Etiology of Periodontal Disease

Dr. Marcel Hallare

Periodontal disease is a pathologic process that affects the periodontium The vast majority of inflammatory diseases of the periodontium results from bacterial infection The dominating causative agents of periodontal disease are microorganisms that colonize the tooth surface (bacterial plaque and products) No systemic disorder is known to be the initiating cause of periodontitis in the absence of bacterial plaque

TOOTH-ACCUMULATED MATERIALS
1. 2. 3. 4. 5.

Bacterial plaque Acquired pellicle Calculus Food debris Materia alba

Bacterial plaque

Two types of plaque that are closely associated with periodontal disease:
1.

2.

Consists of a mat of densely packed, colonized, and colonizing microorganisms that grow on and attach to the tooth Free floating or loosely attached between the soft tissue and teeth

Acquired pellicle

Primarily a protein film that forms on erupted teeth and can be removed by abrasives Quickly reforms after being removed Not removed by forceful rinsing

Calculus

Calcified plaque that is usually covered by a soft layer of bacterial plaque

Food debris

Food matter that is retained in the mouth

Materia alba

(literally, white matter)

A soft mixture of salivary proteins, some bacteria, many desquamated epithelial cells, and occasional disintegrating leukocytes Usually flushed off with forceful water spray

BACTERIAL FACTORS IN PERIODONTAL DISEASE

Morphology of Bacterial Plaque

Under light and SEM, supragingival plaque and subgingival plaque have distinct morphological differences

Supragingival Plaque

Bacterial cells appear to be densely packed on the tooth surface and the deposits may be thick (0.5mm or more) Composition of the microbial deposits includes coccoid and relatively numerous filamentous bacteria

Some filamentous bacteria are covered with coccal organisms, which appear as corncob formations Flagellated forms and spirochetes are observed apically and on the outer surface

Subgingival Plaque

Subgingival plaque in periodontitis patient is composed of an inner and an outer layer The inner layer is tightly adherent bacteria is continuous with, but is thinner and less organized than supragingival plaque

Outside this tightly adherent layer, and adjacent to the soft tissue of the pocket, is a loosely adherent layer of microorganisms This layer consists of numerous spirochetes, gram-negative bacteria, and bacteria grouped into bottle-brush or test-tube brush formations

Microorganisms of Plaque

Young plaque (1-2 days) consists primarily of gram-positive and some gram-negative cocci and rods From 2-4 days of growth, undisturbed plaque changes in the numbers and the types of organisms present

The number or gram-negative cocci and rods increase and fusiform bacilli and filamentous organisms become established From 4-9 days, this ecologically complex population of microorganisms is further complicated by the presence of the increasing number of motile bacteria, namely, spirilla and spirochetes

Other Constituents of Plaque

1. 2. 3. 4. 5. 6.

Epithelial cells White Blood cells Erythrocytes Protozoa Food particles Miscellaneous components

Mechanism of Bacterial Action

1. 2. 3. 4. 5.

Invasion Cytotoxic agent Enzymes Immunopathologic mechanism Combined action

Invasion

Bacterial invasion is not necessary for gingival inflammation to occur All that is required id that enough bacteria (and possibly specific pathogenic bacteria) be fixed to the tooth, near the gingiva, for sufficient length of time to challenge the tissue with their toxic products

Cytotoxic agent

Endotoxins, which are lipopolysaccharide constituents of the cell wall of gramnegative bacteria, can be a direct cause of tissue necrosis, as well as initiator of inflammation by triggering an immunologic response and activation of the complement system

Enzymes

Collagenase depolymerizes collagen

fibers and fibrils, the major formed elements in the gingiva and periodontal ligament Proteases, a family of enzymes, contribute to breakdown of noncollagenous proteins and increase capillary permeability

Hyaluronidase hydrolyzes hyaluronic acid,

an important tissue cementing polysaccharide, and can act as a spreading factor to increase tissue permeability Chondroitinase hydrolyzes chondroitin sulfate, another tissue-cementing polysaccharide

Immunopathologic mechanism

The role of the immunologic response in periodontal disease is not completely understood; however, the potential to cause tissue destruction is apparent

Combined action

It is possible that more than one mechanism may be involved in the initiation and progression of inflammatory periodontal disease

SYSTEMIC FACTORS AND PERIODONTAL DISEASE

Any condition that might reduce the resistance of periodontium to toxic insult should be expected to contribute to the initiation of the inflammation and to influence the rapidity and severity of the disease process

LOCAL CONTRIBUTING FACTORS AND PERIODONTAL DISEASE

1. 2. 3. 4. 5. 6.

Anatomic factors Iatrogenic factors Calculus formation Traumatic factors Chemical injury Excessive occlusal force

Anatomic factors

Root morphology Position of tooth in arch Root proximity

Iatrogenic factors

Operative procedures Restorative materials and restorations Removable partial dentures Fixed partial denture Exodontics Orthodontics

Calculus formation

Important in the progression of disease Serves as a coral reef within which microorganisms can multiply and release their toxic products The rough surface of calculus makes it difficult if not impossible, for the patient to remove associated bacterial plaque

Traumatic factors

Toothbrush abrasion Factitious disease Food impaction

Chemical injury

Indiscriminate use of topically applied aspirin tablets, strong mouthwashes, and various escharotic drugs may result in ulceration of the gingival tissue

Excessive occlusal force

Neoplasms

Renewal of Gingival Epithelium

The oral epithelium undergoes continuous renewal Its thickness is maintained by a balance between new cell formation in the basal and spinous layers and the shedding of old cells at the surface

Mitotic activity exhibits a 24-hour periodicity, with highest and lowest rates occurring in the morning and evening respectively Mitotic rate is highest in nonkeratinized areas and is increased in gingivitis, without significant gender differences

 Turnover

times of tissue:
5-6 days 10-12 days 1-6 days

palate, tongue, cheek gingiva junctional epithelium

The End