Oral Osteomicrobiology: The Role of Oral Microbiota in Alveolar Bone Homeostasis

Abstract

Osteomicrobiology is a new research field in which the aim is to explore the role of microbiota in bone homeostasis. The alveolar bone is that part of the maxilla and mandible that supports the teeth. It is now evident that naturally occurring alveolar bone loss is considerably stunted in germ-free mice compared with specific-pathogen-free mice. Recently, the roles of oral microbiota in modulating host defense systems and alveolar bone homeostasis have attracted increasing attention. Moreover, the mechanistic understanding of oral microbiota in mediating alveolar bone remodeling processes is undergoing rapid progress due to the advancement in technology. In this review, to provide insight into the role of oral microbiota in alveolar bone homeostasis, we introduced the term “oral osteomicrobiology.” We discussed regulation of alveolar bone development and bone loss by oral microbiota under physiological and pathological conditions. We also focused on the signaling pathways involved in oral osteomicrobiology and discussed the bridging role of osteoimmunity and influencing factors in this process. Finally, the critical techniques for osteomicrobiological investigations were introduced.

Proof-of-Principle Study Suggesting Potential Anti-Inflammatory Activity of Butyrate and Propionate in Periodontal Cells

“…SCFAs are well-recognized in periodontal research for two reasons: reason one is that propionic and butyric acid are metabolic by-products of anaerobic bacteria reaching approximately 10 and 3 mM, respectively, in the periodontal pocket of diseased subjects [ 15 , 16 ]. Reason two is that butyrate and propionate isolated from dental plaque extracts are harmful to various cell types related to the periodontium in vitro [ 8 , 9 , 10 , 11 , 12 , 13 ] but, on the other hand, have potential beneficial effects, particularly when acting systemically [ 17 , 18 , 19 , 20 , 21 , 22 ]. The current study provides further evidence to support a role for SCFAs in the control of the inflammatory response of periodontal cells.…”

“…Oral administration of berberine in rats increased butyrate level, being associated with less collagen-induced arthritis [ 18 ] and periodontal bone loss [ 19 ]. Apart from the gut microbiome affecting periodontitis [ 20 ], oral microbiota and its metabolites can modulate immunity and alveolar bone homeostasis [ 21 , 22 ]. There is thus uncertainty over whether butyrate and other SCFAs only impede periodontal tissue homeostasis or even support it [ 23 ].…”

On Peri-Implant Bone Loss Theories: Trying To Piece Together the Jigsaw

“…However, the crux of the matter is to avoid osteoclast (over)differentiation and (over)activation, which in fact is provoked by the local release of proinflammatory cytokines, different cell proliferation factors, and other molecules [30][31][32][33]. The overexpression of these proinflammatory mediators results not only from the perio-pathogenic bacterial colonization and activity [33,34], but also as a result of other risk factors such as occlusal overload, presence of cement remnants, poor prosthetic fitting and micromovement, corrosion, and many other factors that are later discussed [13,35,36] It should be also noted at this point, that the insult caused by the oral biofilm is due to complex interactions between bacteria, viruses, fungi, archaea, and protozoa [31,37] and not exclusively by periopathogenic bacteria. This should be considered when selecting a supportive antimicrobial treatment.…”

“…The most reported bacteria associated with PI are obligate anaerobe Gram-negative bacteria, although Grampositive rods and other Gram-positive species could be also involved [27,37,38]. The immune response is triggered by the dysbiosis of the oral microbiota [37]. Peri-implant microbiota and its metabolites can induce the production of proinflammatory cytokines such as IL-1, IL-6, IL-17, tumor necrosis factor alpha (TNF-α), macrophage inflammatory protein (MIP-1), and macrophage chemoattractant protein (MCP-1) by different immune cells, including neutrophils, monocytes, macrophages, dendritic cells, T cells, and B cells, leading to an increased expression of receptor activator of nuclear factor κ B ligand (RANKL) [37][38][39][40][41][42][43].…”

NLRP3 Inflammasome Negatively Regulates RANKL-Induced Osteoclastogenesis of Mouse Bone Marrow Macrophages but Positively Regulates It in the Presence of Lipopolysaccharides

“…It is widely recognized that the NLRP3 inflammasome is involved in bone resorption following infection challenge [ 17 , 18 ]. However, the role of the NLRP3 inflammasome under physiological conditions remains unclear.…”