Animal experiments consistently demonstrated that Vinp treatment significantly attenuated ovariectomy-induced bone loss with a decrease in the osteoclast number and decreases in serum levels of RANKL, TRAP, interleukin-1β, and tumor necrosis factor-alpha, as well as increased serum levels of osteoprotegerin.
In response to pulp exposure, the bone loss and level of MIF mRNA increased in the periradicular periodontitis, which peaked at 14 d, in conjunction with the upregulated expressions of mRNAs for RANKL, proinflammatory cytokines (TNF-α, IL-6, and IL-1β), chemokines (MCP-1 and SDF-1), and MIF's cognate receptors CXCR4 and CD74.
The blockage of androgen receptor significantly increased radiographic bone loss and tissue levels of IL-1α (P <0.05), IL-1β (P <0.001) and IL-10 (P <0.01) compared with the periodontitis group.
Patients with CP and uncontrolled T2D presented severe periodontal disease and inflammation (PPD, p = 0.0072; CAL, p = 0.0480; bone loss, p = 0.0088), higher levels of CASP1 mRNA expression (p = 0.0026), a stronger pattern of staining for NLRP3 and ASC proteins in the epithelium and connective tissues, and significantly higher production of IL-18 (p = 0.0063) and IL-1β (p = 0.0018) in comparison with healthy or CP subjects.
Our findings suggest that blocking IL1β, IL6, and/or TNFα systemically or locally around titanium implants is a promising therapeutic approach for the clinical management of peri-implant bone loss.
Among patients with peri-implantitis, plaque index (p < 0.001), bleeding on probing (p < 0.001), probing depth (p < 0.001), marginal bone loss (p < 0.001), and whole salivary IL-1β (p < 0.001) and IL-6 (p < 0.001) levels were significantly higher in those with diabetes than in those without diabetes.
ALA (100 and 300 mg/kg) intervention to estrogen-deficiency induced bone loss mice (ovariectomized) showed reductions in TRAP+ osteoclasts count, CTX-I expression, levels of IL-1β, IL-2, IL-6, IL10, TNF-α and MCP-1 and iNOS and COX-2.
To compare bleeding on probing (BoP), probing depth (PD; ≥ 4 mm), radiographic (peri-implant crestal bone loss [CBL]), and immunologic inflammatory (interleukin-1beta [IL-1β] and matrix metalloproteinase-9 [MMP-9]) parameters around dental implants with cement-retained (CR) and screw-retained (SR) implant-supported crowns.
Using both in vitro and in vivo studies, we observed that EETs significantly attenuated bone loss and inhibited osteoclast formation and activity, which were associated with a decreased receptor activator of NF-κB ligand (RANKL):osteoprotegerin ratio and serum levels of TNF-α and IL-1β.
We thus conclude that IL-17A is a key mediator of TNF-α-induced bone loss by closely interacting with IL-1 in blocking bone protective T-cell responses.
At the patient level, these were: age, gender, mean bone loss (mean CEJ-BD)(T0), the interleukin-1 (IL-1) genotype, the interaction between mean bone loss, and IL-1 genotype (mean CEJ-BD(T0) x IL-1 genotype).
We therefore investigated whether the idiopathic early marginal bone loss around implants is related to polymorphisms in the IL-1 gene.We performed a case-control study.
This study suggests that in heavy cigarette smokers, carriage of a functionally significant IL-1 gene complex polymorphism is associated with an increased risk for peri-implant bone loss following prosthetic reconstruction and during the supportive periodontal care phase of the treatment.
We have investigated the expression and synthesis of potential bone-resorbing cytokines, interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor (TNF) in rheumatoid arthritic (RA) and osteoarthritic (OA) bone, two common diseases which are associated with bone loss.