PERIODONTAL MICROFLORA

CONTENTS

• Introduction• History • Microbial specificity of Periodontal Disease• Criteria for Association of Periodontal

Pathogens• Microorganism in specific Periodontal

Diseases• Microbial complexes

Introduction

• Periodontal disease comprises a group of inflammatory conditions of supporting tissues of teeth that are caused by bacteria.

• Multiple species that function as pathogens in one site, also may be present in low numbers in healthy sites.

HISTORY

• Anton Van Leeuwenhoek(1632-1723)– developed a microscope and used it to discover microorganisms, cellular structure, blood cells, sperms.

• I didn’t clean my teeth (on purpose) for three days and then took the material that had lodged in small amounts on the gums above my front teeth…. I found a few living animalcules

• The first individual to identify bacteria as the cause of periodontal disease appears to have been the German dentist Adolph Witzel(1847-1906)

• The first true oral microbiologist was Willoughby D. Miller 1853-1907

Teeth are the primary habitat for periopathogens. Indeed, soon after full mouth tooth extraction in patients with severe Periodontitis, key pathogens such as actinobacillus actinomycetemcomitans and P. gingivalis will disappear from their entire natural intraoral habitat.

P. intermedia and their black pigmented prevotella species can remain, but at lower frequencies and number. Therefore, teeth can even be considered as a port of entry for periopathogens.

• Recent studies using newer microbial techniques however indicate that A. a. and P. gingivalis are not entirely eradicated after full mouth extraction; they may remain at very low concentrations.

• The same applies to edentulous infants or full dentures wearers, in whom significant proportions of periodontal pathogens, again except for A. a. and P. gingivalis have been recorded.

Microbial Specificity for Periodontal Disease

“Non Specific Plaque Hypothesis” Walter Loesche, 1976

“Specific Plaque Hypothesis”Walter Loesche , 1976

Non Specific Plaque Hypothesis

• periodontal disease - elaboration of noxious products by the entire plaque flora.

• periodontal disease - plaque accumulation.

Contradiction of Non Specific Plaque Hypothesis

• plaque and calculus - gingivitis never developed destructive Periodontitis

• Site Specificity

• In the presence of uniform host response, these findings were inconsistent with the concept that all plaque was equally pathogenic.

Specific Plaque Hypothesis

• certain plaque – pathogenic• pathogenicity -presence of or increases in

specific microorganisms.

• This concept predicts that plaque harboring specific bacterial pathogens result in a periodontal disease because these microorganisms produce substances that mediate the destruction of host tissues.

CRITERIA FOR ASSOCIATION OF PERIODONTAL

PATHOGENS

• KOCH’S POSTULATES

In I870s, Robert Koch’s criteria by which microorganism can be judged to be a causative agent in human infections.

1. Be routinely isolated from diseased individuals2. Be grown in pure culture in the laboratory3. Produce a similar disease when inoculated into

susceptible laboratory animals4. Be recovered from lesions in a diseased

laboratory animal

• Streptococcus mutans -fulfils Koch’s postulates - dental caries.

• difficulty - other types of diseases,• application of Koch’s postulates- challenged in

recent years.

Why insufficient in Periodontal Disease

• In Periodontitis-1. Inability to culture all organisms associated

with disease.2. Difficulties inherent in defining and culturing

sites of active disease.3. Lack of good animal model system.

• Sigmund Socransky, a researcher at the Forsyth Dental Centre in Boston, proposed criteria by which periodontal microorganism may be judged to be potential pathogens.

SIGMUND SOCRANSKY’S CRITERIA FOR PERIODONTAL PATHOGENS

1. Be associated with disease, as evident by increases in the number of organisms at diseased sites

2. Be eliminated or decreased in sites that demonstrate clinical resolution of disease with treatment

3. Demonstrate a host response, in the form of an alteration in the host cellular or humoral immune response

4. Be capable of causing disease in experimental animal models5. Demonstrate virulence factors responsible for enabling the

microorganism to cause destruction of the periodontal tissues.

Evidence supporting the role for A.actinomycetemcomitans and

P.gingivalis as pathogens in periodontal disease: Socransky’s Criteria

CRITERION A.actinomycetemcomitans

P. gingivalis

ASSOCIATION EVIDENCE SUPPORTING ROLE OF MICRORGANISMS AS PATHOGENS IN PERIODONTAL DISEASE; SOCRANSKY’S CRITERIA

Increased in LAPIncreased in chronic periodontitis lesionsDetected in tissues of LAP

Increased in periodontitis lesionsFound associated with crevicular epithelium

ELIMINATION Suppressed or eliminated in successful therapyfound in recurrent lesions

Suppressed or eliminated in successful therapyfound in recurrent lesions

HOST RESPONSE Increased serum & local antibody, levels in LAP

Increased systemic & local antibody levels in periodontitis

ANIMAL STUDIES Capable of inducing disease in gnotobiotic rats

Found to be important in experimental mixed infections & in periodontitis in the cynomolgus monkey

VIRULENCE FACTORS

Host tissue cell invasion , leukotoxin, collagenase, endotoxin, fibroblast inhibiting factor etc.

Host tissue cell adherence & invasions, collagenase, fibrinolysin, H2S etc.

MICROORGANISMS IN SPECIFIC PERIODONTAL DISEASES

• The total number of bacteria- per gram of plaque- twice in periodontally diseased

• more plaque - diseased sites• suggests- total bacteria load• The difference between periodontal health

and disease also are evident when the morphotypes of bacteria from healthy and diseased sites are examined.

Periodontal Health

• Healthy sites-gram +ve facultative rods & cocci J Slots ,1977.• Members of the genera Streptococcus and

Actiniomycetes (e.g. S. Sanguis, S. Mitis, A. Viscosus, A. Naesleundii).

• Small proportions of gram –ve species i.e. P. Intermedia, F. Nucleatum and Capnocytophaga, Nisseria and Vellionella species.

• Protective or Beneficial species-S. sanguis, C.ochracea, , Vellionella parvula Dzink JL ,1985

Gingivitis

• The initial microbial flora of experimental gingivitis consists of gram +ve rods, gram +ve cocci, and gram –ve cocci. The transition to gingivitis is evident by inflammatory changes and is accompanied first by the appearance of gram –ve rods and filaments, then by spirochetal and motile microorganisms.

• Plaque induced Gingivitis- Harold Loe, 1965 Gram positive - S. intermedia, S. Sanguis, S. Mitis, S.oralis , A.

Viscosus, A. Naesleundii, and P. Micros. etc. Gram negative-F. Nucleatum, P. intermedia,

Capnocytophaga, and V. Parvula, as well as Haemophilus, and Campylobacter species.

• Pregnancy induced gingivitis P. intermedia

Chronic Periodontitis

Spirochetes,P. gingivalis,B. forsythus,A. actinomycetemcomitansP. micros, Treponema and EubacteriumF. NucleatumC. RectusP. IntermediaE. corrodensDesulfobulbus sp. Oral clone R004, deferri bacteres Sp. Oral

clone BH017 and D084, Bacteroides Sp. Oral clone AU126.

• Recent studies have documented an association between chronic periodontitis and viral microorganisms of the herpes virus group, most probably Epstein Barr Virus I (EBV-I) and human cytomegalovirus (HCMV). Further, the presence of subgingival EBV-I and HCMV are associated with high levels of putative bacterial pathogens, including P. Gingivalis. T. Forsythia, P. Intermedia and T. Denticola.

• These data support the hypothesis that viral infection may contribute to periodontal pathogenesis, but the potential role of viral agents remain to be determined.

MICROBIAL SHIFT DURING DISEASE

Comparing the microbiota in health, gingivitis and periodontitis, the following microbial shifts can be identified:

• From gram +ve to gram –ve• From cocci to rods (and at a later stage to spirochetes)• From nonmotile to motile organisms• From facultative anaerobes to obligate anaerobes• From fermenting to proteolytic species

• Localized Aggressive Periodontitis –A.actinomycetemcomitans Socransky, 1977P. gingivalis,F. NucleatumVirus- EB virus (EBV-I), Human cytomegalo virus (HCMV)

• Necrotizing ulcerative gingivitis - spirochetes - P intermedia.

• Abscesses of Periodontium F.nucleatum

P. intermedia, P. gingivalis, P. micros

Microbial Specificity in Periodontitis

• Table provides an overview of the detection frequency for most key pathogens in different forms of periodontal infections. It is immediately obvious that there is no “black or white” situation; most pathogens might be present, but do not necessarily have to be present for specific forms of periodontitis. This overview also illustrates that one cannot use microbial composition to differentiate between different forms of periodontal infections.

Microbial Complexes

microbiota into groups or complexes, - appear to occur together

transition from a healthy oral environment to gingivitis and to periodontal disease is triggered by a specific 'set' or 'complex' of bacterial species

Socransky and Haffajee and colleagues,1998

Thank you

• Clinical periodontology 9th edition carranza.• Clinical periodontology 10th edition carranza• Clinical periodontology 4th edition jan linde.• Clinical periodontology and implantology Rose

and mealey• Subgingival microflora and periodontal

conditions in healthy teenagers. Asikainen S, Alaluusua S, Kari K, Kleemola-Kujala E. Journal of Periodontology 1986 Aug;57(8):505-9

• Microbiology in the management of destructive periodontal disease.van Winkelhoff AJ, de Graaff J. Journal of Clinical Periodontology 1991 Jul;18(6):406-10.