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Periodontal disease represents an inflammatory disease of the tissues supporting the maintenance and functionality of the teeth on the dental arches. The main cause of periodontitis consists in periodontal dysbiosis, which will trigger an inflammatory response, progressively leading to periodontal tissue breakdown. Scaling and root planing represent the gold standard in treating periodontal diseases but, as it was already established, these measures are unable to completely eliminate the subgingival bacterial plaque. Therefore, new adjunctive therapies have emerged, involving systemic and local delivery of various antimicrobial products. This chapter aims to provide current knowledge on the local application of different periodontal supplementary therapies. The chapter focuses on local forms of antimicrobials, such as irrigations, gels or controlled release systems but also on laser/LED-assisted periodontal pocket photodynamic antibacterial therapy (PDT), along with various photosensitizers. Moreover, we present data from current guidelines regarding the recommendations for the main locally delivered antimicrobials.

The relationship between periodontitis and systemic diseases is an important part of clinical periodontal research, which has been growing steadily. Even though the etiologies of periodontal disease and rheumatoid arthritis (RA) differ, these pathologies have many common features, both being multifactorial diseases characterized by localized chronic inflammatory reactions, which are fuelled by an analogous set of cytokines (among many, the most prominent being Tumour Necrosis Factor (TNF), Interleukin (IL) 6 and 17), leading to high systemic circulating concentrations of inflammatory markers such as C-reactive protein (CRP). It was not until the discovery of peptidylarginine deiminase (PAD) mediated citrullination of proteins by Porphyromonas gingivalis that the link between the two diseases was purely speculative. This citrullination initiates a series of events which culminate in the production of anti-citrullinated protein antibodies (ACPA) and, finally, in the clinical manifestation of rheumatoid arthritis. Another common denominator is the bone destruction caused by proinflammatory cytokines secreted by T 17 helper cells (TH17) which is the pathological hallmark of both diseases. Other notable common areas are shared risk factors such as environmental and genetic risk factors. Regarding treatment, neither pathologies have a definitive cure, however, several strategies are employed, some of which are common, such as diet and lifestyle changes, and immunomodulating medication applied locally or systemically.

Periodontal disease is an infectious and inflammatory disease with a high incidence in the global population and an extremely complex etiopathogenesis. Osteoporosis is one of the systemic diseases that can affect the integrity of periodontal tissues. Osteoporosis, as a skeletal disease, causes a reduction in bone mass and microarchitectural changes in the bone. Discussions about the connection between the two diseases affecting the bone began in 1960, but, contrary to the high number of studies, discoveries are still being made regarding the pathophysiological mechanisms that link the two diseases. The chapter proposes a systematized description of data on the influence of osteoporotic disease on the periodontal structures, therapeutic methods to address the patient with periodontal disease and osteoporosis and data on the potential influence of conventional and adjunctive periodontal treatment on systemic parameters in patients with osteoporosis.