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.
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.
In the model that included IL-1 genotype and heavy smoking, none of the clinical parameters added significantly to the model for tooth loss while mobility, probing depth, crown-to-root ratio, and percent bone loss added significantly to the model, which included IL-1 genotype in non-smokers.
Treatment with IL-1ra blocks the bone loss associated with ovariectomy in animals and the IL-1 receptor antagonist gene (IL-1RN) is therefore a potential candidate gene for the regulation of postmenopausal bone loss.