Microbiology of Periodontal diseases

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Information about Microbiology of Periodontal diseases

Published on March 21, 2013

Author: nurved

Source: slideshare.net


At the end of this session, the student should be able to describe:
What is Periodontium and its role
Ecology of Dental Crevice and its role
Conditions that affect Periodontal tissue
Role of Microorganisms in Periodontal Disease
Complex relationship between Plaque and periodontal disease

MICROBIOLOGY OFPERIODONTAL DISEASES Dr. Ali Yaldrum Faculty of Dentistry, SEGi University.

LEARNING OBJECTIVES• At the end of this session, the student should be able to describe: What is Periodontium and its role Ecology of Dental Crevice and its role Conditions that affect Periodontal tissue Role of Microorganisms in Periodontal Disease Complex relationship between Plaque and periodontal disease

The term ‘periodontal diseases’ embraces a number of conditions in which the supporting tissues of the teeth are attacked.

Supporting tissues are• Gingivae• Cementum• Alveolar Bone• Periodontal Ligament Fibers (PDL)

ECOLOGY OF DENTAL CREVICE Ecology of dental crevice is different from other sites in the oral cavity• more anaerobic• bathed in gingival crevicular fluid (GCF) *In diseased state crevice becomes a pocket

• In Periodontal pocket• Low Eh (oxidation reduction potential)• increased flow of GCF ➡in gingivitis: 147% increase ➡in periodontitis: 30 fold increase

GINGIVAL CREVICULAR FLUID GCF contains• humoral and cellular defense factors• proteins & glycoproteins

assachrolytic & proteolytic increased growth & enzyme activity of periodontal pathogen Porphyromonas gingivalisMetabolism ENVIRONMENT Proteolysis Decreased pH increased temperature enhanced attachment of microbes with epithelium slight increase during inf lammation alter the gene expression alter the competitiveness of P. gingivalis periodontal pathogens disturbing the natural balance of subgingival microflora growth of proteolytic gram -ve organisms

• Flow of GCF can remove planktonic microorganisms• Prevotella, Porphyromonas, Fusobacterium spp. adheres to Streptococcus & Actinomyces colonizing cementum• Parvimonas micra adhere crevicular epithelial cells

C X X Tissue destruction D D Gingiva Tooth C Fluid flow C A A Systemic A Modulation of host defences Cellular Immune response – innate and adaptiveFig. 6.16 Pathogenic synergy in the aetiology of periodontal diseases. Bacteria capable of causing tissue damage directly (e.g.species X) may be dependent synergy in the aetiology other cells (e.g. organisms C and D) for essential damage or attachment sites Pathogenic on the presence of of periodontal diseases. Bacteria capable of causing tissue nutrientsso that they can grow and (e.g. speciesremoval forces provided presence of other cells (e.g. organisms C and D)both of these groups of directly resist the X) may be dependent on the by the increased flow of GCF. Similarly, for essential nutrients or attachment sites so that they can grow and resist the removal forces provided by thebacteria may be reliant for their survivalSimilarly, both of these groups ofA and C) to be reliant for the host defences. Individual bacteria increased flow of GCF. on other organisms (e.g. bacteria may modulate their survival on othermay have more than one role(e.g. A and C) to modulatethe host defences. Individual bacteria may have more than one role organisms (e.g. organism C) in the aetiology of disease. (e.g. organism C) in the aetiology of disease.destruction directly (and satisfy Koch’s postulates), that the tongue may act as a reservoir for these peri-while in other pockets, different bacteria could fill odontal pathogens. Some pathogens may also persist

• The main aetiological agent of periodontal disease is microflora inhabiting subgingival plaque.• Host tissues and its specific and non- specific host defense mechanisms play crucial modulating roles.

HOST TISSUE• Dentogingival junction is most vulnerable site for microbial attack but can be maintained healthy with good oral hygiene• Plaque accumulates close to the gingival margin, the host defenses are overcome and gingival inflammation (gingivitis) and subsequent periodontal inflammation with loss of attachment ensues (periodontitis).

Specific Host Defense Factors Non-specific Host Defense Factors PolymorphsB and T Lymphocytes Macrophages Complement system ProteasesAntibodies: IgA, IgG, IgM Lyzozyme LactoferrinIgG, Immunoglobulin G.

Dental Plaque is an essential aetiological agent in the development and progression of periodontal diseases and is shown by the following— Epidemiological data— Clinical Studies— Topical application of antimicrobial agents— Initiation of disease in gnotobiotic animals by peridontopathogenic bacteria

PLAQUE SPECIFIC HYPOTHESIS— In certain disease states such as necrotizing ulcerative gingivitis the key aetiologic agents are fusobacteria and spirochaetes. Direct involvement of Aggregatibacter actinomycetemcomitans in aggressive (juvenile) periodontitis— Disease can be resolved by appropriate antibiotics active against anaerobes (metronidazole) and tetracycline.

NON-SPECIFIC PLAQUE HYPOTHESIS— Collective groups or consortia of different bacteria have the total complement of virulence factors required for periodontal tissue destruction— some bacteria can substitute for others absent from the pathogenic consortium.— This hypothesis implies that plaque will cause disease irrespective of its composition, and it is supported by the clinical findings of numerous bacterial species in diseased periodontal pockets.

the putative pathogens, but also by interfering with response of the host, and (c) connective tissue andthe environmental factors that drive the changes bone metabolism. These interactions are influencedin the balance in the microflora, e.g. such as by reduc- by disease modifiers, which may be genetic (e.g.ing the severity of the inflammatory response, or by neutrophil defects) or environmental (e.g. tobaccoECOLOGICAL PLAQUE HYPOTHESISaltering the redox potential of the pocket to preventthe growth of the obligate anaerobes. Other relevantchanges in the local environment that could perturb smoking) factors. The clinical signs reflect the sum of these interactions, and the severity of the disease can feed back to influence the microbial challenge, Predominantly Gingival Gram positive microflora health Plaque Reduced Low GCF flow reduction inflammation Higher Eh Facultative anaerobes Inflammatory Environmental Ecological response change shift Predominantly Gram negative microflora Plaque Increased High GCF flow Gingivitis accumulation inflammation Lower Eh Obligate anaerobesFig. 6.17 A schematic representation of the ‘ecological plaque hypothesis’ in relation to periodontal disease. Plaqueaccumulation produces an inflammatory host response; this causes changes in the local environmental conditions which favourthe growth of proteolytic and anaerobic Gram negative bacteria. Disease could be prevented by not only targeting the putativepathogens, but also by interfering with the factors driving their selection.134

Ecology of Healthy Gingival Crevice

Ecology in Gingivitis

Ecology in Periodontitis

Oral Microbiology V. parvula A. odontolyticus S. oralis C. rectus S. mitis C. gracillis P. gingivalis E. corrodens P. intermedia T. forsythia P. nigrescens E. nodatum T. denticola Streptococcus spp. S. constellatus P. micros S. gordonii F. nucleatum S. intermedius E. corrodens Aggregatibacterium (Actinobacillus) C. gingivalis actinomycetemcomitans b. C. sputigena C. ochraceae C. concisus A. a serotype aFig. 6.10 The grouping of bacteria into complexes to reflect their relationship with the host in health and periodontal disease.The ‘red complex’ is found most frequently in deep periodontal pockets, and their presence was usually preceded by membersof the ‘orange complex’. Members of the ‘yellow’, ‘green’ and ‘purple’ complexes were generally associated with healthy sites. Purple, Yellow, Green: Healthy Gingival sulcus Red, Orange: Periodontal pocketsand Treponema denticola, and their presence was often approaches has identified low levels of many ofpreceded by members of the orange complex, which the putative pathogens at healthy sites, while evi-was also often found in deeper pockets, but was dence of transmission of organisms such as P.more diverse in membership. In contrast, species gingivalis and A. actinomycetemcomitans betweenof the yellow, green and purple complexes, together spouses has been obtained. However, in either sit-

Plaque-associated gingivitis has been separ ated into three stages• Stage 1: The initial lesion• Stage 2: The ear ly lesion• Stage 3: Established lesion

STAGE 1:THE INITIAL LESION• develops within 4 days of plaque accumulation.• Micro-flor a consists mostly of Gr am-positive cocci (Streptococcus spp.).• Histologically, there is an acute inflammator y reaction.• The lesion is char acter ized by increased flow of GCF, migr ation of PMN leukocytes into the gingival sulcus from the local vasculature .• Adjacent to the junctional and sulcular epithelia, the inflammator y infiltr ate occupies approximately 5-10% of the gingival connective tissue .• This initial lesion is not visible clinically.

STAGE 2: THE EARLY LESION• Appear s after approximately 7 days of plaque accumulation, detectable clinically as gingivitis.• lower oxygen tension and the plaque flor a shifts to more Actinomyces spp., spirochaetes and capnophilic or ganisms.• Histologically, the gingival infiltr ate in the ear ly lesion is dominated by lymphocytes (75%) and macro-phages,few plasma cells• The infiltr ated area occupies approximately 15% of the mar ginal gingival connective tissue , with some local destr uction of collagen.• Migr ation of polymor phonuclear leukocytes into the gingival sulcus and crevicular fluid peaks at 6 to 12 days following the onset of clinically

STAGE 3: ESTABLISHED LESION• After a var iable per iod of time the subgingival microflor a develops into an environment that can suppor t the growth of obligate anaerobes such as Porphyromonas gingivalis and Prevotella inter media.• Histologically, there is a fur ther increase in the size of the inflammator y lesion within the affected gingiva, with a shift to a predominance of plasma cells and B-lymphocytes.• The junctional and pocket epithelia are heavily infiltr ated with neutrophils. Plasma cells are found at the per ipher y of die lesion, while macrophages and lymphocytes are present in the lamina propr ia of the pocket wall.• Established lesions may per sist for months or year s without progression to per iodontitis.

TYPES OF GINGIVITIS• Chronic Marginal gingivitis• Acute Necrotizing Ulcerative gingivitis• Medication influenced gingivitis• Gingivitis associated with systemic diseases• Acute Herpetic gingivostomatitis

PERIODONTITISPer iodontitis may be defined clinically as inflammationof the suppor ting tissues of the teeth.

• Maintains all the features of the established lesion of gingivitis• Migr ation of the junctional epithelium down the root surface , alveolar bone resor ption and subsequent pocket for mation• Char acter ized by progressively destr uctive changes destroying alveolar bone and per iodontal ligament, with an attachment loss of more than 3 mm.• Histologically, the conver sion of the established lesion of gingivitis into per iodontitis is char acter ized by destr uction of the connective tissue attachment to the root surface and by alveolar bone loss.

FORMATION OF DENTAL POCKET• Creates highly anaerobic environment• pH shifts from 6.9 to approximately 7.4 to 7.8 and the pocket is continually bathed by the protein-r ich GCF, which encour ages growth of proteolytic bacter ia.• Subgingival plaque have a dense zone of mostly Gr am-positive bacter ia attached to the tooth surface and a less densely packed zone of mainly Gr am-negative or ganisms next to the gingival surface .

REFERENCESPhilip D. Marsh, Michael V Martin, “Plaque mediated diseases- Dental Caries and Periodontaldiseases” in Oral Microbiology, 5th Edition, Churchil Livingstone, 2009, pp 117-137J. Bagg, T. W. Macfarlane, I. R. Poxton and A. J. Smith, “Periodontal Diseases” in Essentials ofMicrobiology for Dental Students, 2nd Edition, Oxford University Press, 2006 pp 249-259Lakshman Samaranayake, “Microbiology of Periodontal diseases” in Essential Microbiology forDentistry, 3rd Edition, Churchil Livingstone, Elsevier, pp 275 - 287.

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