Periodontal Diseases Symposia Flashcards
What is periodontal health?
Periodontal health is a state free from inflammatory disease. Absence of inflammation associated with gingivitis or periodontitis, as assessed clinically, is a prerequisite for defining periodontal health. Periodontal health can exist before disease commences but equally, periodontal health can be restored to an anatomically reduced periodontium.
What are the determinants for clinical periodontal health?
Microbiological (supra gingival and sub gingival plaque composition), environmental (smoking, medications, stress, nutrition) and host (local and systemic predisposing factors)
What are 4 local predisposing host factors?
- Periodontal pockets
- Dental Restorations
- Root anatomy
- Tooth position and crowding
What are 3 systemic modifying factors?
- Host immune function
- Systemic health
- Genetics
What are controllable factors?
Removal of overhangs, smoking cessation, optimal diabetes control
What are non-controllable factors?
Genetic predisposition, immune status, use of critical medications
What are predisposing factors?
Any agent or condition that contributes to the accumulation of dental plaque e.g. tooth anatomy, tooth position and restorations
What are modifying factors?
Any agent or condition that alters the way in which an individual responds to sub gingival plaque accumulation e/g. smoking, systemic conditions, meds
What are the 4 levels of periodontal health?
- Pristine periodontal health: total absence of clinical inflammation and physiological immune surveillance on a periodontium with normal support (no attachment/bone loss).
- Clinical periodontal health: characterised by absence of minimum levels of clinical inflammation in a periodontium with normal support.
- Periodontal disease stability: in reduced periodontium
- Periodontal disease remission/control in reduced periodontium
What is periodontal disease stability?
A state in which the periodontitis has been successfully treated through control of local and systemic factors resulting in: minimal BoP, optimal improvements in PPD and attachment levels, lack of progressive destruction, control of modifying factors such as reduction in daily cigarette smoking
What is periodontal disease remission/control?
A period in the course of the disease during which treatment has resulted in reduction (not total resolution) of inflammation, some improvements in PPD and attachment levels but not optimal control of local/systemic contributing factors.
In which pts would low disease activity be an acceptable therapeutic goal?
Pts with long-standing disease and/or uncontrolled contributing factors like smoking or diabetes
What is the main risk factor for the onset of periodontitis?
Gingival inflammation in response to bacterial plaque accumulation (microbial biofilms)
What are the clinical features common to dental-plaque induced gingival conditions?
- Inflammation confined to the free and attached gingiva and does not extend beyond the mucogingival junction
- Reversibility of the inflammation by disrupting/removing the plaque
- Presence of high bacterial plaque burden to initiate and/or exacerbate the severity of the lesion
- Systemic modifying factors: e.g. hormones, systemic disorders, drugs which can alter the severity of the lesion.
- Stable (non-changing) attachment levels on a periodontium which may/may not have experienced a loss of attachment or alveolar bone
Common clinical features of plaque induced inflammatory gingivitis
Erythema, oedema, bleeding, tenderness and enlargement
How are plaque induced gingivitis classified?
A. associated with bacterial dental biofilm only
B. potential modifying factors of plaque induced gingivitis: 1. systemic conditions (Sex steroid hormones, puberty, menstrual cycle, pregnancy, oral contraceptives, hyperglycaemia, leukaemia, smoking, malnutrition) and 2. Oral factors enhancing plaque accumulation (prominent subgingival restoration margins, hyposalivation) and 3. drug influenced gingival enlargements
What drugs are primarily associated with gingival enlargements?
- Anti epileptic drugs: phenytoin, sodium valproate
- Particular calcium-channel blocker drugs e.g. nifedipine, verapamil, diltiazem, amlodipine, felodipine
- Immunoregulating drugs e.g. cyclosporin
- High dose oral contraceptives
How are non-dental biofilm induced gingival diseases classified?
a. genetic/developmental disorders
b. specific infections
c. inflammatory and immune conditions
d. reactive processes
e. neoplasms
f. endocrine, nutritional and metabolic diseases
g. traumatic lesions
h. gingival pigmentation
Non-dental biofilm induced gingival diseases: specific infections - Bacterial
Bacterial origin: Necrotising periodontal disease caused by treponema spp., selenomonas spp., Fusobacterium spp., and prevotella intermedia in pts with specific underlying risk factors i.e poor OH, smokig, stress, poor nutrition, compromised immune status e.g. HIV
NUG + NUP + NS = all signify various stages of the same disease process = NPD
Non-dental biofilm induced gingival diseases: specific infections - Viral
Viral origin: usually infect specific individuals in childhood but primary infections can occur in adult life. They may give rise to oral mucosal disease followed by periods of dormancy and sometimes reactivation
- Coxsackie: herpangia does not involve gingiva compared to hand-foot-mouth
- HSV-1 oral manifestations
- VZV: primary infection causes chicken pox, secondary infections causes herpes zoster (shingles)
Non-dental biofilm induced gingival diseases: specific infections - Fungal
Candidosis: most common fungal infection of the oral mucosa mainly caused by C.albicans - normal commensal organism but aso an opportunistic pathogen. Most commonly presents clinically as redness of the attached gingiva often with granular surface
Non-dental biofilm induced gingival diseases: specific infections - Autoimmune
Autoimmune diseases of the skin and mucous membranes: lichen planus inflammatory reaction toward an unidentified antigen in the basal epithelium layer/basement membrane zone. Common mucocutaneous disease with recurrent manifestation on the gingiva.
- Lesions usually bilateral, often involve the gingiva and present as desquamative gingivitis causing pain and discomfort during eating and toothbrushing
- Tailored plaque control regime can be beneficial in reducing symptoms of gingival lichen planus and improving overall quality of life
Non-dental biofilm induced gingival diseases: reactive processes
Reactive processes: epulis ‘exopytic processes originating from the gingiva’ is a non-specific term and histopathology is the basis of a more specific diagnosis. Many are reactive lesions, usually no symptoms however result as a form of exaggerated tissue response to limited local irritation/trauma. The attached gingiva is the most frequently affected location.
True epulides include:
- Fibrous epulis: exophytic, smooth surfaced pink masses of fibrous consistency attached to the gingiva.
- Pyogenic granuloma: most common and shows a preference for the gingiva accounting for 75% of all cases
- Peripheral giant cell granuloma : most prevealent reactive lesion of the oral cavity. The swelling may be sessile or pedunculated, sometimes ulcerated and the appearance may resemble pyogenic granulomas.
Non-dental biofilm induced gingival diseases: Malignant
Squamous cell carcinoma - commonly occurs in edentulous areas and may also occur at sites in which teeth are present. The mobility of adjacent teeth is common and invasion of the underlying alveolar bone is apparent in approx. 50% of cases.
