It is well-known that microbiota dysbiosis is closely associated with numerous diseases in the human body The oral cavity and gut are the two largest microbial habitats, playing a major role in microbiome-associated diseases Even though the oral cavity and gut are continuous regions connected through the gastrointestinal tract, the oral and gut microbiome profiles are well-segregated due to the oral-gut barrier However, the oral microbiota can translocate to the intestinal mucosa in conditions of the oral-gut barrier dysfunction Inversely, the gut-to-oral microbial transmission occurs as well in inter- and intrapersonal manners Recently, it has been reported that oral and gut microbiomes interdependently regulate physiological functions and pathological processes Oral-to-gut and gut-to-oral microbial transmissions can shape and/or reshape the microbial ecosystem in both habitats, eventually modulating pathogenesis of disease However, the oral-gut microbial interaction in pathogenesis has been underappreciated to date Here, we will highlight the oral-gut microbiome crosstalk and its implications in the pathogenesis of the gastrointestinal disease and cancer Better understanding the role of the oral-gut microbiome axis in pathogenesis will be advantageous for precise diagnosis/prognosis and effective treatment

https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/182940/1/T202101615.pdf

Oral–Gut Microbiome Axis in Gastrointestinal Disease and Cancer

Frailty is a highly prevalent condition in the elderly that has been increasingly considered as a crucial public health issue, due to the strict correlation with a higher risk of fragility fractures, hospitalization, and mortality. Among the age-related diseases, sarcopenia and dysphagia are two common pathological conditions in frail older people and could coexist leading to dehydration and malnutrition in these subjects. “Sarcopenic dysphagia” is a complex condition characterized by deglutition impairment due to the loss of mass and strength of swallowing muscles and might be also related to poor oral health status. Moreover, the aging process is strictly related to poor oral health status due to direct impairment of the immune system and wound healing and physical and cognitive impairment might indirectly influence older people’s ability to carry out adequate oral hygiene. Therefore, poor oral health might affect nutrient intake, leading to malnutrition and, consequently, to frailty. In this scenario, sarcopenia, dysphagia, and oral health are closely linked sharing common pathophysiological pathways, disabling sequelae, and frailty. Thus, the aim of the present comprehensive review is to describe the correlation among sarcopenic dysphagia, malnutrition, and oral frailty, characterizing their phenotypically overlapping features, to propose a comprehensive and effective management of elderly frail subjects.

/pdf/sarcopenic-dysphagia-malnutrition-and-oral-frailty-in-2mgtl6tc.pdf

Sarcopenic Dysphagia, Malnutrition, and Oral Frailty in Elderly: A Comprehensive Review

Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast-osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

/pdf/inflammasomes-in-alveolar-bone-loss-2mww24h618.pdf

Inflammasomes in Alveolar Bone Loss

Periodontal disease seems to be correlated with low vitamin D serum levels, preterm birth (PTB) and low birth weight (LBW), although the literature still lacks a consensus. This study aimed to investigate this correlation in a cohort of pregnant women over 20 weeks of gestation from the University Hospital “Maggiore della Carita”, Novara, Italy. We assessed serum levels of vitamin D and oral health status through the following indexes: Oral Hygiene Index (OHI), Plaque Control Record (PCR), Gingival Bleeding Index (GBI), and Community Periodontal Index of Treatment Needs (CPTIN). Moreover, we assessed the number of PTB and LBW among the newborns. Out of 121 pregnant women recruited, 72 (mean age 29.91 ± 3.64 years) were included. There was a statistically significant correlation between preterm and OHI > 3 (p = 0.033), and between LBW and OHI > 3 (p = 0.005) and CPITN = 3 (p = 0.027). Both pregnant women with vitamin D deficiency ((25-hydroxy-vitamin D) < 30 ng/mL) and PTB plus LBW newborns were significantly correlated (p < 0.05) with poor levels of all oral health status indexes during pregnancy. Furthermore, these conditions (women with hypovitaminosis D and combination of PTB and LBW) were shown to be significantly correlated (p < 0.001). Taken together, our findings reported a high prevalence of PTB and LBW with poor oral health and vitamin D deficiency in pregnant women.

Periodontal Disease and Vitamin D Deficiency in Pregnant Women: Which Correlation with Preterm and Low-Weight Birth?

The association between micronutrient intake and the risk of periodontitis has received much attention in recent years. However, most studies focused on the linear relationship between them. This study aimed to explore the dose–response association between micronutrient intake and periodontitis. A total of 8959 participants who underwent a periodontal examination, and reported their micronutrient intake levels were derived from the US National Health and Nutrition Examination Survey (NHANES, 2009–2014) database. Logistic regression was performed to evaluate associations between micronutrient intake and periodontitis after propensity score matching (PSM), and restricted cubic splines (RCS) analysis was conducted to explore the dose–response associations. Following PSM, 5530 participants were included in the RCS analysis. The risk of periodontitis was reduced with sufficient intake of the following micronutrients: vitamin A, vitamin B1, vitamin B2, and vitamin E. In addition, the risk of periodontitis was increased with excessive intake of the following micronutrients: vitamin B1 (1.8 mg/day, males; 1.3 mg/day, females), vitamin C (90 mg/day, males), and copper (1.1 mg/day, combined). In conclusion, a linear association was found between vitamin A, vitamin B2, vitamin C, and copper and periodontitis—namely, a sufficient intake of vitamin A and vitamin B2 might help reduce the prevalence of periodontitis; by contrast, a high intake of vitamin C and copper increased the risk. In addition, a nonlinear dose–response association was found for the incidence of periodontitis with vitamin B1 and vitamin E. When within reasonable limits, supplemental intake helped reduce the prevalence of periodontitis, while excessive intake did not help significantly and might even increase the risk. However, confounding factors, such as health awareness, should still be considered.

/pdf/abnormal-micronutrient-intake-is-associated-with-the-risk-of-247heirx.pdf

Abnormal Micronutrient Intake Is Associated with the Risk of Periodontitis: A Dose–response Association Study Based on NHANES 2009–2014

AIMS Existing epidemiological studies have suggested that periodontal disease (PD) may be a risk indicator for colorectal cancer (CRC). However, no formal systematic review and meta-analysis have been performed. Therefore, we aimed to evaluate the association between PD and CRC risk in this study. MATERIALS AND METHODS We used the PubMed, EMBASE, Cochrane Library and Web of Science to search for related articles published from 1 January 1966 to 16 July 2020. Stata (Version 15) software was used to calculate the total risk ratio (RR) and 95% confidence interval (CI) of the included studies through the random-effects model to assess the association between PD and CRC risk. RESULTS Nine studies were included in the narrative synthesis, and seven studies were included in the meta-analysis. Results showed that PD significantly increased the risk of CRC by 44% (RR, 1.44; 95% CI, 1.18-1.76; I2 , 55.2%). CONCLUSION We found an association between PD and CRC. PD can be a potential risk indicator for the occurrence and development of CRC, and further studies are needed to assess causality. Hence, effective periodontal treatment could be a valuable preventive measure for CRC.

Is periodontal disease a risk indicator for colorectal cancer? A systematic review and meta-analysis

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Is periodontal disease a risk indicator for colorectal cancer? A systematic review and meta-analysis