Periodontal Diseases and Conditions Flashcards
1
Q
Periodontal Disease: Incidence, major risk factors
A
- 20% of 14-17yo in the US are found to have attachment loss of at least 2mm at one or more sites. The number and severity of affected sites increase steadily with age, demonstrating that chronic periodontitis often begin in adolescence.
- Chronic periodontitis responds well to oral hygiene measures and can more easily be arrested in its early stages when attachment loss is minimal and deep pockets have not developed.
- Smoking is a major risk factor in periodontitis, and smoking is increasing among adolescents, particularly females.
2
Q
Aggressive Periodontitis
A
- Rare, rapidly progressing forms of periodontitis also affect children and adolescents.
- Both periodontitis as a manifestation of systemic disease and aggressive periodontitis affecting children who are otherwise healthy occur in the pediatric population.
- Rapid attachment and bone loss with familial aggregation, phagocyte abnormalities and hyper-responsive macrophage phenotype
3
Q
LAP in permanent dentition: Characteristics
A
- Formerly called localized juvenile periodontitis, is characterized by the loss of attachment and bone around the permanent incisors and first permanent molars.
- Permanent incisors and first permanent molars and no more than 2 other teeth.
- Distinctive radiographic appearance. Rapid attachment loss, occurring at 3x the rate of chronic disease. Inflammation is not as extreme as that occurring in periodontitis associated with systemic disease, such as neutropenia, but both inflammation and plaque accumulation are often greater than those found in the typical teenager.
- Usually detected in early adolescence, but retrospective examination of earlier radiographs has sometimes revealed undetected disease in the primary dentition. This suggests that LAP of permanent dentition and LAP of primary dentition are the same disease entity, differing only in the age of onset or detection.
4
Q
LAP in permanent dentition: Prevalence, etiology
A
- Prevalence: 1%. Most commonly occurring in the African American population.
- In some cases, appears to be inherited as an autosomal dominant trait and LAP has been linked to a neutrophil chemotactic defect. LAP may progress to generalized aggressive periodontitis or remain localized.
- Linked to high numbers of Aggregatibacter actinomycetemcomitans and successful treatment correlates well with eradication of the bacteria.
- No evidence of systemic disease, some populations (Brandywine) is associated with specific gene on chromosome 4, higher in African Americans
- AA and bacteroides species the most highly virulent strains***
- Functional defects reported in neutrophils from patients with LAgP ***
- Anomalies in chemotaxis, phagocytosis, bactericidal activity, and superoxide production
- Molecular markers of LAgP with low numbers of chemoattractant receptors and low GP 110***
5
Q
LAP in permanent dentition: Treatment
A
- Treatment: Local measures in combination with systemic antibiotic therapy and microbiological monitoring.
- Metronidazole alone or in combination with amoxicillin appears to be more effective in arresting disease progression. Localized surgical intervention is necessary to manage residual effects.
- Tx: tetracycline (staining!), tetra with metronidazole, metronidazole and amox***
- With surgical and non-surgical root debridement, maintenance every 4 months
6
Q
Generalized aggressive periodontitis
A
- Adolescents and teenagers.
- In young adults, formerly called rapidly progressive periodontitis.
- Affects the entire dentition and is not self-limiting. Heavy accumulations of plaque and calculus, and inflammation may be severe.
- NOT associated with high levels of A. actinomycetemcomitans; microbiological profile is closer to that of chronic disease.
- Manage aggressively with local therapy and systemic antibiotics
7
Q
LAP in primary dentition: Characteristics, associations, etiology, who does it typically affect? Where does it manifest?
A
- Characterized by localized loss of attachment in the primary dentition.
- Manifests in the molar area, where localized, usually bilaterally symmetric loss of attachment occurs.
- Most commonly occurring in the African American population.
- Usually accompanied by mild to moderate inflammation. Heavier than average plaque deposits may be visible, calculus may be present
- Commonly diagnosed during the late primary dentition or early transitional dentition.
- May progress in the permanent dentition and is probably the same disease entity, differing only in the age of onset or diagnosis.
- Believed to be the result of a bacterial infection combined with specific but minor host immunologic defects.
- Some cases are associated with systemic genetic diseases.
8
Q
LAP in primary dentition: Treatment
A
- Treatment:
- Antibiotics with local debridement
- Tetracyclines are *contraindicated* because of potential staining developing permanent teeth.
- Metronidazole is antibiotic of choice.
9
Q
Acute Necrotizing Ulcerative Gingivitis: Dental management
A
- Local debridement (ultrasonic scaling)
- NSAIDs for pain
- Penicillin or metronidazole for systemic involvement
10
Q
Acute Necrotizing Ulcerative Gingivitis/Periodontitis: Clinical features, peak incidence
A
AKA Vincent’s infection, pyorrhea, or trench mouth
- Characterized by rapid onset of painful gingivitis with interproximal and marginal necrosis and ulceration.
- Fever, lymphadenopathy, malaise, fiery red gingiva, extreme oral pain, hypersalivation, unmistakable fetor oris
- Punched out, ulcerated, and covered with a grayish pseudomembrane
- May progress into necrotizing ulcerative periodontitis in immunocompromised individuals (increased stress; HIV-infected patients).
- Peak incidence in late teens and 20s in developed countries
- Common in young children in less developed countries.
- This multifactorial disease has a bacterial population high in fusiform bacillae, Prevotella intermedia and spirochetes.
11
Q
Necrotizing Ulcerative Gingivitis/Periodontitis: Predisposing factors
A
- Predisposing factors:
- Malnutrition
- Viral infections
- Stress
- Lack of sleep
- Smoking
12
Q
Necrotizing Ulcerative Gingivitis/Periodontitis: Bacterial association
A
High levels of spirochetes and Prevotella intermedia
13
Q
Necrotizing Ulcerative Gingivitis/Periodontitis: Treatment
A
- Treatment:
- Local debridement and irrigation provides rapid resolution
- Antibiotic therapy with penicillin or metronidazole indicated with elevated temperature
- Stress-reduction
- Rest
Partial loss of interdental papillae can be expected despite normal healing.
14
Q
Plaque-induced gingivitis: Features
A
- Gingival inflammation
- No loss of attachment or bone
- Reversible
15
Q
Plaque-induced gingivitis: Prevalence
A
- Low in early childhood
- Peaks during puberty
- 60% of teenagers have gingival BOP (Handbook)
- Gingivitis 73% in 6-11yo and raises with age
- Adolescence is more 50-90%
- Gingivitis less in girls than boys, probably related with oral hygiene
16
Q
Plaque-induced gingivitis: Etiology
A
- Plaque-dependent
- Individual susceptibility variable
- Reactivity gradually increases with age
- May be related to steroid hormones
- Puberty
- Pregnancy
- Menstruation
- Oral contraceptives
- Local factors may contribute
- Crowding
- Ortho appliances
- Mouthbreathing
- Eruption
- Calculus (~10% of children, ⅓ of teens have calculus)
17
Q
Plaque-induced gingival enlargement: Clinical features
A
- Enlargement of interdental papilla and/or marginal gingiva.
- Ranges from pale and fibrotic to red and friable.
- May be generalized or localized.
18
Q
Plaque-induced gingival enlargement: Etiology
A
Prolonged exposure to plaque
19
Q
Plaque-induced gingival enlargement: Common local contributory factors
A
- Mouth breathing
- Ortho appliances
20
Q
Plaque-induced gingival enlargement: Dental management
A
- Thorough OH
- Electric TB may help
- Gingivectomy or gingivoplasty may be necessary
21
Q
Drug-induced gingival enlargement: Drugs
A
- Phenytoin (dilantin) - anti-epileptic
- Cyclosporin (immunosuppressant)
- Calcium channel blockers (diltiazem, nifedipine, amlodipine)
22
Q
Drug-induced gingival enlargement: Clinical features
A
- Starts as painless enlargement of interdental papilla and marginal gingiva
- Fibro-epithelial growth
- May progress to cover crowns
- Related to plaque-control
- Does not occur in edentulous areas
- Regresses and may disappear after cessation of drug tx
23
Q
Drug-induced gingival enlargement: Treatment
A
- Replace with alternate drug if possible
- Professional prophylaxis and thorough OH
- Daily use of CHX may help
- Gingivectomy or gingivoplasty
24
Q
Pyogenic granuloma
A
Pregnancy tumor
- Painless localized gingival enlargement
- Blue-red color
- Occurs in pregnancy
25
Q
Gingival abscess: Features, onset, dental management
A
- Localized, painful lesion of marginal gingiva or interdental papilla
- Onset: Sudden
- Bacterial infection following gingival trauma, typically caused by embedded foreign object
- Dental management:
- Debridement, irrigation, establishment of drainage
26
Q
Pericoronitis: Clinical features
A
- Inflammation of gingiva covering partially erupted tooth
- Most common around erupting 3rd molars
- Food trap, environment conducive to bacterial growth
- Pericoronal flap becomes inflamed and swollen
- Enlarged flap traumatized by occlusion = very painful
27
Q
Pericoronitis: Dental management
A
- Debridement
- ABX therapy for systemic involvement
- CHX irrigation
28
Q
Vitamin C-deficiency gingivitis: Clinical features
A
- Edematous, spongy gingiva
- Clinical appearance of non-specific gingivitis
- Impaired wound healing
29
Q
Vitamin C-deficiency gingivitis: Dental management
A
- Tx of underlying deficiency
- Plaque control
30
Q
Diabetes and Chronic Periodontitis: Clinical features
A
- Increased incidence of gingivitis
- Increased risk and earlier onset of periodontitis (10-15% of teens)
- Poor metabolic control appears to increase risk of periodontitis
- Plaque and calculus levels comparable to normal controls
31
Q
Diabetes and Chronic Periodontitis: Dental management
A
- Plaque control
- Scaling and root planing
32
Q
Hypophosphatasia + Periodontal Disease: Clinical features
A
- Genetic disorder
- Early loss of primary teeth occurs in almost all reported cases.
-
Five levels of severity:
- Perinatal (lethal)
- Infantile
- Childhood
- Adult
- Odontohypophosphatasia
- Phenotypes range from severe bone abnormalities leading to neonatal death, to isolated premature loss of deciduous teeth (odontohypophosphatasia) – early loss of primary teeth may be the first clinical sign in mild forms.
- Abnormal cementum formation leads to early loss of primary teeth.
- Teeth are exfoliated with intact roots, usually before root formation is complete.
- Teeth lost in order of eruption.
- Most likely to affect primary incisors but may affect additional teeth.
- Pulp chambers may be abnormally large.
33
Q
Hypophosphatasia + Periodontal Disease: Etiology
A
Deficient or defective tissue non-specific alkaline phosphatase (TNSALP)
34
Q
Hypophosphatasia + Periodontal Disease: Diagnosis
A
- Low serum alkaline phosphatase (normal values vary with age, so normal control values must be adjusted for age).
- Increased phosphoethanolamine in urine or elevated pyridoxal phosphate in serum.
- Deficient or defective cementum by histologic examination.
- Characteristic defects on radiographic examination of bones.
35
Q
Hypophosphatasia + Periodontal Disease: Dental prognosis
A
- In odontohypophosphatasia permanent dentition may be normal.
- Poor dentition reported in more severe forms.
