Periodontology Flashcards
gingival disease can be split into 2 categories
- plaque induced
- non-plaque induced
plaque induced gingival disease
modified by systemic factors - endocrine system i.e. puberty, pregnancy / blood dyscrasias i.e. acute monocytic leukaemia
modified by medication - phenytonin in epilepsy, ciclosporin in immunosuppression, nifedipine in Ca channel blockers
non plaque induced gingival disease
infection - gonorrhoea/syphilis, PHG, gingival candidiasis
genetic - hereditary gingival fibromatosis
manifestation of systemic conditions - lichen planus, toothpaste allergy causing desquamative gingivitis
traumatic lesions - physical / chemical
difference in chronic and aggressive periodontitis
chronic - destruction is consistent with local factors i.e. plaque/disease progresses at a slow or moderate approach
aggressive - clinically healthy ptx but there will be rapid attachment loss and bone destruction. standard pattern follows 6s and incisors
periodontitis as a manifestation of systemic disease
haematological disorders - chronic lymphocytic leukaemia
genetic disorders -cyclic neutropenia (cycles of low neutrophils), papillon lefevre syndrome (autosomal recessive disease cause by deficiency in cathepsin C - rare ectodermal dysplasia)
localised tooth related factors modifying or predisposing plaque induced gingival diseases/periodontitis (4)
tooth anatomical factors i.e. crowding
restoration margins
orthodontic appliances
partial denture
mucogingival deformities & conditions around teeth (5)
gingival recession
lack or keratinised gingivae
aberrant frenal attachment
excessive gingival display
fibrous tuberosities
what is inflammation
the response of living tissue to injury and can be seen as dilation of blood vessels, increased permeability of vessel walls, inflammatory exudate and emigration of white blood cells from vessels to connective tissues
gingivitis
erythema & bleeding on probing, reti pegs on gingival tissues of the junctional epithelium, inflammation in this area but confined to gingivae and there is no loss of attachment
periodontitis
apical extension of gingival inflammation resulting in connective tissue attachment destruction, apical migration of junctional epithelium, bone loss and true pocket formation which all can lead to tooth mobility
what is ANUG and what can it lead to
acute necrotising ulcerative gingivitis can lead to necrotising periodontitis
signs & symptoms of necrotising perio disease
ptx c/o pain, bleeding, halitosis
o/e punched out crater like ulcers covered in grey slough which when wiped away will leave bleeding tissues - caused by necrosis rather than pocketing, erythema, swelling, interdental papilla destroyed
risk factors for necrotising perio disease (3)
impaired immunity e.g. HIV
smoking
stress
pathogenesis of perio disease
in slough itself fusobacterium sp. are the predominant species of bacteria
treponema sp. & p.intermedia also present
will invade tissues unlike other periodontal diseases & produce endotoxins
either the endotoxins produce the damage or the cytokine/neutrophil response
pocketing no produced just actual tissue destruction
treatment of ANUG
effective debridement
chlorhexidine & OHI
use of antibiotics controversial but if lymphadenopathy / systemic symptoms then metronidazole indicated
periodontal abscess & causes
localised acute exacerbation of pre-existing pocket from chronic periodontitis - caused by trauma to pocket epithelium, obstruction at entrance of pocket, post non-surgical treatment as pocket can tighten obstructing flow out of pocket or cause could be unknown
characteristics of periodontal abscess
pain or biting / constant pain
swelling
discharge causing halitosis
bad taste in mouth
o/e - swelling adjacent to periodontal pocket, tooth may be TTP, may be tooth mobility from LoA from inflammation
periapical v periodontal abscess
if there is chronic periodontitis with a pocket adjacent to the swelling then it is likely to be a periodontal abscess especially if tooth is vital
treatment of periodontal abscess
drain abscess (by pocket if possible)
gentle subgingival debridement
hot saline mouthwash
follow up with HPT
surgery if indicated
maintenance
antibiotics for perio abscess
again controversial - unless systemic involvement local measures taken first
amoxycillin 250mg 3-5 days
metronidazole 200mg 3 days
when would you carry out periodontal surgery
only ever indicated when pockets >5mm that persist in presence of excellent OH
must also be at the re evaluation phase 4-6wks after completing non surgical phase
if OH still poor at this stage then supportive care with cause related therapy is indicated
post periodontal surgery
chlorhexidine mouthwash 1-2wks, analgesia for 1-2days, antibiotics may be indicated, after 1wk sutures removed and normal mechanical plaque removal begins
at 2-4wks a long junctional epithelium will attach and probing depth will reduce, gingival recession as a result but gain in clinical attachment levels
infra bony defect & management
bone loss around tooth due to perio disease (may have 1/2/3 bone walls)
3 wall bony defect more likely to heal by repair as they can more easily form a clot and have bony infill from all 3 walls
managed by - closed/open root surface debridement with healing by repair // pocket elimination with osseous resection // regenerative techniques