title: Effect of periodontal therapy on the course of cyclosporin-induced gingival overgrowth: role of ABCB1 and PAI-1 gene polymorphisms.
abstract: OBJECTIVE
  Etiological periodontal therapy is effective in reducing cyclosporin A-induced gingival overgrowth, but a high variability among subjects has been observed. This study aimed to evaluate the role of polymorphisms in PAI-1 and A BCB1 genes on the course of this side effect following periodontal therapy.
  
  
  METHODS
  Forty-five transplant patients were subjected to nonsurgical periodontal therapy and evaluated for hypertrophy index, probing depths, bleeding, and plaque scores at baseline, and after 3 and 6 months. A BCB1 (C3435T and G2677T) and PAI-1 (4G/5G) polymorphisms were studied with polymerase chain reaction-restriction fragment length polymorphism and allele-specific polymerase chain reaction respectively.
  
  
  RESULTS
  All the monitored periodontal indexes decreased significantly during the six months. Modeling of hypertrophy index by linearmixed- effect models (allowing non-normal distribution of the outcome variable hypertrophy index) resulted in the selection as the most significant model, of the one comprising the independent variables: time, C 3435T genotype, and their interaction term. This model indicated that C 3435T-mutated patients had significantly higher baseline hypertrophy index values (90% Markov chain Monte C arlo empirical confidence intervals: 5.08, 30.00). The decrease in hypertrophy index values over time showed a trend toward being faster in mutated than nonmutated patients (interaction time: C 3435T nonmutated, 90% Markov chain Monte C arlo empirical confidence interval: -11.08, -0.40). When hypertrophy index values were normalized, the significance and trend were lost. No effect of the A BCB1 G2677T and PAI-1 4G/5G polymorphisms was observed.
  
  
  CONCLUSIONS
  These preliminary results suggest that C 3435T polymorphism is a genetic factor that could influence the course of cyclosporin A-induced gingival overgrowth in transplant patients subjected to periodontal therapy.
authors: Dipartimento Universitario Clinico di Scienze Mediche, Chirurgiche e della Salute, University of Trieste, Trieste, Italy.
authors: Sara
authors: S
authors: De Iudicibus
authors: Gabriele
authors: G
authors: Stocco
authors: Gaetano
authors: G
authors: Castronovo
authors: Camillo
authors: C
authors: Pico
authors: Roberto
authors: R
authors: Racano
authors: Massimo
authors: M
authors: Borelli
authors: Lorenzo
authors: L
authors: Bevilacqua
authors: Roberto
authors: R
authors: Di Lenarda
authors: Fiora
authors: F
authors: Bartoli
authors: Giuliana
authors: G
authors: Decorti
mesh_terms: D018435:ATP Binding Cassette Transporter, Subfamily B; D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000235:genetics*; D000328:Adult; D000368:Aged; D064591:Allografts; D016572:Cyclosporine / Q000009:adverse effects*; D005260:Female; D019214:Gingival Overgrowth / Q000139:chemically induced* / Q000235:genetics* / Q000628:therapy; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D016014:Linear Models; D008297:Male; D008390:Markov Chains; D008875:Middle Aged; D009154:Mutation; D016377:Organ Transplantation; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic
chemical_list: C513055:ABCB1 protein, human; D018435:ATP Binding Cassette Transporter, Subfamily B; D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D007166:Immunosuppressive Agents; D017395:Plasminogen Activator Inhibitor 1; D016572:Cyclosporine