Perio Emergency Flashcards
Necrotizing perio disease
Necrotizing gingivitis
Necrotizing periodontitis
Necrotizing stomatitis
Prevalence:
Most commonly in young adults
Higher in developing countries
Clinical characteristic:
Inflammatory, destructive, ulcerative necrotic tissue
Punched out appearance
Painful
Rapidly developing
Bleeding easily provoked
Foetor ex ore- the smell
Within inflammation: fibrin, necrotic tissue, leukocytes, erythrocytes, masses of bacteria
First lesions often in mandibular anterior region
Confined to top of a few interdental papillae
Often signs of pre existing chronic gingivitis
Papillae rapidly swell-rounded contour
Zone between marginal necrosis and uneffected gingival usually exhibits a well demarcated narrow erythematous zone (linear erythema)
Hyperaemia due to dilation of vessels in the gingival connective tissue in the periphery of the necrotic lesions
Extensive gingival necrosis can coincide with loss of crestal alveolar bone
Usually is the interproximal necrotic depression as papillae separated in one facial and one lingual portion- in this stage: PDL and LoA is involved
Sequestrum formation- in severe cases: it is necrotic bone that becomes loose and removed by forceps after some time
Involvement of alveolar mucosal in severe cases (immunocompromised, malnourished…)- necrotizing stomatitis
Other symptoms:
Swelling of lymph nodes, fever, malaise, poor OH, large amounts of plaque
Differential diagnosis
Confusing between necrotizing periodontal disease and primary herpetic gingivostomatitis
Other:
Desquamative gingivitis
Benign mucous membrane pemphigoid
Streptococcal gingivitis
All are clinically distinct from NPD
Microbiology of necrotizing perio disease
Constant flora:
Treponema spp.
Selenomonas spp.
Fusobacterium spp.
Prevotella intermedia
Host responses and predisposing factors
Systemic disease
Poor OH
Pre existing gingivitis
Phycological stress and inadequate sleep
Smoking and alcohol
Treatment for necrotizing perio
Acute phase:
Scaling at first appointment
Advise hydrogen peroxide 3% or chlorhexidine 0.2% mouthwash
Consider antibiotic use: metronidazole 400mg 3x/day for 3 days (in severe, persistent)
Maintenance phase:
Normal perio maintenance
Severe periodontitis - severe, grade C
Grade c- rapid rate of progression
Characterized by early age onset and a distinctive familiar tendency
It is quite rare
Occurs in age less than 35 years olds but is detectable in all age and ethnic groups
Early onset implies that etiological agents have been able to cause clinically detectable levels of disease over a relatively short time
-implies infection with highly virulent microbialbiofilm and/or a high level of susceptibility to periodontal disease
Diagnosis requires exclusion of presence of systemic disease that may impair host defences and lead to premature bone loss
Secondary features reported:
Amount of microbial deposits that are inconsistent with the severity of periodontal destruction
Elevated proportions of Aaa and Porphyromonas gingivalis
Phagocyte abnormalities
Hyper-responsive macrophage phenotype including elevated production of prostaglandin E2 and interleukin 1beta in response to bacterial endotoxins
Progression of attachment loss and bone loss may be self- arresting
Localised vs generalized severe periodontitis
Local:
Circumpubertal onset, localised first molars/incisor presentation with interproximal bone loss on at least 2 permanent teeth and involving no more than 2 other than first molars and incisors
Robust serum antibody response to infecting agents
Generalized:
Usually affecting persons under 30 but might be older
Generalized interproximal attachments affecting at least three permanent teeth other than first molars and incisors
Pronounced episodic nature of the destruction of attachment and alveolar bone
Poor serum antibody response to infecting agents
Further tests to aid diagnosis and description of disease for severe periodontitis
Radiography
Microbiology
Immunology
Habit history (smoking)
Bacterial etiology of sever periodontitis
Aa (aggregatibacter actinomycetemcomitrans)
Isolated in perio lesions from more than 90% of localised severe periodontitis
Produces several potentially pathogenic substances including leukotoxin capable of translocating across epithelial membranes
There is elevated levels of serum antibodies to Aa in severe periodontitis pts
But Aa can be detected in subgingival plaque without disease
Porphyromonas gingivalis and tannerella forsythia are frequently associated with generalized disease
Bacteria damages the periodontium directly by themselves or their products on the host tissue and/or as a result of tissue damaging host defense mechanisms
Principles of intervention
Diagnosis is the key
Success of treatment is dependant on early diagnosis, therapy to eliminate or suppress infecting microorganisms and providing an environment that can be maintained
Referral to specialist clinic should be considered
Abscesses in periodontium
Abscesses are one of the main reasons for a pt to seek emergency treatment
Can be:
1. Periodontitis -related abscess: acute infection originates from bacteria present at the subgingival biofilm in a deepened periodontal pocket
2. Non-periodontitis related abscess: acute infection originates from bacteria coming from another local source, such as a foreign body impaction,root canal bacterial colonisation
Periodontal abscess
Represents a period of active tissue breakdown and it is the result of an acute exacerbation of chronic disease
Usually due to the marginal closure of a deep periodontal pocket that prevents proper drainage
Characterized by local accumulation of neutrophils, remnants of tissue breakdown and pis formation
Different pathological mechanisms can lead to abscess formation in the periodontium:
1. Exacerbation of chronic disease
2. Post therapy periodontal abscess
- scaling remnants are left
- antibiotic use: is done without appropriate scaling
Prevalence:
Up to 14% of emergency dental treatment
More often in molars sites
Important as might influence prognosis of the affected tooth
* If occurs in teeth with residual deep pockets and reduced periodontal support this additional destruction is frequently the main reason for tooth XLA
Pathogenesis and microbiology of perio abscess
Abscess will contain bacterial bacterial products, inflammatory cells tissue breakdown products and serum
Majority are strict anaerobes similar to chronic periodontal lesions
Diagnosis of perio abscess
Presence of ovoid elevation in the periodontal tissue along the lateral side of the root
Suppuration: normally through the pocket opening, either spontaneous or when pressure is applied
Clinical symptoms:
Pain, tenderness, swelling, TTP, increased mobility
Radiographic appearance:
Normal to pronounced bone loss
Differential diagnosis (to perio abscess)
Other abscess - e.g. periapical
Lateral periapical cyst
Vertical root fracture
Perio-endo leison
