Hidradenitis suppurativa (HS) is a chronic, inflammatory skin condition characterized by painful nodules which suppurate and later develop into scar tissues followed by the development of hypodermal tracts. Although the mechanisms behind HS are not fully understood, it is known that dietary factors play important roles in flare frequency and severity. We hypothesize that the high fat diet (HFD) causes dysbiosis, systemic inflammation, and hyperhomocysteinemia (HHcy) in susceptible individuals, which subsequently elevate inflammatory cytokines such as IL-1β, IL-6, IL-17, and tumor necrosis factor alpha (TNF-α). This increase in dysbiosis-led inflammation coupled with a dysregulation of the 1-carbon metabolism results in an increase in matrix metalloproteinases MMP-2, MMP-8, and MMP-9 along with tissue matrix remodeling in the development and maintenance of the lesions and tracts. This manuscript weaves together the potential roles played by the gut microbiome, HHcy, MMPs, and the 1-carbon metabolism toward HS disease causation in susceptible individuals.

Periodontal disease results from poor oral hygiene and is characterized by a destructive process in periodontium that includes gingiva, alveolar mucosa, cementum, periodontal ligament and alveolar bone. Notably, destructive event in alveolar bone has been linked to homocysteine (Hcy) metabolism however; it has not been fully investigated. Therefore; implication of Hcy towards initiation, progression and maintenance of periodontal disease remains incompletely understood. Higher Hcy (or hyperhomocysteinemia; HHcy) exerts deleterious effects on gum health and teeth. Firstly, increased proinflammatory cytokines production such as TNF-α, IL-1β, IL-6 and IL-8 leads to an inflammatory cascade that affects methionine (Met) and Hcy metabolism (i.e. 1-carbon metabolism) leading to HHcy. Secondly, metabolic dysregulation during chronic conditions increases inflammation leading to decrease in vitamins, specifically B6, B12 and folic acid that play important roles in Hcy metabolism. Also, given the folate level in HHcy state that is important during dysbiosis, these two conditions appear to be intimately related, and in this context HHcy induced dysbiosis may be one of the potential causes of periodontal disease. This paper sums-up the link between periodontitis and HHcy, with a special emphasis on “oral-gut microbiome axis” and the potential probiotic intervention towards warding-off some of the serious periodontal disease conditions

Hyperhomocysteinemia (HHcy) affects bone remodeling since destructive process in cortical alveolar bone has been linked with it, however; the mechanism remains at large. HHcy increases pro-inflammatory cytokines viz. TNF-α, IL-1b, IL-6 and IL-8 that leads to a cascade that negatively impacts methionine-metabolism and homocysteine cycling. Further, chronic inflammation decreases vitamins B12, B6 and folic acid that are required for methionine-homocysteine homeostasis. This study aims to investigate a HHcy mouse model (cystathionine β-synthase deficient; CBS+/-) for studying the potential pathophysiological changes, if any, in the periodontium (gingiva, periodontal ligament, cement and alveolar bone). We compared periodontium, side-by-side; CBS+/- model with that of wild-type; WT (C57BL/6J) mice. Histology and histomorphometry of mandibular bone along with gene expression analyses were carried out. Also, pro-angiogenic proteins and metalloproteinases were studied. To our knowledge, this research shows, for the first time, a direct connection between periodontal disease during CBS deficiency thereby suggesting the existence of disease drivers during hyperhomocysteinemic condition. Our findings offer opportunities to develop diagnostics/therapeutics for the people who suffer from chronic metabolic disorders like HHcy.

Although a high-fat diet (HFD) induces gut dysbiosis and cardiovascular system remodeling, the precise mechanism is unclear. We hypothesize that HFD instigates dysbiosis and cardiac muscle remodeling by inducing matrix metalloproteinases (MMPs), which leads to an increase in white adipose tissue, and treatment with lactobacillus (a ketone body donor from lactate; the substrate for the mitochondria) reverses dysbiosis-induced cardiac injury, in part, by increasing lipolysis (PGC-1α, and UCP1) and adipose tissue browning and decreasing lipogenesis. To test this hypothesis, we used wild type (WT) mice fed with HFD for 16 weeks with/without a probiotic (PB) in water. Cardiac injury was measured by CKMB activity which was found to be robust in HFD-fed mice. Interestingly, CKMB activity was normalized post PB treatment. Levels of free fatty acids (FFAs) and methylation were increased but butyrate was decreased in HFD mice, suggesting an epigenetically governed 1-carbon metabolism along with dysbiosis. Levels of PGC-1α and UCP1 were measured by Western blot analysis, and MMP activity was scored via zymography. Collagen histology was also performed. Contraction of the isolated myocytes was measured employing the ion-optic system, and functions of the heart were estimated by echocardiography. Our results suggest that mice on HFD gained weight and exhibited an increase in blood pressure. These effects were normalized by PB. Levels of fibrosis and MMP-2 activity were robust in HFD mice, and treatment with PB mitigated the fibrosis. Myocyte calcium-dependent contraction was disrupted by HFD, and treatment with PB could restore its function. We conclude that HFD induces dysbiosis, and treatment with PB creates eubiosis and browning of the adipose tissue.

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Diabetes mellitus, a chronic disease considered by the World Health Organization to be an epidemic, is now recognized as one of the factors behind the onset of periodontal disease. The connection between periodontal disease, which is an irreversible inflammatory disease of the supporting tissue of the teeth, and systemic diseases is reflected in the existence of common risk factors, subgingival dental biofilm, as a constant source of proinflamma-tory cytokines synthesized intensely in inflammatory periodontium. Diabetes mellitus leads to increased oxidative stress in periodontal tissues causing worsening of the disease and periodontopathy exacerbates deficiency of pancreatic β-cells. The most important role in primary inflammatory response in the pathogenesis of periodontopathy is played by neutrophils. Neutrophils cause periodontium destruction by the release of enzymes (matrix metalloproteinases), cytotoxic substances (free radicals, reactive oxygen and nitrogen species) and the expression of membrane receptors. Matrix metalloproteinases within the “protease network” are critical to many physiological and pathological processes, including immunity, inflammation, bone resorption and wound healing. Matrix metalloproteinases levels are elevated in patients with metabolic syndrome and diabetes mellitus, which may contribute to more frequent complications. In this paper, the review of available literature data shows the correlation between periodontal disease and diabetes mellitus, as well as the role of matrix metalloproteinases and oxidative stress in these. In this regard, determining the value of matrix metalloproteinases may be helpful in the diagnosis of periodontal disease complicated by diabetes mellitus. Also, the parameters of oxidative stress could help to clarify the mechanisms of pathogenesis and etiology of periodontal disease, or indicate the potential benefit of antioxidant supplementation in these individuals. As the role of matrix metalloproteinases has not been fully clarified in the pathogenesis of periodontopathy, additional studies will be needed to indicate their importance.

Reconstruction of defects in the maxillofacial region following traumatic injuries, craniofacial deformities, defects from tumor removal, or infections in the maxillofacial area represents a major challenge for surgeons. Various materials have been studied for the reconstruction of defects in the maxillofacial area. Biodegradable metals have been widely researched due to their excellent biological properties. Magnesium (Mg) and Mg-based materials have been extensively studied for tissue regeneration procedures due to biodegradability, mechanical characteristics, osteogenic capacity, biocompatibility, and antibacterial properties. The aim of this review was to analyze and discuss the applications of Mg and Mg-based materials in reconstructive oral and maxillofacial surgery in the fields of guided bone regeneration, dental implantology, fixation of facial bone fractures and soft tissue regeneration.