Etiology of the periodontal disease
P.D. diseases are group of inflammatory conditions caused by M.O. that form what is called (Dental plaque)Dental Plaque It’s the main etiological factor of P.D. diseases & any associated factors whether local or systemic that enhance the accumulation of D.P. will aggravate the diseaseLoe in 1965; experimental gingivitis
Dental plaque Bacterial aggregation on teeth & other solid surfaces in the oral cavity including removable & fixed restorationComposed of:
bacteria
leukocytes
Desquamated epith.cell
Dental plaque
It is the root of most dental evils Materia alba soft accumulation of bacteria & tissue cells (leukocytes & desquamated epithelial cells) that: 1. Lack organized structure of D.P. 2. Easily displaced with a water spray Dental Calculus mineralized D.P.Dental plaque
Supra & subgingival plaque Supragingival Whitish to yellowish layer that extend along the G. margin, its difficult to identify if present in small amount, such amount varies among individuals & sites Subgingival Thin layer that only revealed by explorer (probe) or by displacing soft tissue (gingivae)Microbiology of suprag. plaque
P. samples during Loe study In day 1: Great proportion of G+ cocci: Strept. oralis gp.: S. mitis , S. sanguis, S. oralis G+ rods: Actinomyces viscosus A. naeslundii
With the increasing no. of G-ve anaerobic cocci (Veillonella , Neisseria), G-ve rodes (Prevotella intermedia, Fusobacterium nucleatum Capnocytophaga & Haemophilus)
Microbiology of suprag.p.
In day 3 No. of G-ve cocci & rods increase with reduction in no. of G+ve cocci & rods & appearance of filamentsMicrobiology of suprag.p.
At day 9 Increasing in G-ve cocci & rods with appearance of spirals & spirochetes (obligate anaerobes like Borrelia, Treponema & Leptospira) with significant reduction in no. of G+ve cocci & rods Remaining period up to 3 weeks Showed no changesMicrobiology of suprag. P.
After 24hs a clinically demonstrable layer of M.O. which is adhered at this time that represent; Previously attached & then detached bacteria Those irreversibly adherent M.O. which are started to multiply Bacteria that are arrived later, trapped & aggregatedMicrobiology of suprag. P.
Increased no. of G-ve rods that grow in deeper layers next to tooth may be attributed to changes in growth conditions due to development of G. inflammation (increased G. fluid with swelled gingiva) [ S.Sanguis produces H2O2 which is lethal to A.a. ,so high no. of such bacteria could be seen in an inactive site]Microbiology of subgingival P.
It starts from already occurring supragingival p. so its composition partly influenced by supragingival p. But there are different growth conditions such as 1- Limited access that allows growth of anaerobic bacteria 2- The nutrition supplied from G. exudate 3- Limited or no detachment which allow growth of motile bacteriaWith progression of D.P. there is decreasing in G+ve & increasing in facultative anaerobes such as G-ve rods (A.a.), total anaerobes such as spirochetes & rods like Bacteroids & Fusobacterium
Formation of supragingival d.p.
D.P. seen after 1-2 days, on G. 1/3 of tooth surface Location & rate formation vary among individuals & factors such as: oral hygiene and host factors including diet, salivary composition & flow rate D.P. continue to accumulate until a balance is reached between force of removal & that of formationAcquired pellicle A.P.it’s a glycoprotein layer derived from saliva & G. fluid, it has an ion-regulating function between tooth & saliva and contains antibody, complement & lysozyme Adhere by electrostatic Van der Waals & hydrophobic forces, where hydroxy appetite crystals have –ve charged phosphate gp. that interact with +ve charged component of S. & G.F. macromolecules
Salivary mucin Has protective action to the mucosa as it acts as a lubricant & prevents bacterial attachment to mucosa
Initial bacteria within few hours bact. will be found on A.P. where G+ve (S.sanguis & A. viscosus) are adhered to A.P. by adhesines
A. viscosus posses fimbriae, there are adhesins on these fimbriae which bound to protein on A.P. Continuous growth will occur with a transition from aerobic environment to highly O2-deprived environment(anaerobic)
2ndary colonizer
Prevotella intermedia (obligate anaerobe) Prevotella loescheii (obligate anaerobe) Fusobacterium nucleatum (obligate anaerobe), Porphyromonas gingivalis (obligate anaerobe)Those bacteria are adhered to M.O.by coaggregation (that occur through chemical interaction of protein & C.H.O. molecules on bacterial cell surface like coaggregation of F.n. with P.g.
Structure of dental plaque
Supragingival plaque Corncob structure in which the F.n. formes the inner core & coccal cell (Strept. cocci) or P.g. attached along its surface G+ve cocci & rods are seen on tooth sur. while G-ve rods, filaments & spirochetes on the outer surface of mature massStructure of dental plaque
350 different bacterial species + yeasts, protozoa & viruses, host cells like epithelial cells, macrophages & other leukocytes Intercellular matrix (20- 30%), organic & inorganic materials derived from S., G.F. & bacterial products
Organic Glycoprotein, albumin, lipids (membrane of M.O., host cell, food debris), bacterial vesicles (toxins & enzymes)
Polysaccharides (levan, glucan) synthesized by Strept. mutans gp. (S.m., S. sobrinus) from dietary sucrose Levan : Storage of energy Glucan Dextan: energy source, Mutan: Skeleton in the matrix that allows aggregation of bact.