Volume 71 • Number 4 Interleukin-1 Gene Polymorphisms and Long-Term Stability Following Guided Tissue Regeneration Therapy* Massimo De Sanctis and Giovanni Zucchelli 606 Background: Specific interleukin (IL)-1 gene polymorphisms are associ- ated with an increased susceptibility to severe periodontitis, increased inflam- mation, and increased likelihood of tooth loss during the maintenance phase after conventional periodontal therapy. The aim of the present study was to evaluate the impact of genotype on the maintenance of gained clinical attach- ment obtained after guided tissue regeneration (GTR) surgical therapy in deep intrabony defects. Methods: Forty deep (≥4 mm) interproximal angular bony defects with presurgical clinical attachment loss of >8 mm were treated by GTR using a non-absorbable expanded polytetrafluoroethylene (ePTFE) membrane. Mem- branes were surgically removed 4 to 6 weeks after surgery. Afterwards patients were placed on monthly recall for the first year and every 3 months for the following 3 years. At the 4-year re-evaluation, a IL-1 genetic susceptibility test was performed on all patients. Results: Fourteen (35% of the 40 patients) were genotype-positive (+). At baseline no statistically significant differences were found between patients with different genotypes in full mouth plaque score (FMPS), full mouth bleed- ing score (FMBS), clinical attachment level (CAL), probing depth (PD), or gin- gival recession. At year 1 follow up visit, no statistically significant differences were noted between genotype + and genotype - patients in FMPS, FMBS, amount of CAL gain, decrease in PD, or increase in gingival recession. Six- teen patients had membrane exposure after the GTR procedures. In these patients, the amount of CAL gain (P <0.001) and PD reduction (P <0.01) 1 year after surgery was significantly lower than those observed in patients without membrane exposure. At the year 4 follow-up visit, no significant dif- ferences were found between genotype negative and positive patients in FMPS or FMBS and both groups showed a significant loss in CAL (P <0.001) and increase in PD (P <0.001) when compared to year 1 visit. No change in gingival recession was noted. Genotype + patients showed significantly more CAL loss (P <0.002) and increase in PD (P <0.001) between the years 1 and 4 when compared to genotype - patients. A significant association between genotype and stability of the regenerated attachment was also demonstrated. Conclusions: The results of this study demonstrate that genotype expres- sion did not effect GTR treatment response at 1 year, but had a great impact on long-term stability (year 4). In a 3-year period, patients with positive IL- 1 genotype lost about 50% of the first year gained CAL and were about 10 times more likely of experiencing ≥2 mm CAL loss when compared to oral hygiene matched genotype-negative patients. J Periodontol 2000;71:606-613. KEY WORDS Periodontal attachment loss/prevention and control; genotype; periodontitis/ etiology; tooth loss/prevention and control; polymorphism, gene. * Department of Periodontology, Bologna University, Bologna, Italy. T he ultimate goal in peri- odontal therapy is to regenerate the attach- ment apparatus lost to peri- odontal disease. Application of the principles of guided tissue regeneration (GTR) in the treat- ment of vertical bony defects has been shown to result in significant and predictable gain of clinical attachment and bone fill. 1-7 It has been demonstrated that these clinical improve- ments can be maintained over time in patients enrolled in peri- odontal maintenance pro- grams. 8-10 Furthermore, high plaque and bleeding on probing scores, 6,9 cigarette smoking, 11 and lack of compliance 9,12 are frequently associated with clin- ical attachment loss. Among inherent patient factors, genetic characteristics have not yet been evaluated in relation to the response to GTR therapy or to the long-term results. With the discovery of a specific genetic marker for susceptibil- ity to periodontitis and the availability of a laboratory test † for identifying this marker, it has now become possible to assess the patient’s genetic risk. † PST, Interleukin Genetics, San Antonio, TX.