Microbial interaction with the host in periodontal diseases

Malik Hudieb, BDS, PhD

Department of Preventive Dentistry Faculty of Dentistry Jordan University of Science and Technology

Pathogenesis..
Periodontal diseases:

Bacterial Plaque

Host response

Immune system

Inflammation

Clinical signs

Pathogenesis..
Periodontal diseases: Bacterial Plaque

Host tissues

Host Response

Pathogenesis..
Periodontal diseases: Bacterial Plaque

Host tissues

Protective or Destructive?

Host Response

So..
The presence of periodontal pathogens alone is
insufficient to cause the tissue destruction seen in periodontitis. It is the bodys response to the periodontal pathogens that is the cause of nearly all the destruction seen in periodontitis.

Bacterial Virulence Factors

Virulence factorsmechanisms that
enable the bacteria to colonize and invade

the tissues of the periodontium

Minor cause of periodontal destruction

Bacterial Virulence Factors:

Characteristics of the bacteria, themselves Products produced by the bacteria

Bacterial Characteristics
Bacterial invasion factorsallow
bacterium to actively penetrate the

epithelium lining of the pocket wall and

enter the gingival connective tissue

Peptidesfound in the bacterial cell

membrane

Bacterial Products
Exotoxinsharmful proteins (potent
toxin) released from the bacterial cell

Enzymesproteins that catalyze chemical reactions that are harmful to the bodys cells

Bacterial Colonization (biofilm)

Bacterial Colonization

Coaggregation of Bacteria
Coaggregationthe cell-to-cell adherence of one oral bacterium to another.
Coaggregation is NOT random, each bacterial strain only has a limited set of bacteria to which they are able to adhere.

Coaggregation of Bacteria
Early Intermediate Late

Early Colonizers
The first bacteria to colonize the tooth
surface are nonpathogenic. Periodontal pathogens are UNABLE to colonize the biofilm alone.
Tooth/ or hard tissue NonPathogenic Pathogenic

Colonization of the Pellicle

Early Gram-positive: Actinomyces viscosus
Attaches to fimbriae to proline rich proteins on saliva coated tooth surfaces.

Streptococcus sanguis

Streptococcal SpeciesEarly Colonizers

Many streptococcal species have the
ability to attach to the tooth pellicle

Other early colonizers coaggregate with the streptococcal species.

The Importance of Early Colonizers

Free-floating periodontal pathogens cannot cause disease.
Every time the biofilm is disrupted, the process must start all over again with the early colonizers.

Intermediate and Late Colonizers

Like the early colonizers, the intermediate
and late bacterial colonizers must join the

biofilm in the proper sequence.

Many of the periodontal pathogens are late colonizers of the biofilm.

Intermediate Coaggregation
Bacteria begin to multiply.

Gram-Negative Organisms
Gram-negative bacteria join: Fusobacterium nucleatum Prevotella intermedia

Gram-Negative Organisms
Gram-negative bacteria colonize Porphyromonas gingivalis Capnocytophaga gingivalis

Socranskys Microbial Complexes

Biochemical Mediators

 Biochemical mediators are biologically

active compounds secreted by the immune

cells that activate the bodys inflammatory

response.

Biochemical Mediators
Released by the immune cells to activate the inflammatory response.

Inflammatory mediators of importance in

periodontal disease are
Cytokines Prostaglandins Matrix metalloproteinases (MMPs)

Cytokines
Cell signalling protein molecules Powerful mediators produced by immune cells Influence the behavior of other cells Signal to the immune system to send more phagocytes to site of infection

Cytokines (cont.)
Produced by many different cellsPMNs, macrophages, B lymphocytes, epithelial cells, gingival fibroblasts, and osteoblasts Produced in response to tissue injury Cytokines important in periodontal disease include IL-1, IL-6, IL-8, and TNF-alpha.

Functions of Cytokines
Recruit cells (PMNs and macrophages) to infection site

Increase vascular permeability that increases movement of immune cells into the tissues Can initiate tissue destruction and bone loss in chronic infections, such as periodontal disease

Prostaglandins
Potent inflammatory mediators Series of prostaglandinsD, E, F, G, H, I Most cells can produce prostaglandins (arachidonic acid in the cell membrane)

Macrophages and fibroblasts

Functions of Prostaglandins
Increase permeability and dilatation of blood vessels to promote increased movement of immune cells and complement to the infection site

Trigger osteoclastsbone-consuming
cellsto destroy the alveolar bone

Functions of Prostaglandins
Promote the overproduction of destructive MMP enzymes Prostaglandins of the E series (PGE) initiate most of the alveolar bone destruction in periodontitis.

Matrix Metalloproteinases (MMPs)

Family of at least 12 different enzymes Produced by various cells of the body PMNs, macrophages, fibroblasts, JE cells Enzymes act together to breakdown connective tissue matrix (collagen,gelatin, elastin)

Function of MMPs in Health

In health, MMPs facilitate normal turnover of

the periodontal connective tissue matrix.

MMPsChronic Bacterial Infection

MMPs are released Overproduction of MMPs results in breakdown of connective tissue of the periodontium.

MMPsChronic Bacterial Infection

High MMP levels result in extensive collagen
destruction in the periodontal tissues.

Gingival recession, pocket formation, and tooth mobility.

Host Response in Periodontal Disease

Initial

Bacteria colonize the tooth near the

gingival margin.
Bacteria initiate host response. PMNs pass from bloodstream into the gingival connective tissue.

PMNs release cytokines that

destroy gingival connective tissue, allowing PMNs to move quickly through the tissue.

PMNs migrate into the sulcus and

phagocytize bacteria.

Early

 Bacteria penetrate into the connective tissue. PMNs release cytokines causing more localized destruction of the connective tissue. Macrophages release cytokines, PGE2, and

MMPs.

Established

Plaque biofilm extends subgingivally

Host cells produce more toxic

chemicalscytokines, PGE2,
and MMPs.

Increase in proportions of gram-negative anaerobes.

Advanced

Cytokines destroy the connective tissue and PDL fibers.

Cytokines, PGE2, and MMPs destroy the connective tissue and bone.

PGE2 initiates bone destruction.

Specific microorganisms: P.gingivalis, T.forsythus, T.denticola, P.intermedia, A.a,F.nucleatum, E.corroens, C. rectus

Mechanisms of Alveolar Bone Destruction

 Macrophages produce cytokines, PGE2, and MMPs. This will stimulate fibroblasts to secrete PGE2 and MMP. Destruction of the connective tissue. PGE2 stimulates osteoclasts to resorb the alveolar bone.

Let us remember that..

For the periodontium to remain healthy,

the bacterial infection must be controlled

so as not to trigger a chronic,

exaggerated host immune response. The bodys immune response to the

bacteria causes most of the tissue

destruction in the periodontal tissues.