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Enrico G. RIOD O. Text -. Chapter 1. Chapter 2. Chapter 3. Chapter 4. Clinical case. Clinical cases. Volume I I. Chapter 9. Chapter 1 0. The function of keratinized and attached gingiv a Gingival recessio n Sullivan and Atkins Classificatio n Miller Classificatio n Surgical instrument s Frenulectomy Pedicle soft tissue grafts Coronally positioned Laterally positioned Bipapillar Free soft tissue graft s Connective tissue graft s.

Chapter 1 2. Chapter 1 3. Chapter 1 4. Chapter 1 5. The mechanis m of periodonta l destruction. The term "periodontal disease" describes a group of diseases initiatin g in and remaining confined to the periodontal tissue. The majority are inflam- matory lesions caused by microorganisms accumulating in the pericrevicula r area. Periodontal disease can be divided into :. Although more than species of bacteria have been isolated in the mouth , human periodontal infections are apparently caused by a specific microbial infection.

Epithelial attachment 0. Ideal gingival morphology and diagrammatic representation : pink colour, scalloped margin , "orange peel" appearance, papillae in the interdental spaces, adequate band of keratinized gingiva. The gingival sulcus is shallow 0. The distance from the bottom of the sulcus to the osseous crest is known as the biological width 2.

A healthy gingival condition known as "pristine gingiva" is an ideal sit - uation in which there is no bacterial plaque and the gingival tissue is histologi - cally perfect, without inflammatory infiltration. It can be achieved only under experimental conditions and through meticulous oral hygiene.

A small quantity of. If removed daily, th e plaque does not have time to proliferate an d reach the sulcus, modi- fying its qualitative characteristics. If the bacterial plaque is not constantly removed, it proliferates an d spreads in the gingival sulcus.

Two subgingival plaque components have bee n identified : a part adhering to the root of the tooth and a free or fluctuating par t Listgarten, J. Perio Supragingival plaqu e. Plaqu e. Supragingiva l. Subgingival - adherent. Subgingival - not adheren t. Subgingival plaque.

Quantity of plaqu e. Quality of plaqu e. Plaque retainin g factor. Bacterial product s. Positive Response. Intact tissue s. Exudatio n. Immune respons e. Deficient Respons e. PMN defect s. Hypersensitivity reactions. Systemic disease s. The presence of specific bacteria in the sulcus is a vital element in determining inflammatory peri - odontal diseases Loe - Theilade - Socransky - Listgarten - Newman.

On the other hand, the presence o f microorganisms is not in itself sufficient to cause the destruction of tooth support tissue. The bacterial flora, in fact, triggers off a complex immune response in the host organism and it is this response which leads to the destruction of periodontal tissues Taichman - Page - Schroeder - Toto - Levine -Genco.

Healthy condition. Subgingival plaqu e. Disease condition. Impairment of the Sulcular Epitheliu m. The enzymes produced by the subgingival bacterial plaque destroy the mucopolysaccharides in the ground substance between the cells of the junc- tional epithelium, allowing bacterial components acting as antigens endotox - ins, fragments of bacterial capsule, etc.

This further increases vessel permeability, enabling the PMNs to leak from th e blood vessels and reach the crevice through the connective tissue and junc- tional epithelium.

During this phase, there is an increase in crevicular fluid. Bacterial plaque enzyme s. Collecting crevicular fluid with blotting paper. Crevicular leukocyte s. During the gingiviti s development period, a gradual increase in th e number of leukocytes i n the crevice and in th e flow of crevicular flui d can be observed.

Epithelial cells in the desquamation phase. Epithelial cells. Ground substance. Epithelial cell in the desquamatio n phase: note the underlying groun d substance. Plaque Enzymes. Destroy the mucopolysaccharides o f the ground substanc e.

Polymorphonuclear Leukocytes P M N s. Gingival blood vessel : the PMNs can be observed on the inne r. The perivascular tissue is infiltrated. Stimulated by chemoactive substances, the PMNs migrate through th e connective tissue and accumulate in the junctional epitheli- um and the sulcus, pe'iforming their phagocytic function. Polymorphonuclear leukocytes in th e non-migratory phase. Animal histologic preparation. Polymorphonuclear leukocytes in diapedetic phase. Epithelial attachment and connective attachment.

Phagocytosis of a bacterium by a polymorphonuclear leukocyte. Inflammation localized coronally to the transseptal fibres. Probing and X-ray examination do not indicate loss of periodontal support. The PMN accumulation and activity in the pericrevicular zone lead t o the release of various enzymes with a damaging action both on the bacteri a and on the tissue of the host organism.

Macrophages and lymphocytes also begin to move towards the site. The former have a phagocytic action, neutralizing the enzymes released by th e PMNs.

The latter neutralize an enormous number of antigens. Supragingival plaque. X PMN s. Marginal gingivitis Note the plaque in the pericrevicular zone and the red and edematous gingival margin. Histologic perfectio n. Normal healthy gingiva. Initial lesion. Early gingiviti s. Early lesion. Stable lesio n. Stable gingivitis. A number of neutrophil s. Slight infiltrat e. Mac : Lymph.


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