervision of : Dr. Majdi Kamel

2. What’s the Dental plaque ? Dental Plaque is an adherent intercellular matrix consisting primarily of proliferating microorganisms, along with a scattering of epithelial cells , leukocytes and macrophages .

3. What’s the Dental plaque ? CAN ALSO be defined as the soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable and fixed restorations .

4. Dental Plaque is a( host-associated biofilm).

5. What’s Biofilms ? Biofilms are defined as “ Matrix—enclosed bacterial populations adherent to each other and or/to surface or interfaces (by Costerton ).

6. What’s Biofilms ? Biofilm is defined ALSO as the relatively undefinable microbial community associated with a tooth surface or any other hard, non-shedding material.

7. Dental Plaque As A Biofilm

8. Dental plaque Structure Dental plaque is now considered to be a complex and dynamic microbial community , It contains areas of high and low bacterial biomass interlaced with Aqueous channels of bact. Colony.

9. Types of dental plaque Based on its relationship to the gingival margin, plaque is differentiated into two categories : supragingival plaque subgingival plaque

10. 1- Supragingival plaque Is further differentiated into: Coronal plaque , is only the( tooth surface ). Marginal plaque , which is( associated with the tooth surface at the gingival margin ).

11. 1- Supragingival plaque It can be detected clinically only after it has reached a certain thickness . Small amounts of plaque can be visualized by using disclosing agents . The color varies from gray to yellowish-grey to yellow .

12. Disclosing Agents

13. 1- Supragingival plaque The rate of formation and location of plaque vary among individuals and is influenced by diet, age, factors, salivary secretion oral hygiene, tooth alignment, systemic diseases and host factors.

14. 2- Subgingival plaque Can be further differentiated into: Attached plaque Unattached subgingival plaque It is usually thin, contained within the gingival sulci or periodontal pocket and thus CANNOT be detected by direct observation. Its presence can be identified only by running the end of a probe around gingival margin

15. a-Attached plaque Attached plaque can be: tooth. Epithelium. connective tissue associated.

16. 1- Tooth-associated Subgingival Plaque The structure is similar to the supragingival plaque. The flora is dominated by Gram-positive cocci, rods, filamentous bacteria and some/few Gram-negative cocci and rods. This flora is associated with calculus formation, root caries and root resorption .

17. 2- Epithelium-associated Subgingival Plaque This type is loosely adherent because; it lacks the interbacterial matrix and is in direct association with the gingival epithelium, extending from the gingival margin to the junctional epithelium. This plaque predominantly contains Gram-negative rods and cocci, as well as a large number of flagellated bacteria and Spirochetes.

18. 3- Connective Tissue-associated Plaque It is usually demonstrated in ANUG and localized aggressive periodontitis patients. The clinical significance is unclear .

19. b- Unattached plaque The unattached plaque can be seen anywhere.

20. * Thus * The tooth-associated subgingival plaque is most important in calculus formation, root caries and slowly progressive periodontal destruction, whereas unattached bacterial component is associated with rapid periodontal destruction.

21. COMPOSITION OF DENTAL PLAQUE Bacteria + Intercellular matrix = Dental plaque

22. Bacteria make up approximately 70 to 80 percent of total material. One mg of dental plaque is estimated to contain 250 million bacteria . Other than bacteria, mycoplasma, fungi, protozoa and viruses may be present. The material among the bacteria in dental plaque is termed as intermicrobial/ cellular matrix. It contains organic and inorganic portions.

23. 1- The ORGANIC matrix The ORGANIC matrix is composed of protein— polysaccharide complex produced by microorganisms. Carbohydrates in the form of levans (fructans) provide smainly energy while glucans (dextran) provide NOT only energy, but also act as the organic skeleton of plaque. Other carbohydrates are galactose and rhamnose. Glycoproteins provide the protein component and small amounts of lipids are also present.

24. 2- The INORGANIC matrix Inorganic components include, primarily calcium, phosphorus with small amounts of magnesium, potassium and sodium.

25. Formation/Development of Dental Plaque Pellicle is the initial organic structure that forms on the surfaces of the teeth and artificial prosthesis. The FIRST stage in pellicle formation involves adsorption of salivary proteins to apatite surfaces. This results from the electrostatic ionic interaction between hydroxyapatite surface which has negatively charged phosphate groups that interacts with opposite charged groups in the salivary macromolecules.

26. The mean pellicle thickness varies from 100 nm at 2 hours to 500 to 1,000 nm. e transition from pellicle to dental plaque is extremely rapid . The FIRST components include mainly cocci with small number of epithelial cells and PMNL’s  they form a monolayer within a few hours , and the attached bacteria proliferate and form small colonies of cocci. With time other types of microorganisms proliferate and form different microcolonies

27. Hence, in dental plaque development, two adhesion processes are required. First , bacteria must adhere to the Sl . No. Tooth-associated subgingival plaque Epithelium-associated plaque

28. 1 . Gram-positive bacteria predominates Gram- positive and Gram-negative bacteria. 2. Does not extend to junctional epithelium Extends to junctional epithelium. 3. May penetrate cementum May penetrate epithelium and connective tissue. 4. Associated with calculus formation and root caries Associated with gingivitis and periodontitis.30

29. Bacterial attachment via electrostatic interactions pellicle surface and become sufficiently attached to withstand oral cleansing forces. Second , they must grow and adhere to each other to allow plaque accumulation.

30. First step in plaque formation is: Adhesion and attachment Of Bacteria

31. Bacterial Adherence During initial adherence, interactions occur mainly between specific bacteria and the pellicle. They are: 1- Bacterial Attachment via Electrostatic Interactions Oral bacteria bear an overall net negative charge, negatively charged components of the bacterial surface and negatively charged components of pellicle become linked by cations such as calcium

32. 2- Bacterial Attachment via Hydrophobic Interactions These interactions are based on the close structural fit between molecules on the pellicle and bacterial surfaces. The nature of the hydrophobicity of the cell is not clearly known. The contributing factor might be lipoteichoic acid (LTA ), which may provide a long hydrophobic area . Lectins in the bacterial surfaces recognize specific carbohydrate structure in the pellicle and become linked.

33. Adhesion and attachment Adhesion and attachment occurs between: Bacteria and clean tooth surface Bacteria and pellicle Bacteria and same species Bacteria and different species Bacteria and matrix.

34. Next step in plaque formation is: Growth and Accumulation Of Bacteria

35. Growth and Accumulation of Bacteria Once the bacteria is adhered to the pellicle, subsequent growth leads to bacterial accumulation and increased plaque mass. Dental plaque growth depends on : Growth via adhesion of new bacteria Growth via multiplication of attached bacteria.

36. The initial bacteria that colonize the pellicle surface are mostly gram-positive facultative microorganisms such as morphologic arrangement of the flora in supragingival plaque described as “ corncob” formations , characterized by central core consisting of rod-shaped bacterial cells, e.g. Fusobacterium - nucleatum and coccal cells , e.g. streptococci which attaches along the surface of the rod-shaped cell.

37. The subgingival plaque differs from supragingival plaque , in that it contains many large filaments with flagella and is rich in Spirochetes . Tooth-associated plaque is similar to supragingival plaque; whereas tissue-associated plaque is covered with flagellated bacteria without a well-defined extracellular matrix and numerous bristle—brush formations .

38. This arrangement is also called as “ test tube brush ” formation characterized by large filaments that forms the long axis; and short filaments or gram-negative rods embedded in a amorphous matrix

39. Structural and Microscopic Prosperities Of Dental Plaque 1-Supragingival Plaque

40. 1- Supragingival Plaque It is usually adherent to the tooth surface. It contains gram positive cocci and gram-negative rods and filaments. The strongly influences the growth, accumulation and pathologic potential of subgingival plaque , especially in the early stages of gingivitis and periodontitis.

41. Clinical Significance Of Dental Plaque The microbial aggregations on the tooth surface if prevented from maturing may become compatible with gingival health. Supragingival plaque if allowed to grow and mature, may induce gingivitis and can lead to the formation of a microenvironment that permits the development of subgingival plaque.

42. Therefore, supragingival plaque Actinomycesviscosus and Streptococcus sanguis , as the plaque matures, secondary colonization of Prevotella intermedia , Capnocytophaga , Porphyromonasgingivalis takes place. This ability of bacteria to adhere to different species and genera of microorganisms is known as coaggregation

43. 2- Subgingival Plaque Structural and Microscopic Prosperities Of Dental Plaque

44. 2- Subgingival Plaque In association with the presence of supragingival plaque, there are inflammatory changes that modify the anatomic relationships of the gingival margin and tooth surface . This result in enlarged gingiva, which increases the space for bacterial colonization and also protects bacteria from normal cleansing mechanisms .

45. They derive nutrients from gingival crevicular fluid. Many of these microorganisms lack the adherence ability and utilizes supragingival plaque bacteria as a means of colonization of the subgingival area. Electron microscopic studies have demonstrated the existence of an organic material called cuticle between the root surface and subgingival plaque. It is covered by a dense layer of microorganisms and is believed to be a remnant or secretary product of the junctional epithelial cells.

46. Microbial Specificity Of Periodontal Diseases Walter Loesche proposed the nonspecific and specific plaque hypothesis in 1976. The nonspecific plaque hypothesis states that it is the total bulk of plaque, which determines the pathogenicity rather than the individual species within it. In other words, all plaque is equally pathogenic .

47. According to this, when only small amounts of plaque are present, the products released by this gets neutralized by the host. Similarly, large amounts of plaque would produce large amounts of noxious products, which would overwhelm the host’s defenses. However , several authors have contradicted this concept. First , many patients have considerable amounts of plaque and calculus as well as gingivitis , but only a minority suffer from destructive periodontal disease even then in only few sites.

48. This paradox might be explained by specific plaque hypothesis, which states that destructive periodontal disease is a result of specific microbial pathogens in plaque. Thus , although the amount of plaque present correlates well with disease severity , it correlates poorly in individual patients.

49. But it is the nonspecific plaque hypothesis, which forms the basis for virtually all the current modalities for treatment, and prevention, which relies on the principle of reducing plaque scores to a minimum. Thus , although the nonspecific plaque hypothesis has been discarded in favor of the specific plaque hypothesis, much clinical treatment is still based on the nonspecific plaque hypothesis.

50. Specific Plaque Hypothesis It states that, not all plaque is pathogenic. Its pathogenicity depends on the presence of certain specific microbial pathogens in plaque . This is based on the fact that, the specific microorganisms responsible for periodontal diseases release certain damaging factors that mediates the destruction of the host tissue.

51. This concept was accepted easily due to the recognition of Actinobacillus actinomycetemcomitans as a possible pathogen responsible for localized juvenile periodontitis.

52. What Makes Dental plaque Pathogenic ? The following are the possible pathogenic mechanisms by which the plaque microorganisms can cause periodontal disease: a. Physical nature of plaque. b. Invasion of tissues by bacteria. c. Release of toxic and inflammatory substances. d. Role of bacterial specificity.

53. Microorganisms associated with periodontal diseases It is well accepted that a plaque bacteria is the primary etiologic agent in periodontal disease. Bacteria are seen in the oral cavity from birth to death. It is estimated that about 400 different species are capable of colonizing in the mouth.

54. Counts in subgingival sites range from about 103 in healthy sulci to greater than 108 in deep periodontal pockets. It has not been possible to identify and study all the organisms present in the bacterial plaque, of nearly 400 species; only 30 of them are considered to be periodontopathic. Koch’s postulates, generally used to identify the periodontopathogenecity of a microorganism, are not applicable in periodontal disease, as more than one organism is involved in periodontal diseases.

55. Hence, Socransky (1977) had proposed the following criteria for identifying the possible causative organisms in periodontal diseases: 1. The number of etiologic organisms in the diseased site must be increased and conversely the number o forganisms must be reduced or absent in healthy sites. 2. If the etiologic organism is eliminated or suppressed, the disease should stop. 3. Presence of specific antibodies to those microorganisms. 4. Presence of virulence factors associated with certain microorganisms (e.g. toxins, enzymes, etc.). 5. In vitro or animal experiments should be able to demonstrate the human disease process.

56. There are many speculations regarding the pathogens responsible for periodontitis whether they could be exogenous or components of indigenous flora. To explain this controversy, two theories have been proposed . 1- According to the first theory, periodontopathic organisms are a part of indigenous flora and they tend to overgrow during the disease progression.

57. 2- The second proposal is that, they are not components of indigenous oral flora, but are exogenous pathogens derived from outside sources. This concept hints that the quantity of plaque is not necessary for disease onset. Instead , the site should be contaminated with specific periodontopathogens.

58. Recent reports have demonstrated a possibility of viral etiology in periodontitis and implicated viruses are Epstein Barr virus, human cytomegalovirus and mixed herpes viral infections. Viral infection can contribute to periodontitis by altering the functions of neutrophil, macrophages and lymphocytes which in turn promotes the overgrowth of periodontopathic organisms in the subgingival flora. The other possibility is that, the viral infection can destroy the oral epithelial cells thus disrupting the barrier function of the periodontium.

59. Bacteria Associated with Periodontal Health and Disease Wolinella recta Campylobacter rectus (C . rectus) Bacteroidesgingivalis Porphyromonasgingivalis (P . gingivalis ) BacteroidesintermediusPrevotellaintermedia (P . intermedia ) BacteroidesmelaninogenicusPrevotellamelaninogenica (P . melaninogenica ) BacteroidesforsythusTannerellaforsythus ActinobacillusAggregatibacter actinomycetemcomitansactinomycetemcomitans

60. Health Actinomyces ( viscosus and naeslundii ) Streptococcus ( S. mitis and S. sangius ) Veillonellaparvula , small amounts of gram-negative Species are also found.

61. Chronic Gingivitis Gram-positive (56%), Gram-negative (44%) organisms are found. Predominant gram-positive species include, S. sangius , S. mitis , S. oralis , A. viscosus , A. naeslundii , Peptostreptococcus micros. Gram-negative Organisms Fusobacteriumnulceatum Prevotellaintermedia Veillonellaparvula as well as Haemophilus , Capnocytophaga and Campylobacter species. Pregnancy-associated Gingivitis Prevotellaintermedia .

62. Acute Necrotizing Ulcerative Gingivitis Spirochetes Prevotellaintermedia . Adult Periodontitis Porphyromonasgingivalis Bacteroides ( Tannerella ) forsythus Prevotellaintermedia Campylobacter rectus Eikenellacorrodens Fusobacteriumnucleatum Actinobacillusactinomycetemcomitans Peptostreptococcus micros Treponema , and Eubacterium species .

63. Acute Necrotizing Ulcerative Gingivitis Chronic Adult Periodontitis

64. Viruses EBV-1 ( Ebstein -Barr virus) HCMV (Human cytomegalovirus). Localized aggressive Periodontitis Actinobacillus ( Aggregatibacter ) actinomycetemcomitans Porphyromonasgingivalis Eikenellacorrodens Campylobacter rectus Fusobacteriumnucleatum Bacteroidescapillus Eubacteriumbrachy Capnocytophaga Herpes virus.

65. Generalized aggressive Periodontitis Actinobacillus ( Aggregatibacter ) actinomycetemcomitans Porphyromonasgingivalis Prevotellaintermedia Capnocytophaga Eikenellacorrodens Neisseria .

66. Localized aggressive Periodontitis Generalized aggressive Periodontitis

67. Refractory Periodontitis Actinobacillusactinomycetemcomitans Bacteroidesforsythus Porphyromonasgingivalis Prevotellaintermedia Wolinella recta. Abscesses of the Periodontium Fusobacteriumnucleatum Prevotellaintermedia Peptostreptococcus micros Bacteroidesforsythus Porphyromonasgingivalis .

68. Refractory Periodontitis Abscesses of the Periodontium

69. Edit By : Ghadah Abulqumsan Reham Altayep Noor Abdurrahman