Abstract

Periodontitis is an inflammatory disease associated with a dysbiosis of the oral flora characterized by a chronic sustained inflammation leading to destruction of tooth-supporting tissues. Over the last decade, an association between periodontitis and systemic disorders such as cardiovascular diseases, rheumatoid arthritis and obesity has been demonstrated. The role of periodontal pathogens, notably Porphyromonas gingivalis (P. gingivalis), in the onset or exacerbation of systemic diseases has been proposed. P. gingivalis expresses several virulence factors that promote its survival, spreading, and sustaining systemic inflammation. Recently, the impact of periodontitis on gut dysbiosis has also been suggested as a potential mechanism underlying the systemic influence of periodontitis. New therapeutic strategies for periodontitis and other dysbiotic conditions, including the use of beneficial microbes to restore healthy microbial flora, may pave the way to improved therapeutic outcomes and more thorough patient management.

Highlights

  • Periodontitis is an oral inflammatory disease of infectious origin affecting periodontium, characterized by gingival swelling and bleeding, periodontal pocket formation and clinical attachment loss, destruction of tooth-supporting tissue and to tooth loss [1,2]

  • Periodontitis is among the most common diseases worldwide, with its severe form affecting approximately 11% of the global population [3]. This disease represents a major public health issue as periodontitis has been correlated with decreased oral health and related quality of life [4]

  • In the context of periodontal inflammation, the contribution of microbiome dysbiosis is under investigation due to the molecular mechanisms underlying this microbiome state being poorly understood

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Summary

Introduction

Periodontitis is an oral inflammatory disease of infectious origin affecting periodontium, characterized by gingival swelling and bleeding, periodontal pocket formation and clinical attachment loss, destruction of tooth-supporting tissue and to tooth loss [1,2]. There is overwhelming evidence to support that periodontal pathogens, P. gingivalis, play a role in the progression of the disease by allowing for the accumulation of inflammatory cytokines and autoreactive antibodies, leading to the tissue destruction associated with RA [69,82,83,84]. It has been demonstrated in numerous animal models of experimental arthritis that arthritis can be treated by targeting P. gingivalis and its numerous virulence factors, supporting the need for further investigation into the effects of nonsurgical periodontal treatment and the progression of RA in human trials. Due to the ability of periodontal treatment to change the serum metabolome, the effects on the composition of the microbiome should be investigated

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