Probiotics Ameliorate Alveolar Bone Loss by Regulating Gut Microbiota

Abstract

BackgroundEstrogen deficiency is an etiological factor of postmenopausal osteoporosis (PMO), which not only decreases bone density in vertebrae and long bone, but also aggravates inflammatory bone loss in alveolar bone. Recent evidence has suggested the critical role of gut microbiota in osteoimmunology, and modulation of gut microbiota may have positive influence on bone metabolisms. The present study aimed to evaluate the therapeutic effects of probiotics on alveolar bone loss under estrogen-deficient condition. Inflammatory alveolar bone loss induced by either chronic periodontitis or apical periodontitis was established in ovariectomized (OVX) rats, which were gavage-fed with probiotics daily until sacrifice. Gut microbiota and gut permeability, as well as alveolar bone loss and the related osteoimmune were evaluated to investigate the effects and underlying mechanisms by which probiotics counter the alveolar bone loss under estrogen-deficiency. ResultsWe found that administration of probiotics significantly prevented periodontal and apical bone resorption in OVX rats. Administration of probiotics significantly enriched butyrate-producing genera and enhanced gut butyrate production, resulting in improved intestinal barrier and decreased gut permeability in the OVX rats. Furthermore, the estrogen deprivation-induced inflammatory responses were suppressed in probiotics-treated OVX rats, as reflected by reduced serum levels of inflammatory cytokines and a balanced distribution of CD4+IL-17A+Th17 cells and CD4+CD25+Foxp3+Treg cells in the bone marrow. ConclusionOur data demonstrate that probiotics can effectively attenuate alveolar bone loss by modulating gut microbiota and further regulating osteoimmune, and thus represent a promising adjuvant in the treatment of alveolar bone loss under estrogen-deficiency.

Dynamics of Mmp8 and Osteopontin Content in Oral Liquid of Patients With Oral Diseases in the Presence of Oncopathology

“…In turn, pH has a medium-strength feedback relationship with MMP8 and a direct medium-strength relationship with osteopontin. MMP8 and osteopontin have strong feedback, meaning that an elevation in one of them may indicate a decrease in osteopontin [11,12,15].…”

“…The last decade reports have stated the high level of microorganisms as one of the main factors contributing to the development of diseases associated with the bone tissue destruction and their pathological procession. It is believed that pathological changes in the periodontium occur with an increase in microbial attack caused by the accumulation of microorganisms (biofilm formation) [11,12]. The slackening of specific and nonspecific mechanisms of local and general protection is mostly associated with increased activity of microbial assemblies that results in the development of a clinically pronounced inflammatory reaction.…”

Probiotics and Prebiotics: Any Role in Menopause-Related Diseases?

“…In fact, the increase in permeability which occurs in the intestinal dysbiosis of menopause prompts the activation of Th17 lymphocytes and the release of TNF-α and RANKL, ultimately leading to enhanced osteoclastogenesis and bone resorption [50]. Similar mechanisms are effective at the level of alveolar bone where they are responsible for bone resorption and the progression of the disease [51]. By reducing the plasma levels of cytokines, probiotics may also positively impact on cardiovascular risk which is increased by systemic microinflammation [52][53][54].…”

Systemic antibiotics increase microbiota pathogenicity and oral bone loss

“…18,22 Dysbiosis of the gut microbiota in ovariectomized (OVX) rats aggravates periodontitis through a Th17/Treg imbalance, while probiotics or berberine can improve the gut microbiota and reverse the Th17/Treg imbalance, reducing alveolar bone loss. 23 These studies indicate that a Th17/Treg imbalance might aggravate periodontitis and might be linked to the microbiota.…”