Peridontics : 4/basic Concepts In Periodontal Diseases Pathology/ First Semester

Front 1

define pathoenesis

Back 1

The development of a disease and the chain of events that led to this disease.

The cellular events and reactions and other pathological mechanisms occurring in the development of disease. Includes the study of the relationship between:
the cause --> the lesions --> the clinical signs.

Front 2

healthy gingiva reperesnts a state of balance between ... ?

Back 2

the host response and the bacerial plaque

Front 3

define dental plaque

Back 3

An organized biofilm, (undefinable microbial community ) that adheres to teeth, prostheses, and hard oral surfaces and is found in the periodontal pockets

Front 4

list the composition of dental plaque

Back 4

The composition is affected by the surrounding environment.

1) -Microorganisms: 70% (mainly bacteria)

2) -Organic components:
polysaccharide-protein matrix, bacterial by-products such as enzymes, food debris and desquamated cells.

3)-Inorganic components such as calcium and phosphate.

Front 5

talk more about the oragnic compoents of the detnal plaque

Back 5

polysaccharides - produced by bacteria

glycoproteins - from saliva and initially coats the clean tooth (Pellicle)

lipids - debris from membranes of disrupted bacterial and host cells

Front 6

talk more about the inorganic components of plaque matrix

Back 6

Primarily calcium, phosphorus, with trace amounts of other minerals such as sodium, potassium, and fluoride.

Inorganic components of subgingival plaque is from crevicular fluid. (Subgingival Calculus is dark because of blood products associated with hemorrhage)

Front 7

talk about the intial and secondary colonzation

Back 7

Initial bacterial colonization of dental pellicle is predominantly gram-positive facultative spp, Actinomyces species and Streptococci.

Secondary colonization by gram-negative anaerobic spp. Prevotella intermedia, Capnocytophaga spp., fusobacterium nucleatum, P.gingivalis.

Front 8

MICROBIAL SPECIFICITY OF PERIODONTAL DISEASES

Back 8

Nonspecific Plaque Hypothesis – Small amounts of plaque can be neutralized Large amounts of plaque produce disease.

Specific Plaque Hypothesis – Plaque which includes certain types of bacteria is pathogenic. These bacteria produce more substances that cause the destruction of periodontal tissues.

Front 9

MECHANISMS OF HOST TISSUE DAMAGE

Back 9

Production of metabolic by-products: (ammonia, volatile sulfur compounds, fatty acids)

Production of enzymes (proteases).

Induction of the production of host enzymes.

Induction of release of inflammatory mediators

Front 10

Evidence of the relationship of plaque to periodontal disease

Back 10

Experimental gingivitis

Peri-implant mucositis

Germ free animals→ optimal dental and gingival health. (isolators)

Front 11

Is treatment of periodontal disease based on the non-specific or specific plaque hypotheses?

Back 11

the specific
BUT NOT SURE

Front 12

Host’s Defense Mechanisms : list the defense mechanisms

Back 12

The intact barriers (junctional epithelium)

The regular shedding of epithelial tissues

Saliva

The gingival crevice fluid

Front 13

The immune system

Back 13

Innate immune system : provides an immediate, but non-specific response

Adaptive immune system
–Adapts the response to a specific pathogen

Front 14

talk more about the Innate immunity

Back 14

Inflammation is one of the first responses
–Redness, swelling, heat and pain
–Chemical and cellular response
–Neutrophils
–Macrophages
–Dendritic cells

Front 15

Talk about the gingival cervical fluid

Back 15

Initially considered as a transudate

Recent studies: it is an inflammatory exudate, with minimal or no presence in healthy gingiva.

Front 16

Talk about the compisiton of the gingival cervical fluid

Back 16

Cellular elements: bacteria, desquamated epithelial cells, leukocytes

Electrolytes: K, Na, Ca

Organic compounds: carbohydrates and proteins, metabolic and bacterial products

Front 17

Host response

Back 17

Gingivitis and periodontitis are inflammatory responses in periodontal tissues induced by microorganisms in dental plaque (involving leukocytes, lymphocytes, production of antibodies).

Production of inflammatory mediators (IL-1, TNF, Prostaglandins).

Front 18

Inflammation

Back 18

The vascular & cellular responses of inflammation are mediated by chemical factors (derived from blood plasma or some cells) & triggered by inflammatory stimulus.

Tissue injury or cell death---> Release mediators

Front 19

Cardinal Signs of Inflammation

Back 19

Redness : Hyperaemia

Warm : Hyperaemia.

Pain : Nerve, Chemical mediators

Swelling : Exudation

Loss of Function: Pain

Front 20

talk about the changes that accompany the Inflammation

Back 20

Increase blood flow (redness and warmth).

Increase vascular permeability (swelling, pain & loss of function).

Leukocytic Infiltration.

Front 21

talk about the Mechanism of Inflammation

Back 21

1.Vaso dilatation
2.Exudation - Edema
3.Emigration of cells
4.Chemotaxis

Front 22

Stages of periodontal diseases ---> GENERALLY

Back 22

Stage 1: The Initial Lesion.
•Stage 2: The Early Lesion.
•Stage 3: The Established Lesion.
•Stage 4: The Advanced Lesion.

Front 23

The Initial Lesion

Back 23

Subclinical gingivitis

Changes in junctional epithelium and perivascular connective tissue

Increased migration of leukocytes (PMN).

Plaque formation on the cervical 3ed

24 hours --> dentogingival plexus :
1) increased exudate
•2)The flow of GCF increases.

Front 24

The Early Lesion

Back 24

Within several days of plaque accumulation


Dentogingival plexus --->dilated, increased in no.

PMN migration to perio pocket and phagocytosis of bacteria.

Redness of the marginal gingiva (erythema), BOP

Lymphocytes and PMNs are the predominate

Degeneration of fibroblasts and breakdown of collagen fibers (70%) (mainly circular and dento-gingival fiber groups).

leukocyte infiltration

Proliferation of basal cells (junctional and sulcular epithelium) --> mechanical barrier

Epithelial rete pegs can be seen invading the coronal portion of the lesion in the connective tissue

Loss of the coronal portion of the junctional epithelium.

Front 25

The Established Lesion

Back 25

Chronic gingivitis

Congested blood vessels.

-Impaired venous return
-Extravasation of RBCs

GCF flow is increased

Leukocyte exudate:
-Dominated by plasma cells
-Old human individual, plasma cells

Rete pegs extend deeper into the connective tissue

The pocket epithelium:
•Not attached to the tooth surface
•Harbors large numbers of leukocytes
•Allows for a further apical migration of the biofilm
•Compared to the junctional epithelium:
--- more permeable.
--- may be ulcerated.

Front 26

talk about the types of established lesions

Back 26

Two types of established lesion:
•One remains stable for months or years,
•Second becomes more active and converts more rapidly to destructive advanced lesion

Front 27

The Advanced Lesion

Back 27

Loss of connective tissue attachment and alveolar bone

Extensive damage to collagen fibers

The pocket epithelium migrates apically from the cemento-enamel junction

It is generally accepted that plasma cells are the dominant cell type in the advanced lesion

Front 28

Saliva

Back 28

•Protective in nature.
•Mechanically cleanses the exposed oral surfaces.
•Buffers acids produced by bacteria.
•Antibacterial factors: inorganic and organic
•Lysozyme: hydrolytic enzyme of the bacterial cell wall.
•Salivary antibodies: IgA predominantly.

Front 29

Significance of saliva in periodontal pathology

Back 29

Influence on plaque initiation and maturation.
•Influence on calculus formation.
•Xerostomia→increased incidence of dental caries, periodontal disease and delayed wound healing.