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Periodontics (Disease Classification (Severity Mild (<4 mm) …
Periodontics
Disease Classification
Severity
Mild (<4 mm)
Moderate (4-6 mm)
Severe (>6 mm)
Site
Localized (30% sites)
Generalized (>30% sites)
Role of Bacteria
= The ONLY ETIOLOGICAL AGENT
the pattern of accumulation is predictable
changes in biofilm species popn
disruption of biofilm regularly prevents disease
periodontitis is HOST MODULATED
Characteristics
= Colour, Contour, Consistency, BOP, Attachment Level
Gingivitis = Red, blunted/puffy, soft w/ BOP
Peri-Implant Mucositis = Red, blunted/puffy, soft w/ BOP
Periodontitis = assoc. Bone Loss
Peri-Implantitis = assoc. bone loss
See NEW 2018 Classification
Acute Conditions of Periodontium
Abcesses
Gingival Abscess
- localized purulent infection - w/ swelling, pain assoc. w/ foreign body
Periodontal Abscess
localized purulent infection assoc. w/ periodontal pocket
assoc. tissue breakdown (PDL, Al. bone)
nb: diabetes is a risk factor
Perio-endo lesion
Hx of a periodontal and periapical lesion
Ex w/ bone loss, furcation, radiolucencies
nb. primary perio/secondary endo ... ect
Periocoronal Abscess
- localized purulent infection surrounding the crown of a partially erupted tooth
assoc. swollen opeculum +/- systemic symptoms
Vertical Root Fracture
Periodontal tissue breakdown
requires toluidine blue to diagnose
Necrotising Disease
NUG (necrotising ulcertaive ginigivtis)
rapidly destructive, complex, interdental necrosis (cratering), pain bleeding
NUP (necrotising ulcerative periodontitis)
necrosis progresses into the PDL & Al. bone leading to further invasion and infection
Non-bacterial Infections
Viral
Herpes Gingivostomatitisitis (primary and secondary herpes labalis)
Herpes Zoster (VZV)
Fungal
Candidosis (opportunist organism)
pseudomembranous (semi adherent, whitish)
erythromatous (red, painful)
Other
Burns
Allergies
IgE mediated response
Self-inflicted injureis
Pathogenesis of Disease
plaque
soft adherent deposits, embedded in a polysaccharide matrix as part of an eco-community
theories =
Non-specific, plaque will cause disease irrespective of composition
Specific, plaque w/ specific pathogens will cause disease
Ecological, pathogens and the environment cause disease
Major Pathogens
eg. A. actionomycetem...
eg. P. gingivalis
e.g. T. forsythia
Minor Pathogens
eg. Fusobacterium n.
eg. Prevotella intermedia
host response
initiated by the presence of bacteria and the release of their products (LPS, toxins, bacterial enzymes)
normal healthy gingiva
subclinical inflam w/ microbial colonization
early gingivitis
(4-7 days) increased infiltration + JE proliferation
established gingivitis
(>21 days) clinical inflam, leukocyte infiltration, plasma/nuetrophil migration
periodontitis
apical migration of JE(pocket), predominate plasma, bone loss
Risk Factors
Local (predisposing)
= hinder the removal of plaque
e.g. plaque retentive features
rotated teeth, crowding, calculus, high frenulum attachment, orthodontic appliance, overhangs, root grooves, rough restorations, deep pockets, RPds
Systemic (modifying)
= alters the course of disease
e.g behavioral/lifestyle
smoking
Smokers are 2-8 times more likely to have periodontitis
smokers have a reduced vascularity, therefore less BOP
reduced neutrophil migration results in reduced healing (<28%)
2nd hand smoking & cannabis smoking risks
Stress
impaired immune function and altered behaviour
e.g. environmental exposure
medications
altered immune response
Sex hormones
i.e. menstration = increased inflam
i.e pregnacy = cause gingivitis
Immuno supressants
i.e HIV can develope ANUG and Periodontis
e.g. inherited characteristics
Diabetes
Both Type 1 and 2 are risks
AGE - advanced glycated end products due to poor glycemic control results in poor periodontal health
altered vascular function
altered inflammatory response
delayed wound healing
Genetic susceptibility
some individual are genetically predisposed to be more at risk
accounts for 50% of variation of disease in popn
e.g Loe et al
Recession and Hypersensitivity
Recession
Define
= Displacement of the soft tissue margins apically from the CEJ with oral exposure of root surface.
Aetiology**
Mechanical factors, periodontal disease, keratinised tissues, tooth malabsorbtion, iatrogenic factors, frenulum attachment, occlusal trauma
Hypersensitivity
Contributing factors
Exposure of cementum or dentine (i.e gingival recession, pathologic, traumatic, procedural)
Anatomy of CEJ (i.e meeting of CEJ)
Loss of cementum (i.e abrasion, erosion, caries, RP/SC
Loss of enamel (i.e wear, parafunctional, fractures)
Define
The transient pain arising from exposed dentine, typically in response to chemical, thermal, tactile or osmotic stimuli that could not possible be anything else
Management
1st determine severity; 2nd Id etiology factor and remove it; 3rd desensitize nerve
Avoiding pain stimulus
Occluding Dentinal tubules
coagulation, mineralization, surface coating
Desenitizing nerve
potassium salts
Other Agents
Calcium Hydroxide, Potassium nitrate, Fluoride
induces hypermineralization of dentine (reducing tubule size) or cementum
Treatment Outline
Establishing the disease activity and progression will be able to determine presence inflammation and attachment loss
Acknowledge to the patient the nature of the disease, Tx required, maintenance and monitoring, Px(influencing attitude)
Control Phase Therapy SC/RP, overhang removal and Home Care Instruction(nb. this is a critical aspect of success of tx)