Subjects with GAgP significantly benefit from the adjunctive use of MTZ and AMX. The short-term advantages are observed in the clinical and microbiological parameters.

This literature review provides an overview of the current scenario regarding the impact of smoking on the progression and treatment of periodontitis; clinical, microbiological and immunological data from studies from our and other groups are presented. In general, preclinical and clinical data are unanimous in demonstrating that smokers present increased susceptibility, greater severity and faster progression of periodontal disease compared with nonsmokers. The evidence further demonstrates that smokers lose more teeth and have a less favorable response to therapy than do nonsmokers. Although it is well established that smoking significantly impacts on the onset, progression and outcome of periodontal disease, the mechanisms involved remain unclear. More importantly, some of the reported deleterious effects of smoking on periodontal tissues have been reported to be reversible upon participation in smoking-cessation programs. Therefore, clinicians should strongly advise smokers to enroll in cessation strategies, even temporarily, in order to improve the overall outcome.

Mechanical therapies alone were effective in treating mucositis and peri-implantitis over a period of 3 months. The open debridement procedure showed clinical and microbiological benefits on the treatment of peri-implantitis and could be safely used as a standard control group for future studies.

A. actinomycetemcomitans seems to be associated with the onset of LAgP, and Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Campylobacter gracilis, Eubacterium nodatum and Prevotella intermedia play an important role in disease progression. Successful treatment of LAgP would involve a reduction in these pathogens and an increase in the Actinomyces species.

Periodontitis mainly influenced the circulating levels of resistin and adiponectin, whereas both obesity and periodontitis affected the circulating levels of leptin in favor of proinflammation. In addition, obesity upregulated the local levels of TNF-α.

Obesity may modulate systemic and periodontal levels of adipokines in favour of pro-inflammation, independently of periodontal therapy. SRP did not affect the circulating levels of adipokines in patients with or without obesity.

The data of the present study suggest no adjunctive benefit of AZM in the treatment of generalized ChP.

The proposed anti-infective therapies may locally modulate the levels of TNF-alpha and the OPG/RANKL ratio and improve clinical parameters around peri-implant tissues.