Acute Periodontal Conditions Flashcards
What do all acute periodontal conditions have in common?
They cause pain and rapid periodontal destruction.
How are acute periodontal lesions distinct from other forms of periodontitis?
They are rapid onset
They cause rapid destruction of periodontal tissues
They cause pain or discomfort which prompts patients to seek urgent care
What is the definition of an abscess?
Localized accumulation of pus in the periodontal tissues (gingival wall of a periodontal sulcus/pocket) resulting in a significant tissue breakdown.
How are abscesses of the periodontium classified?
Location: Gingival and periodontal abscesses.
Course of the lesion: Acute and chronic
Number of abscesses: Single and multiple
How are gingival abscesses different from periodontal abscesses?
Gingival abscess - don’t have previous attachment loss (healthy or gingivits but not tissue destruction)
Previous periodontitis - then the patient has
periodontal abscess
What causes periodontal abscesses?
Impaction: Dental floss, orthodontic elastic, popcorn hulls.
Harmful habits: Wire or nail biting
Orthodontic factors: Orthodontic forces on a cross-bite.
How big of an issue is a periodontal abscess?
14% of all dental emergencies are periodontal abscesses.
It is the third most prevalent dental infection in the UK
37% of patients are under maintenance
Who are periodontal abscesses seen most often in?
Associated with probing depths deeper than 6mm and are more common in molar sites (furcations)
What adverse outcomes can periodontal abscesses lead to?
Can lead to tooth loss.
It is the main reason for tooth extraction in maintenance patients for questionable prognoses teeth.
Potential risk for bacteremia
What are potential etiologies of periodontal abscesses?
Acute exacerbation of untreated periodontitis
Acute exacerbation of maintenance patients
After periodontal debridement (incomplete or debris pushed)
After systemic antimicrobial intake
After surgical therapy (membrane or suture contamination)
Uncontrolled diabetic patient HbA1c 10+ (if they are periodontitis patients)
Impact of foreign bodies
How does a periodontal abscess develop?
Invasion of bacteria to soft tissue (pocket) -> Development of inflammatory process -> Inflammatory products lead to (PMN influx, production of pus, connective tissue destruction, encapsulation of bacterial infection) -> Rapid rate of destruction pending of bacterial growth, virulence and pH
Do periodontal abscesses have a distinct pathophysiology when compared to other periodontitis lesions?
Periodontal abscesses involve entry of bacterio or foreign body into the soft tissues surrounding the periodontal pocket which leads to PMNs and other immune cells. If the neutrophils fail to control the influx of bacteria or to clear the foreign body, degranulation, necrosis, and further neutrophil influx may occur. This leads to formation of pus and if the pus is not drained it forms into an abscess. This lesion resolves more rapidly because it creates a low pH environment within the abscess which leads to rapid enzymatic disruption of surrounding connective tissues and has a greater potential for resolution if quickly managed.
How does the microbiology of abscesses look?
It is polymicrobial Gram negative, rod predominant anaerobic bacteria
EXTRA INFO:
*4 complexes are possible with different bacterial content:
Red complex: Consist mostly of P gingivalis which is the most prevalent and T forshythia as well as treponema species.
Orange complex: Consists of P intermedia and F nucleatum
Yellow complex*
From Clinical and microbiological characterization of periodontal abscesses
How can a periodontal abscess be diagnosed?
Evaluation of symptoms: Discomfort, pain, tenderness, swelling, tooth mobility, tooth elevation, sensitivity to palpation.
Clinical findings:
Ovoid elevation lateral / labial to a tooth, or diffuse swelling or redness, BOP.
Suppuration, deep periodontal pocket and signs of periodontitis and mobility.
Radiographic examination: Normal appearance, some bone loss
Other: Fever, malaise, lymphadenopathy, elevated leukocyte number.
History of previous dental or antibiotic intake.
What are some differential diagnoses of periodontal abscesses?
Other abscesses of the mouth such as: Periapical abscess, Lateral periapical cyst, Vertical root fracture,
Post operative infection
Other serious dental conditions such as Osteomyelitis, ONJ, Squamous cell carcinoma, Metastatic carcinoma, Head and neck cancer, Eosinophilic granuloma, Pyogenic Granuloma
How can other periodontal abscesses ruled out?
Proper assessment: Caries or deep restorations, periodontal probing, pulp tests, abscess location, radiographic examination, general periodontal condition, and control the HbA1c
How can other serious dental conditions be ruled out?
Biopsy if not responding
How is a periodontal abscess treated?
Drainage through pocker or incision compression.
Meticulous periodontal debridement and removal of foreign body if that is the cause.
Extraction: Severe damage and/or hopeless prognosis.
Surgical procedures if needed.
Analgesics
Systemic antimicrobials adjunctive to treatment (especially if there is a fever and swollen lymph nodes)
Sole AB: if there is diffuse infection and inadequate draining.
How is an acute gingival abscess treated?
If it is very localized and there is no previous periodontitis:
Object should be eliminated, drained by incision, and scaling should be done through the sulcus and drained. Followed by warm saline risk and follow up 24 - 48 hours later.
Analgesics can be used but no ABs because it is very localized.
How should pericoronal abscesses due to impacted third molars be treated?
Drainage + irrigation
Antimicrobials
Depending on the prognosis: Removal of the peri-coronal tissue and extraction.
How can pericoronal abscesses due to impacted 3rd molars be detected?
Causes accumulation of pus around a pericoronal tissue, trismus, and pain
What is necrotizing periodontal disease known as?
Vincent’s Disease
Trench mouth disease
Necrotising gingivo-stomatitis
Fuso-spirochaetal stomatitis
Ulcerative membranous gingivitis
Acute Ulcerative gingivitis
Necrotising ulcerative gingivitis
Acute necrotising ulcerative gingivitis (ANUG)
How can necrotizing periodontal diseases be classified?
Location: Necrotizing gingivitis (only gingival tissue), Necrotizing periodontitis (progression to PDL and alveolar bone), and necrotizing stomatitis (deeper beyond the MGL)
What is necrotizing gingivitis?
An acute inflammatory process of the gingival tissues characterized by presence of necrosis/ulcer of the interdental papillae, gingival bleeding and pain.
What is necrotizing periodontitis?
An inflammatory condition of the periodontium characterized by presence of necrosis/ulcer of the interdental papillae, gingival bleeding, halitosis, pain, and rapid bone loss. Other signs/symptoms associated with this condition include pseudomembrane formation, lymphadenopathy, and fever.
What is necrotizing stomatitis?
A severe inflammatory condition of the periodontium and the oral cavity in which soft tissue necrosis extends beyond the gingiva and bone denudation may occur through the alveolar mucosa, with larger areas of osteitis and formation of bone sequestrum.
Do necrotizing periodontal diseases have a distinct pathophysiology when compared to periodontitis lesions?
Yes, necrotizing gingivitis lesions are characterized by presence of ulcers within the stratified squamous epithelium and the superficial layer of the gingival connective tissue surrounded by non-specific acute inflammatory infiltrate. 4 zones have been described
Who are necrotizing periodontal diseases most commonly seen in?
Strongly associated with impairment in the host immune system:
1) In chronically, severely immuno compromised patients.
2) In temporarily or moderately compromised patients.
Why must necrotizing periodontal diseases be controlled immediately?
They are the most severe oral biofilm related condition and must be controlled immediately to avoid progression
What are the predisposing factors to necrotizing periodontal diseases?
Military personnel
Students
HIV+
Malnutrition
Smoking
How common are necrotizing periodontal diseases?
14% prevalence in WWII
Developed countries less than 0.5%
Developing countries 1.7 to 1.5%
Chile 6 - 7%
NP less frequent 0 - 11% HIV+
What are the likely outcomes of necrotizing periodontal diseases?
Susceptible to recurrence
Can become chronic
Can lead to cancrum oris or noma (Systemic diseases-malnutrition)
Can be treated
How does NPD occur? (Aetiology)
Spirochetes and fusiform bacteria
Invasion of epithelium and connective tissues
Necrotic tissue perfect microbiological niche
Active periodontal destruction by activation host response
What bacteria are seen in necrotizing periodontal diseases?
Spirochetes such as:
Treponema species
Selenomona species
Fusobacterium species
P intermedia
Possible role of viruses
What does the histology of NPD look like?
epithelial and connective tissue ulcers surrounded by non-specific acute inflammatory infiltrate.
4 zones:
Zone 1: Superficial bacterial zone
Zone 2: Neutrophil rich zone
Zone 3: Necrotic zone
Zone 4: Spirochete infiltration zone
What are the predisposing factors for NPD?
Poor oral hygieve + Immune suppression.
How is Necrotizing periodontal gingivitis diagnosed?
Based on clinical findings:
Necrosis and ulcers on free gingiva,
SPECIALLY tip of interdental papilla
Spontaneous or easy gingival bleeding
Rapid onset pain
Pouch out appearance
Marginal erythema
Pseudomembrane Whitish / yellow
Halitosis
Lymphadenopathies, fever and discomfort
How is Necrotizing periodontitis diagnosed?
Necrosis and Ulcers as NG
Extent to PDL and alveolar bone
Attachment loss
Pocket pending on extension of necrosis
Open interdental papilla
Necrosis in the middle (crater)
Interdental bone exposed and denuded
Crater favors plaque accumulation
Bone sequestrum
How is Necrotizing stomatitis diagnosed?
Denudation extending throuhg alveolar mucosa
Bone sequestrum
Loose bone fragments
Interdental or labial palatal
How is acute condition controlled of NPD?
Immediate treatment needed to arrest disease process and destruction:
Control patient discomfort and pain.
Periodontal debridement under LA
Use of power instrumentation devices
Restricted oral hygiene (chlorhexidine mouth-rinses)
Antibiotics adjunctive to treatment (metronidazole 400 mg)
Recall and reassessment 24 to 48 hours
How is pre-existing condition treated for NPD?
Control gingivitis or periodontitis
OHI
Control local predisposing factors
Control existing systemic predisposing factors
What corrective treatment is used for NPD?
Correct altered gingival topography
Gingivectomy
Gingivoplasty
Regenerative / resective surgery
What happens during maintenance phase of NPD?
Control predisposing factors
Ensure patient is complying with treatment
How should HIV patients be treated differently?
Screening for HIV
Irrigation of disease sites with iodine-povidone
Metronidazole is still a choice
Opportunistic candida overgrowth so check for that
What causes primary herpetic infection and where does it present?
HSV-1
May present labially or intraorally
How does primary herpetic gingivo-stomatitis present?
Dysphagia, fever, malaise, submandibular adenopathy.
Children 2 - 5 years
Oral vesicles (erosion - ulcers)
How is primary herpetic gingivo stomatitis treated?
Treat if symptomatic
Use antiviral agents, nutritional support
What are the signs of recurrent herpetic infection?
Intraoral or labial
Discomfor itching, stinging, vesicle, erosion, ulceration
No treatment or topical antiviral agents
What do allergic reactions in the mouth look like?
In the mouth urticarial, angioedema. Erythema
multiforme
Contact allergy (Medications, Metals, materials)
Allergies associated to toothpaste, mouth rinse, chewing gum
Burning Itching stinging
