Local Systemic Factors
Primary Etiology: bacterial plaque

Secondary Etiology: local and systemic factors
No concrete evidence that any of the contributing (secondary) factors can initiate periodontal disease by themselves
They enhance the ability/virulence of the bacterial plaque to cause periodontal disease
Primary and secondary etiologic factors should be listed on the Baseline form under risk assessment
Local Factors: make plaque removal more difficult
Calculus
Caries
Iatrogenic
Anatomical features
Trauma
Supragingival Calculus
70-90% inorganic
75.9% calcium phosphate
4 main crystal forms
58% hydroxyapatite
21% magnesium whitlockite
12% octacalcium
9% brushite
Hampers plaque removal
Subgingival Calculus
Similar composition as supra
More mag. whitlockite
No salivary proteins
Higher calcium to phosphate ratio
Harder to remove
Hampers plaque removal
Caries
Caries which approximated the gingival margin can complicate plaque removal
Lesions should be repaired early in therapy to allow easier plaque removal
Iatrogenic Factors
Open margins
Overhanging margins
Open contacts/food impactions
Over contoured restorations
Tooth Positions
Crowding
Tipping
Tooth proximity
Tooth Associated Anatomical Factors
Furcation involvement, enamel pearls, enamel projections and developmental grooves and concavities
Furcation Involvement

Enamel Pearls
1.1 to 5.7% of permanent molars
75% on maxillary third molars

Enamel Projections
28.6% of mandibular molars
17% of maxillary molars

Concavities


Developmental Grooves
5.6% of maxillary lateral incisors
3.4% of maxillary central incisors

Soft Tissue Anatomical Factors
Inadequate attached gingiva, clefts, enlargements and craters
Clefts

Gingival Enlargements

Soft Tissue Craters

Systemic Conditions and Periodontal Disease
Endocrine Conditions
Hematologic Disorders
Neutrophil Disorders
Smoking
Medications
Nutrition
Stress
Heredity
Obesity
Endocrine Conditions
Diabetes
Hormonal
Hormonal Conditions
Puberty
Pregnancy
Estrogen deficiency
Puberty Gingivitis
Peaks at 11-13 years of age
Related to hormonal changes
Both male and female
Pregnancy Gingivitis
Increased hormone levels in gingival crevicular fluid associated with dramatic increases in P. intermedia, which use hormones as growth factors
Estrogen Deficiency/Osteoporosis
Bone mass peaks age 20-30
Reduction accelerates at menopause
Estrogen is protective
Estrogen deficiency is a possible modifying factor in alveolar bone loss

Diabetes
Increased incidence of gingivitis/periodontitis
Defective PMN chemotaxis
Enlarged gingiva
Periodontal abscesses
2,273 Pima Indians
60% prevalence with diabetes
36% prevalence without diabetes

Obesity and Periodontal Disease
Significant association for young group (18-24)
OR 1.0 for BMI 18.5-24.9 kg/m2 (reference)
OR 1.76 for BMI > 30 kg/m2 (P<0.01)
OR 0.21 for BMI < 18.5 kg/m2 (P<0.01)
OR 2.27 for high waist circumference (P<0.001)
Hematologic Disorders
Leukemia
Gingival Enlargement
4% overall
Rare for chronic
67% acute monocytic
Gingival Bleeding
18% acute
4% chronic
Neutrophil Disorders

The neutrophil is the first line of defense to combat acute bacterial infection
Neutrophil dysfunction results in severe periodontitis
Drug Manifestations
Phenytoin (Dilantin)
Cyclosporine
Nifedipine (Calcium Channel Blockers)
Cannabis
Oral contraceptives
Phenytoin (Dilantin)
Enlargement occurs in about 50% of patients
Genetic predisposition suspected
Evidence links pathogenesis to direct effect on fibroblasts, inactivation of collagenase, and plaque-induced inflammation
Nifedipine
Enlargement occurs in 20% of patients taking nifedipine
Enlargement also seen with other calcium-channel blockers (Amlodipine)
Cyclosporine (Immunosuppressant)
More vascularized than phenytoin induced enlargement
20-70% occurence
Plasma cell infiltrate suggests hypersensitivity response
HIV Associated Periodontal Disease
Linear gingival erythema
Necrotizing gingivitis
Necrotizing periodontitis
Linear Gingival Erythema
Persistent, linear, easily bleeding, erythematous gingivitis
Possible etiologic role for candidial species

Necrotizing Gingivitis and Periodontitis


Stress and Periodontal Disease
Systematic review
14 of 58 articles analyzed
No meta-analysis
57% found a positive relation
29% found a positive and negative relation
14% found a negative relation
Possible Biologic Mechanisms
Poorer Oral Hygiene
Stress may alter immune response
Neutrophil impairment
Monocyte upregulation
Smoking
Important periodontal risk factor
Increased incidence and severity of periodontitis
Poorer response to therapy
Associated with NUG
Nicotine can impair neutrophil phagocytosis
Decreased bleeding on probing

Nutritional Factors
Efforts to associate periodontal disease with nutritional deficiencies have yielded conflicting results
In theory, poor nutrition lowers resistance to periodontal disease
Poor nutrition may slow the healing process


Conclusion: results suggest that low dietary intake of calcium results in more severe periodontal disease
Genetics
Identical twins studies suggest that more than 40% of the clinical signs of disease severity are the result of genetic factors
Hereditary Gingival Fibromatosis
