Histopathology and Pathogenesis Flashcards
1
Q
What is pristine gingiva?
A
- intact layer of epithelium lining the gingival crevice
- no inflammatory cells in the connective tissue
- continuous sparse migration of neutrophil leucocytes into the coronal part of the junctional epithelium and gingival crevice
2
Q
What is normal healthy gingiva?
A
- a small number of inflammatory cells in the junctional epithelium and connective tissue
- gingivitis is not clinically detectable, but inflammatory changes can be detected microscopically
3
Q
What is early gingivitis?
A
- seen after 10-20 days of plaque accumulation
- increased number of inflammatory cells in the tissue
- increased number of neutrophils emigrating into the gingival crevice
- junctional epithelium becomes thicker
- gingival connective tissue becomes more heavily infiltrated with inflammatory cells and dilated blood vessels
4
Q
What is established gingivitis?
A
- more dense infiltration of inflammatory cells in the connective tissue
- plasma cells much more evident
- collagen loss increases due to an outpouring of collagenase enzyme
- epithelium lining the gingival crevice continues to increase in thickness
5
Q
What is periodontitis histopathologically?
A
- apical migration of junctional epithelium
- first stage of attachment loss
- dense infiltrate of inflammatory cells can be seen with plasma cells now dominant
- bone loss begins to occur
6
Q
What are predisposing factors to necrotising disease?
A
- poor OH
- cigarette smoking
- raised stress levels
- malnutrition
- fatigue
- immune dysfunction or suppression
- pre-existing gingivitis
- systemic conditions e.g. leukaemia or HIV
7
Q
What are the clinical features of necrotising gingivitis?
A
- visible change in gingival contour
- loss of knife edge margin
- bleeding
- pain
- loss of apex of papilla giving punched out appearance
- a grey pseudomembranous slough
- unpleasant odour (foetor oris)
- swollen lymph nodes
- pyrexia (fever)
May form a sequestrum
8
Q
What is a sequestrum?
A
Fragment of dead bone, caused by destruction/necrosis of periodontal ligament and bone, rapid and may lead to interproximal or facial bone
9
Q
How is necrotising diseases treated?
A
- OHI
- smoking cessation
- debridement, easiest to use an ultrasonic
- hydrogen peroxide: mouth rinse or applied directly to ulcerated tissue, beneficial due to mechanical cleansing properties, ability to release oxygen into the area, damaging the anaerobic infecting organisms
- chlorhexidine mouthwash: reduces plaque growth, patient may not be able to brush effectively due to pain but cannot penetrate pseudomembranous slough
- systemic antibiotics if pt is generally unwell: metronidazole 400mg 3X daily for 3-7 days, penicillin and tetracyclines also effective
10
Q
What is acute herpetic gingivostomatitis?
A
- presents with pyrexia, lymph gland involvement, flu-like symptoms, stomatitis, oral ulceration especially on keratinised tissue, gingivitis and pain
- caused by herpes simplex virus
- highly contagious, spread by oral lesions
- Tx: maintaining adequate fluid intake, antipyretics, topical antiseptics
- antiviral drugs such as aciclovir are not normally prescribed unless immunocompromised
11
Q
What are the different abscesses of the periodontium?
A
- gingival abscess: caused by trauma form a foreign body
- periodontal abscess: arising from an established periodontal pocket
- pericoronal abscess: flap of gum overlying partially erupted 3rd molar
12
Q
Name some bacterial complexes present in dental plaque, likely to cause periodontal disease:
A
- Porphyromonas gingivalis
- tannerella forsythus
- treponema denticola
- prevotella intermedia
- fusobacterium nucleatum