7 Etiology of Periodontal Disease

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    Etiology of PeriodontalDisease

    Dr. Marcel Hallare

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    Periodontal disease is a pathologic processthat affects the periodontium

    The vast majority of inflammatory diseasesof the periodontium results from bacterial

    infection The dominating causative agents of

    periodontal disease are microorganisms thatcolonize the tooth surface (bacterial plaque

    and products) No systemic disorder is known to be the

    initiating cause of periodontitis in theabsence of bacterial plaque

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    TOOTH-ACCUMULATED MATERIALS

    1. Bacterial plaque2. Acquired pellicle

    3. Calculus

    4.

    Food debris5. Materia alba

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    Bacterial plaque

    Two types of plaque that are closelyassociated with periodontal disease:

    1. Consists of a mat of densely packed,colonized, and colonizing microorganismsthat grow on and attach to the tooth

    2. Free floating or loosely attached betweenthe soft tissue and teeth

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    Acquired pellicle

    Primarily a protein film that forms onerupted teeth and can be removed byabrasives

    Quickly reforms after being removed

    Not removed by forceful rinsing

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    Calculus

    Calcified plaque that is usually coveredby a soft layer of bacterial plaque

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    Food debris

    Food matter that is retained in the mouth

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    Materia alba

    (literally, white matter)A soft mixture of salivary proteins, some

    bacteria, many desquamated epithelialcells, and occasional disintegrating

    leukocytes Usually flushed off with forceful water

    spray

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    BACTERIAL FACTORS INPERIODONTAL DISEASE

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    Morphology of BacterialPlaque

    Under light and SEM, supragingivalplaque and subgingival plaque havedistinct morphological differences

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    Supragingival Plaque

    Bacterial cells appear to be denselypacked on the tooth surface and thedeposits may be thick (0.5mm or more)

    Composition of the microbial deposits

    includes coccoid and relatively numerousfilamentous bacteria

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    Some filamentous bacteria are coveredwith coccal organisms, which appear as

    corncob formations

    Flagellated forms and spirochetes areobserved apically and on the outer

    surface

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    Subgingival Plaque

    Subgingival plaque in periodontitispatient is composed of an inner and anouter layer

    The inner layer is tightly adherent

    bacteria is continuous with, but is thinnerand less organized than supragingivalplaque

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    Outside this tightly adherent layer, andadjacent to the soft tissue of the pocket,is a loosely adherent layer ofmicroorganisms

    This layer consists of numerousspirochetes, gram-negative bacteria, and

    bacteria grouped into bottle-brush ortest-tube brush formations

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    Microorganisms of Plaque

    Young plaque (1-2 days) consistsprimarily of gram-positive and somegram-negative cocci and rods

    From 2-4 days of growth, undisturbed

    plaque changes in the numbers and thetypes of organisms present

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    The number or gram-negative cocci androds increase and fusiform bacilli and

    filamentous organisms becomeestablished

    From 4-9 days, this ecologically complexpopulation of microorganisms is further

    complicated by the presence of theincreasing number of motile bacteria,namely, spirilla and spirochetes

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    1. Epithelial cells2. White Blood cells

    3. Erythrocytes

    4. Protozoa

    5. Food particles

    6. Miscellaneous components

    Other Constituents of Plaque

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    Mechanism of Bacterial Action

    1. Invasion2. Cytotoxic agent

    3. Enzymes

    4. Immunopathologic mechanism

    5. Combined action

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    Invasion

    Bacterial invasion is not necessary forgingival inflammation to occur

    All that is required id that enoughbacteria (and possibly specific pathogenic

    bacteria) be fixed to the tooth, near thegingiva, for sufficient length of time tochallenge the tissue with their toxicproducts

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    Cytotoxic agent

    Endotoxins, which are lipopolysaccharideconstituents of the cell wall of gram-negative bacteria, can be a direct causeof tissue necrosis, as well as initiator of

    inflammation by triggering animmunologic response and activation ofthe complement system

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    Enzymes

    Collagenasedepolymerizes collagen

    fibers and fibrils, the major formedelements in the gingiva and periodontalligament

    Proteases, a family of enzymes,contribute to breakdown of non-collagenous proteins and increasecapillary permeability

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    Hyaluronidasehydrolyzes hyaluronic acid,an important tissue cementingpolysaccharide, and can act as a

    spreading factor to increase tissuepermeability

    Chondroitinasehydrolyzes chondroitin

    sulfate, another tissue-cementingpolysaccharide

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    Immunopathologic mechanism

    The role of the immunologic response inperiodontal disease is not completelyunderstood; however, the potential tocause tissue destruction is apparent

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    Combined action

    It is possible that more than onemechanism may be involved in theinitiation and progression of inflammatoryperiodontal disease

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    SYSTEMIC FACTORS ANDPERIODONTAL DISEASE

    Any condition that might reduce theresistance of periodontium to toxic insultshould be expected to contribute to theinitiation of the inflammation and to

    influence the rapidity and severity of thedisease process

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    LOCAL CONTRIBUTING FACTORSAND PERIODONTAL DISEASE

    1. Anatomic factors2. Iatrogenic factors

    3. Calculus formation

    4. Traumatic factors

    5. Chemical injury

    6. Excessive occlusal force

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    Anatomic factors

    Root morphology Position of tooth in arch

    Root proximity

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    Iatrogenic factors

    Operative procedures Restorative materials and restorations

    Removable partial dentures

    Fixed partial denture Exodontics

    Orthodontics

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    Calculus formation

    Important in the progression of disease Serves as a coral reef within which

    microorganisms can multiply and releasetheir toxic products

    The rough surface of calculus makes itdifficult if not impossible, for the patientto remove associated bacterial plaque

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    Traumatic factors

    Toothbrush abrasion Factitious disease

    Food impaction

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    Chemical injury

    Indiscriminate use of topically appliedaspirin tablets, strong mouthwashes, andvarious escharotic drugs may result inulceration of the gingival tissue

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    Excessive occlusal force

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    Neoplasms

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    Renewal of GingivalEpithelium

    The oral epithelium undergoescontinuous renewal

    Its thickness is maintained by a balancebetween new cell formation in the basal

    and spinous layers and the shedding ofold cells at the surface

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    Mitotic activity exhibits a 24-hourperiodicity, with highest and lowest ratesoccurring in the morning and eveningrespectively

    Mitotic rate is highest in nonkeratinizedareas and is increased in gingivitis,without significant gender differences

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    Turnover times of tissue:

    palate, tongue, cheek 5-6 days

    gingiva 10-12 days

    junctional epithelium 1-6 days

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    The End