Hyperbaric oxygen therapy modulates serum OPG/RANKL in femoral head necrosis patients

Abstract

Hyperbaric oxygen therapy (HBOT) has beneficial effects on avascular necrosis of femoral head (ANFH), but its mechanism of action is still unclear. We investigated if HBOT upregulates serum osteoprotegerin (OPG) and/or inhibits osteoclast activation. 23 patients with unilateral ANFH at stage I, II and III consented to the study: the patients received standard HBOT. Serum OPG levels were obtained at the beginning of HBOT (T0), after 15 sessions (T1), 30 sessions (T2), after a 30-day break (T3), and after 60 sessions (T4). Magnetic resonance imaging (MRI) was obtained at T0 and about one year from the end of HBO treatments. Lesion size was compared between pre- and post-HBOT. 19 patients completed the study. HBOT reduced pain symptoms in all patients. HBOT significantly reduced lesion size in all stage I and II patients and in 2 of 11 stage III patients. HBOT increased serum OPG levels but receptor activator of nuclear factor kappa-B ligand (RANKL) levels did not change.

Hyperbaric Oxygen Therapy Improves the Osteogenic and Vasculogenic Properties of Mesenchymal Stem Cells in the Presence of Inflammation In Vitro

“…Current treatments are typically invasive and, depending on the bone-affecting disease, they involve grafting, surgery, debridement, and/or pharmacotherapy [2]. Recently, hyperbaric oxygen (HBO) has been proposed as an adjunctive therapy in the management of several conditions requiring bone healing [3][4][5][6]. The HBO therapy is the noninvasive administration of 100% O 2 at pressures greater than one atmosphere absolute (ATA).…”

Protective effect of Agrimonia pilosa polysaccharides on dexamethasone‐treated MC3T3‐E1 cells via Wnt/β‐Catenin pathway

“…6,7 Numerous in vitro and in vivo studies also strongly suggested that GCs were able to inhibit the growth and differentiation of bone cells, thus affecting the reconstruction and resorption of bones and decreasing the bone conversion rate, which further leads to bone destruction, and the deposit of apoptotic bone cells. 6,7 Numerous in vitro and in vivo studies also strongly suggested that GCs were able to inhibit the growth and differentiation of bone cells, thus affecting the reconstruction and resorption of bones and decreasing the bone conversion rate, which further leads to bone destruction, and the deposit of apoptotic bone cells.…”

“…role in the initiation and pathogenesis of femoral head necrosis. 6,7 Numerous in vitro and in vivo studies also strongly suggested that GCs were able to inhibit the growth and differentiation of bone cells, thus affecting the reconstruction and resorption of bones and decreasing the bone conversion rate, which further leads to bone destruction, and the deposit of apoptotic bone cells. 8 Therefore, it is critical to understand the pathological mechanisms underpinning this condition and to develop proper therapeutics to disrupt the progression of SANFH.…”

The Impact of Hyperbaric Oxygen Therapy on Serum C-Reactive Protein Levels, Osteoprotegerin Expression, and Osteoclast Numbers in Induced-Periodontitis Diabetic Rats

“…OPG, the soluble decoy receptor for RANKL, inhibits RANKL binding to receptor activator of NF-kB (RANK) and prevents osteoclastogenesis and bone resorption. [32][33][34] RANK-RANKL/OPG ratios and the level of other inflammatory cytokines, such as TNF, constitute critical mediators of osteoclastogenesis in diabetes with periodontal disease. 11,35,36 The RANKL/OPG ratio has been reported to increase in periodontal diseases such as periodontitis.…”