Abstract

The aim of this retrospective case series was to evaluate the clinical efficacy of nanohydroxyapatite powder (NHA) in combination with polylactic acid/polyglycolic acid copolymer (PLGA) as a bone replacement graft in the surgical treatment of intrabony periodontal defects. Medical charts were screened following inclusion and exclusion criteria. Periodontal parameters and periapical radiographs taken before surgery and at 12-month follow-up were collected. Intra-group comparisons were performed using a two-tailed Wilcoxon signed-rank test. Twenty-five patients (13 males, 12 females, mean age 55.1 ± 10.5 years) were included in the final analysis. Mean probing depth (PD) and clinical attachment level (CAL) at baseline were 8.32 ± 1.41 mm and 9.96 ± 1.69 mm, respectively. Twelve months after surgery, mean PD was 4.04 ± 0.84 mm and CAL was 6.24 ± 1.71 mm. Both PD and CAL variations gave statistically significant results (p < 0.00001). The mean radiographic defect depth was 5.54 ± 1.55 mm and 1.48 ± 1.38 mm at baseline and at 12-month follow-up, respectively (p < 0.0001). This case series, with the limitations inherent in the study design, showed that the combination of NHA and PLGA, used as bone replacement graft in intrabony periodontal defects, may give significant improvements of periodontal parameters at 12-month follow-up.

Highlights

  • Periodontitis is a chronic inflammatory disease caused by infection of the supporting tissues around teeth

  • Medical records and periodontal charts of all patients treated with the combination nanohydroxyapatite powder (NHA)/polyglycolic acid copolymer (PLGA)

  • Heavy smokers (>10 cigarettes a day), pipe and/or cigar smokers; alcohol and/or drug abusers; medical conditions that could affect wound healing at the time of surgery; insufficient information found in medical records; patients who did not comply to scheduled recall visits after surgery

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Summary

Introduction

Periodontitis is a chronic inflammatory disease caused by infection of the supporting tissues around teeth. The infection begins with colonization and growth of a small group of predominantly. Gram-negative anaerobic bacteria and spirochetes [1]. These bacteria, organized in biofilms with other commensal species, colonize the root surface, eliciting a chronic inflammation which leads to the progressive destruction of alveolar bone and collagen fibers of the periodontal ligament, and to the formation of periodontal pockets [2]. The inflammatory process is regulated by several biomolecular response mediators that may induce a quite disproportional reaction, leading to connective tissue damage [4,5,6,7,8].

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