Abstract

Relevance. The administration of antibiotics in implantology is indicated to prevent suppurative inflammation conditions. Two regimens are commonly used: a single preoperative dose or prolonged postoperative antibiotic administration. Due to ethical constraints, certain parameters of antibiotic efficacy cannot be directly evaluated within clinical trials. These include the status of the implant-mandibular segment microbiome and the histological parameters of the tissue's inflammatory response at the implant site.Materials and methods. This study employed a miniature pig model comprising 10 males. The cohort was equally divided into two groups of five animals each. Group 1 received a single preoperative dose of amoxicillin/clavulanic acid 2 ml per 20 kg body weight. Group 2 received the same initial dose prior to implantation, followed by a daily postoperative dose of amoxicillin/clavulanic acid at 1 ml per 20 kg body weight for five days. Each animal received six dental implants. An implant site microbiological test was performed pre-surgery, on Day 1, 3, 7 and 14 post-surgery. Core needle biopsies for histological examination of the tissues were performed on the same postoperative days.Results. Microbiological testing revealed that Group 2 exhibited lower levels of Streptococcus spp. on Day 3 (p = 0.04) and Porphyromonas spp. on Day 7 (p = 0.04). Group 1 demonstrated reduced levels of Fusobacterium spp. on Day 1 (p = 0.02) and Porphyromonas spp. both pre-surgery (p = 0.04) and on Day 1 (p = 0.012). Comparative analysis of histological assays from the implant sites indicated identical tissue inflammatory responses, regardless of the antibiotic prophylaxis regimen.Conclusion. Both the single-dose and the prolonged antibiotic prophylaxis regimens, using amoxicillin/clavulanic acid for dental implantation, demonstrated similar histological patterns of tissue inflammation at the implant site, along with comparable microbiota profiles within the implant site. The oral mucosa exhibited an increased population of Staphylococcus spp. and Streptococcus spp., which might contribute to the development of resistant strains, as well as Candida spp., potentially increasing the risk of candidiasis infection onset.

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