Abstract
BackgroundPro-inflammatory cytokines possess osteoclastogenic or anti-osteoclastogenic activities. They influence osteoclasts directly or via the receptor activator of nuclear factor κB (RANK), RANK ligand (RANKL) and osteoprotegerin (OPG) system. Recent evidence suggests that inflammation may play a role in osteoporosis (OP) and osteoarthritis (OA). We aimed therefore to determine whether there is a difference between both groups: first, in the expression of the osteoclastogenic and anti-osteoclastogenic cytokines, second, in correlation of these cytokines with bone mineral density (BMD) and levels of bone turnover markers (BTM) and third, in correlation between the expression of these cytokines and osteoclast specific genes and RANK/RANKL/OPG genes.MethodsHuman bone samples from 54 age and sex matched patients with OP or OA were collected during hip arthroplasty surgery. The expression of 25 genes encoding pro-inflammatory cytokines, their receptors, osteoclast specific genes and RANK/RANKL/OPG genes was measured using quantitative real-time PCR. Total hip, femoral neck and lumbar spine BMD and BTM in blood samples were measured. The comparison between OP and OA was assessed using Student's t-test or Mann-Whitney U test and correlations between gene expression, BMD and BTM were determined using nonparametric correlation.ResultsThe results demonstrated a higher expression of interleukin (IL)-6 and IL-1α in OP, and interferon (IFN)-γ in OA (p < 0.0005). Negative correlations of total hip BMD with tumor necrosis factor-α (TNF-α) in OA and with RANKL/RANK in OP were found (p < 0.05). Significant correlations with BTM were shown for IL-1α and IFN-γ in OP (rho = 0.608 and -0.634) and for TNF-α, IL-6 and transforming growth factor-β1 (TGF-β1) in OA (rho = 0.591, -0.521 and 0.636). Results showed OP specific negative correlations (IFN-γ with ITGB3, IFN-β1 with CTSK, tartrate resistant acid phosphatase (TRAP), CALCR, RANK, RANKL, IL-1α with CTSK, OPG, IL-17A with CALCR) and positive (TGF-β1 with CTSK, TRAP, RANK), and OA specific negative (IL-1α with osteoclast associated immunoglobulin-like receptor (OSCAR), TNF-α with RANK, RANKL, OPG) and positive (IL-6 with RANK, RANKL, OPG) correlations.ConclusionsOur results demonstrate that the relationship between osteoclastogenic and anti-osteoclastogenic pro-inflammatory cytokines differs in human OP and OA bone and could present an important factor for characteristics of OP and OA bone phenotypes.
Highlights
Pro-inflammatory cytokines possess osteoclastogenic or anti-osteoclastogenic activities
OP and OA are two contrasting bone phenotypes in terms of bone mineral density (BMD) [33], and both have only recently been considered as inflammatory bone disorders [3,4] in which osteoclastogenic and anti-osteoclastogenic cytokines might play important roles. Given these observations the aim of our study was to investigate, whether there is a difference between OP and OA: first, in the expression of the osteoclastogenic and anti-osteoclastogenic cytokines, second, in correlation of these cytokines with BMD and levels of bone turnover markers (BTM) and third, in correlation of these cytokines with osteoclast specific genes and Receptor activator of nuclear factor κB (RANK)/RANK ligand (RANKL)/OPG genes
The two groups differed in body mass index (BMI) and BMD values of the hip, femoral neck and lumbar spine, these values being significantly lower in OP than in OA
Summary
Pro-inflammatory cytokines possess osteoclastogenic or anti-osteoclastogenic activities. They influence osteoclasts directly or via the receptor activator of nuclear factor B (RANK), RANK ligand (RANKL) and osteoprotegerin (OPG) system. Osteoclasts are influenced by a variety of pro-inflammatory osteoclastogenic and anti-osteoclastogenic cytokines that can either stimulate or suppress their activity [1]. As the immune system is triggered during estrogen deficiency or inflammation, both osteoporosis (OP) and osteoarthritis (OA) are being recently considered as inflammation driven bone disorders [3,4]. Serum IL-6 accounted for up to 34% of the total variance of change in bone mineral density (BMD) after the menopause [10]. Blockade of TNF and IL-1 reduced bone resorption in postmenopausal OP women [11]
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