Abstract
Causes of the progression of periodontitis such as an imbalance between the immune response by the host by the release of inflammatory mediators in the response of the oral pathogenic dysbiotic biofilm have been identified. New insights on specific cell signaling pathways that appear during periodontitis have attracted the attention of researchers in the study of new personalised approaches for the treatment of periodontitis. The gold standard of non-surgical therapy of periodontitis involves the removal of supra and subgingival biofilm through professional scaling and root planing (SRP) and oral hygiene instructions. In order to improve periodontal clinical outcomes and overcome the limitations of traditional SRP, additional adjuvants have been developed in recent decades, including local or systemic antibiotics, antiseptics, probiotics, anti-inflammatory and anti-resorptive drugs and host modulation therapies. This review is aimed to update the current and recent evolution of therapies of management of periodontitis based on the adjunctive and target therapies. Moreover, we discuss the advances in host modulation of periodontitis and the impact of targeting epigenetic mechanisms approaches for a personalised therapeutic success in the management of periodontitis. In conclusion, the future goal in periodontology will be to combine and personalise the periodontal treatments to the colonising microbial profile and to the specific response of the individual patient.
Highlights
Periodontitis is a disease with an infectious aetiology characterised by inflammation of the supporting tissues of a tooth that can lead, if not properly treated, to the destruction of both periodontal tissues and alveolar bone, and, in the long term, cause tooth loss [1].periodontitis’s onset and subsequent progression occur as a host’s unbalanced immune reaction to a dysbiotic organised biofilm
It has been previously shown that the mechanical disruption of supra- and subgingival biofilm by the non-surgical periodontal therapy performed by scaling and root planing (SRP) alone can reduce the plaque index (PI) and the bleeding on probing (BOP) in around 45% of periodontal sites [28]
The treatment of periodontal disease in its various forms has evolved over the past century, initially on an empirical basis and on an increasing number of studies based on scientific evidence
Summary
Periodontitis is a disease with an infectious aetiology characterised by inflammation of the supporting tissues of a tooth that can lead, if not properly treated, to the destruction of both periodontal tissues and alveolar bone, and, in the long term, cause tooth loss [1].periodontitis’s onset and subsequent progression occur as a host’s unbalanced immune reaction to a dysbiotic organised biofilm. Among the main known periodontal pathogens, there are bacteria such as Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis (P.gingivalis), which produce multiple factors underlying the tissue damage found during periodontitis such as peptidoglycans, various integrins and outer membrane proteins, lipopolysaccharide and cellular superficial fimbriae degradation connective tissue [3,4,5,6,7] Once these pathogenic bacteria trigger immune and inflammatory processes, the body induces leukocytes, fibroblasts or other inflammatory cells to release various substances in order to protect tissues from infection, including metalloproteinases, cytokines, transglutaminases, prostaglandins and proteolytic enzymes [8]. The inflammatory-related mediators can control the release of ligand-receptor factor Kappa B (NF-KB), RANKL and osteoprotegerin, which stimulate osteoclastic activity by inducing alveolar bone destruction [15]
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