Probiotics enhance alveolar bone microarchitecture, intestinal morphology and estradiol levels in osteoporotic animals.

BACKGROUND AND OBJECTIVE: Osteoporosis is associated with bone microarchitecture alterations, and the depletion of estrogen during menopause is a major contributing factor to its development. The literature highlights the noteworthy role of gut microbiota in bone metabolism, particularly in the progression of osteoporosis. Periodontal disease leads to alveolar bone loss, which may be influenced by estrogen deficiency, and this mechanism is intricately associated with an imbalance in systemic microbiota. The aim of this study was to evaluate the effects of Bifidobacterium animalis subsp. lactis HN019 (B. lactis HN019) and Lacticaseibacillus casei 01 (L. casei 01) administrations on an osteoporosis animal model. MATERIALS AND METHODS: Thirty-three female rats were randomly divided into three groups: control (C-OVX), C-OVX-HN019 and C-OVX-LC01. All animals were ovariectomized. In groups C-OVX-HN019 and C-OVX-LC01, the probiotics were administered for 4 months. All animals were euthanized after 16 weeks from ovariectomy. Microtomographic, histopathological and immunohistochemical examinations were conducted on periodontal tissues, whereas histomorphometry, histopathological and immunohistochemical analyses were carried out on the intestine. The levels of estradiol were assessed in blood using an immunoenzymatic assay. The data were subjected to statistical analyses (p < .05). RESULTS: The C-OVX-LC01 group exhibited a significant reduction in alveolar bone porosity and an increase in connective tissue density compared to C-OVX (p < .05). The C-OVX-HN019 and C-OVX-LC01 groups presented reduced expression of TRAP and RANKL compared to the C-OVX (p < .05). The C-OVX group presented villi defects, mild neutrophil infiltration, decrease in both villous height and intestinal crypts and reduced expression of intestinal junctional epithelium markers e-cadherin and claudin 01 compared to C-OVX-HN019 and C-OVX-LC01 (p < .05). The C-OVX group had lower estradiol levels than C-OVX-HN019 and C-OVX-LC01 (p < .05). CONCLUSION: The probiotic therapy promoted a reduction in alveolar bone destruction and intestinal permeability as well as an increase in estradiol levels in ovariectomized rats. Specifically, the probiotic strain Lacticaseibacillus casei 01 exhibited greater effectiveness compared to Bifidobacterium animalis subsp. lactis HN019, indicating strain-dependent outcomes.

Effects of Prebiotic Therapy on Gastrointestinal Microbiome of Individuals with Different Inflammatory Conditions: A Systematic Review of Randomized Controlled Trials.

Prebiotics are substrates selectively utilized by host microorganisms conferring a health benefit. The effects of prebiotics on the gut microbiome of individuals with inflammatory processes need further investigations. The purpose of this study was to evaluate the effects of prebiotics on the gastrointestinal microbiome of individuals with some types of inflammatory conditions. Randomized controlled clinical trials (RCTs) evaluating the effects of different prebiotics on the gut microbiome were included. A systematic review of the literature including searches in PubMed/MEDLINE, EMBASE, Cochrane Library, Web of Science, and Scopus databases was performed until 23 March 2023. The risk of bias was assessed using the Cochrane Collaboration's criteria. Qualitative data was tabulated to facilitate comparisons and represented in the form of descriptive statistics and summary tables. Thirty trials, ranging from 12 to 135 patients, were included. The most commonly used prebiotic type was inulin-type fructans, and the treatment duration ranged from 1 to 36 weeks. The majority of the trials investigated the gut microbiome using 16 s rRNA gene sequencing on the Illumina Miseq platform. In general, prebiotic therapy exerted positive effects on inflammatory conditions. An increase in Bifidobacterium genus was the most common shift in bacterial composition observed. Within the limits of this systematic review, it can be suggested that prebiotic therapy presents the potential to favorably modulate the gastrointestinal microbiome of individuals with different types of inflammatory conditions.

Effects of Bifidobacterium animalis subsp. lactis HN019 on ligature-induced periodontitis in rats with experimental rheumatoid arthritis.

The purpose of this study was to evaluate the effects of systemic administration of the probiotic Bifidobacterium animalis subsp. lactis HN019 (HN019) on ligature-induced periodontitis in rats with experimental rheumatoid arthritis (RA). 28 rats were divided into four groups (n=7): RA (rheumatoid arthritis), RA/PROB (probiotic), RA/EP (experimental periodontitis) and RA/EP/PROB. From day zero, HN019 was added daily to the water of the PROB groups animals until the end of the experiment. From day seven, RA was induced. On day 28, in EP groups, ligatures were positioned around mandibular first molars and remained in position for 11 days, in order to induce periodontitis. The animals were euthanised on day 39. Microtomographic, histomorphometric, immunoenzymatic and microbiological analyses were performed. Data were statistically analysed (P<0.05). Group RA/EP/PROB presented reduced alveolar bone loss, tumour necrosis factor-α and interleukin (IL)-6 levels and increased IL-17 levels when compared with group RA/EP. There were no significant differences regarding connective tissue attachment level and IL-10 levels between groups RA/EP and RA/EP/PROB. Group RA/PROB showed decreased anti-citrullinated protein antibodies levels when compared with groups RA and RA/EP. Group RA/EP/PROB presented a higher rate of aerobic/anaerobic bacteria than group RA/EP. Systemic administration of HN019 promoted a protective effect against periodontal tissue destruction, decreasing both bone loss and inflammatory mediators and increasing the proportion of bacteria compatible with periodontal health, in rats with experimental RA and EP.

Effect of curcumin on bone tissue in the diabetic rat: repair of peri-implant and critical-sized defects.

This study determined the effect of curcumin on bone healing in animals with diabetes mellitus (DM). One hundred rats were divided into five groups: DM+PLAC, DM+CURC, DM+INS, DM+CURC+INS, and non-DM (CURC, curcumin; PLAC, placebo; INS, insulin). Critical calvarial defects were created and titanium implants were inserted into the tibiae. Calvarial defects were analyzed histometrically, and BMP-2, OPN, OPG, RANKL, Runx2, Osx, ß-catenin, Lrp-5, and Dkk1 mRNA levels were quantified by PCR. The implants were removed for a torque evaluation, the peri-implant tissue was collected for mRNA quantification of the same bone-related markers, and the tibiae were submitted to micro-computed tomography. The DM+CURC+INS and non-DM groups exhibited greater closure of the calvaria when compared to the DM+PLAC group (P<0.05). Increased retention of implants was observed in the DM+CURC, DM+CURC+INS, and non-DM groups when compared to the DM+PLAC group (P<0.05). CURC improved bone volume and increased bone-implant contact when compared to DM+PLAC (P<0.05). In calvarial samples, CURC favourably modulated RANKL/OPG and Dkk1 and improved ß-catenin levels when compared to DM+PLAC (P<0.05). In peri-implant samples, Dkk1 and RANKL/OPG were down-regulated and BMP-2 up-regulated by CURC when compared to DM+PLAC (P<0.05). CURC reverses the harmful effects of DM in bone healing, contributing to the modulation of bone-related markers.

Rosuvastatin promotes benefits on induced periodontitis in hypertensive rats.

BACKGROUND AND OBJECTIVE: The potential benefits of statins in modulating periodontal disease is supported by in vitro and clinical studies showing statins can induce a lower expression of proinflammatory cytokines and matrix metalloproteinases. The aim of this study was to evaluate the effects of rosuvastatin (ST) on ligature-induced periodontitis in spontaneously hypertensive rats (SHR). MATERIAL AND METHODS: Fifty-four adult male rats were divided into three groups: SHR-C, SHR-L and SHR-L-ST (C, control; L, ligature groups). In the SHR-L-ST group, animals were treated with daily 2 mg/kg ST administration. In L groups, a ligature remained around mandibular first molars for 10 d. Each group was divided for killing at 10 or 21 d postoperatively. Microtomographic and histometric analyses were performed. Osteoclastogenesis was evaluated by tartrate-resistant acid phosphatase assay and gene expression of 84 proinflammatory mediators by polymerase chain reaction array. RESULTS: The SHR-L-ST group showed reduced bone loss and attachment loss in comparison with the SHR-L group at both 10 and 21 d postoperatively (p < 0.05). ST decreased the amount of tartrate-resistant acid phosphatase-positive cells compared with the SHR-L group at both 10 and 21 d (p < 0.05). The SHR-L-ST group presented 14 genes differentially expressed when compared with SHR-L group, featuring a downregulated gene profile at 10 d. CONCLUSION: Statin therapy may promote a protective effect against alveolar bone and connective tissue attachment losses attributable to periodontitis in hypertensive rats through inflammatory gene profile modulation.

Bone healing in critical-size defects treated with platelet-rich plasma activated by two different methods. A histologic and histometric study in rat calvaria.

BACKGROUND AND OBJECTIVE: The purpose of this study was to analyze histologically the influence of platelet-rich plasma (PRP) coagulated with two different activators on bone healing in surgically created critical-size defects (CSD) in rat calvaria. MATERIAL AND METHODS: Forty-eight rats were divided into three groups: C, PRP-C and PRP-T. An 8 mm diameter CSD was created in the calvarium of each animal. In group C, the defect was filled by a blood clot only. In groups PRP-C and PRP-T, the defect was filled with PRP activated with either calcium chloride or thromboplastin solution, respectively. Each group was divided into two subgroups (n = 8 per subgroup) and killed at either 4 or 12 weeks postoperatively. Histologic and histometric analyses were performed. The amount of new bone formed was calculated as a percentage of the total area of the original defect. Percentage data were transformed into arccosine for statistical analysis (analysis of variance, Tukey's post hoc test, p < 0.05). RESULTS: No defect completely regenerated with bone. Group PRP-C had a statistically greater amount of bone formation than groups C and PRP-T at both time points of analysis. No statistically significant differences were observed between groups C and PRP-T. CONCLUSION: It can be concluded that the type of activator used to initiate PRP clot formation influences its biological effect on bone healing in CSD in rat calvaria.

Bone healing in critical-size defects treated with platelet-rich plasma: a histologic and histometric study in rat calvaria.

BACKGROUND AND OBJECTIVE: The purpose of this study was to analyze histologically the influence of autologous platelet-rich plasma on bone healing in surgically created critical-size defects in rat calvaria. MATERIAL AND METHODS: Thirty-two rats were divided into two groups: the control group (group C) and the platelet-rich plasma group. An 8-mm-diameter critical-size defect was created in the calvarium of each animal. In group C the defect was filled by a blood clot only. In the platelet-rich plasma group, 0.35 mL of platelet-rich plasma was placed in the defect and covered by 0.35 mL of platelet-poor plasma. Both groups were divided into subgroups (n = 8) and killed at either 4 or 12 wk postoperatively. Histometric (using image-analysis software) and histologic analyses were performed. The amount of new bone formed was calculated as a percentage of the total area of the original defect. Percentage data were transformed into arccosine for statistical analysis (analysis of variance, Tukey, p < 0.05). RESULTS: No defect completely regenerated with bone. The platelet-rich plasma group had a statistically greater amount of bone formation than group C at both 4 wk (17.68% vs. 7.20%, respectively) and 12 wk (24.69% vs. 11.65%, respectively) postoperatively. CONCLUSION: Within the limits of this study, it can be concluded that platelet-rich plasma placed in the defects and covered by platelet-poor plasma significantly enhanced bone healing in critical-size defects in rat calvaria.