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Aim: To assess factors contributing to tooth loss 20 years after active periodontal therapy (APT) on tooth level. Materials and Methods: After an initial retrospective analysis 10 years after APT, patients were monitored for 10 more years. At clinical re‐evaluation 20 years after APT, tooth‐related factors (tooth type, location, bone loss, furcation involvement, abutment status) and patient‐related factors (gender, smoking, adherence) were investigated. Descriptive statistical analysis and a mixed logistic regression analysis were performed with tooth loss as primary outcome variable. Results: The study included 69 patients (42 female/27 male). 39 patients were non‐adherent (56.5%), and 11 were active smokers (15.9%). A total of 198 out of 1611 teeth were lost. Tooth loss was significantly highest (p <.01) in molars (21.1%), multi‐rooted teeth with furcation involvement (23.5%) and abutment teeth (fixed: 27.6%, removable: 36.4%). 37.6% of teeth with initial bone loss >60% were lost during 20 years. Adherent patients showed less frequent tooth loss than non‐adherent patients (OR 0.371; p <.01). Conclusion: Even teeth with an initial bone loss over 60% could be retained in approximately two thirds for 20 years. This should be kept in mind when assigning prognosis and establishing a treatment plan. [ABSTRACT FROM AUTHOR]

Objective. To determine the association between the interleukin (IL)-1-polymorphism and the severity of periodontal disease prior to active periodontal therapy. Materials and methods. Two hundred and six patients with obtained baseline x-rays were tested for IL-1-polymorphism. Relative bone loss before active periodontal treatment was measured with a Schei ruler and classified in five groups. Descriptive statistics and backward stepwise linear regression analyses were performed. Results. Forty-nine patients with moderate (mChP), 79 with severe chronic (sChP) and 78 with aggressive periodontitis (AgP) were included. Age correlated significantly with bone loss and number of teeth at baseline. Gender, smoking and IL-1-polymorphism were neither associated with bone loss nor with number of teeth prior to treatment. After adjusting for age as well as gender, AgP was significantly associated with more severe bone loss in untreated periodontal disease ( p == 0.036). In non-smokers, mean number of teeth prior to active periodontal therapy correlated significantly with presence of IL-1 polymorphism. Conclusion. The IL-1-polymorphism is associated with lower number of teeth in non-smokers with untreated periodontal disease. Untreated AgP is associated with more severe bone loss than untreated ChP. [ABSTRACT FROM AUTHOR]

Objectives: Evaluation of patient-related risk factors contributing to tooth loss and recurrence of periodontitis 10.5 years after initial therapy in patients with aggressive periodontitis (AgP). Material and Methods: Eighty-four of 174 patients were included. Re-examination consisted of patient's history, clinical examination and test for interleukin (IL)-1 composite genotype. Patients' charts were searched for regularity of maintenance and initial diagnosis. Statistical analysis was performed using Poisson and logistical regression analysis. Results: The responder rate was 48%. Thirteen of 84 patients presented a localized AgP, 68 were females and 29 smoked. One hundred and thirteen teeth out of 2154 were lost after therapy (1.34 teeth/patient). Age (p = 0.0018), absence of IL-1 composite genotype (p = 0.0091) and educational status (p = 0.0085) were identified as statistically significant risk factors for tooth loss. Twenty patients exhibited recurrence of periodontitis at re-examination. Smoking ( p= 0.0034) and mean Gingival Bleeding Index (GBI) (p = 0.0239) contributed significantly to recurrence of disease. No patient participating regularly in supportive periodontal therapy (SPT) showed disease recurrence. Conclusion: Age, absence of IL-1 composite genotype and low social status are detected as risk factors for tooth loss. Smoking and high mean GBI are associated with an increased risk for recurrence of periodontitis, whereas regular SPT acts as a protective factor. [ABSTRACT FROM AUTHOR]