Abstract
ObjectivesFluorine, an organic trace element, has been shown to unfavourably effect osteoclasts function at a low dose. Use of hydroxyapatite (HA) has been effective in exploring its roles in promoting bone repair. In this study, we used HA modified with fluorine to investigate whether it could influence osteoclastic activity in vitro and ovariectomy‐induced osteoclasts hyperfunction in vivo.Materials and methodsFluorohydroxyapatite (FHA) was obtained and characterized by scanning electron microscope (SEM). Osteoclasts proliferation and apoptosis treated with FHA were assessed by MTT and TUNEL assay. SEM, F‐actin, TRAP activity and bone resorption experiment were performed to determine the influence of FHA on osteoclasts differentiation and function. Moreover, HA and FHA were implanted into ovariectomized osteoporotic and sham surgery rats. Histology and Micro‐CT were examined for further verification.ResultsFluorine released from FHA slowly and sustainably. FHA hampered osteoclasts proliferation, promoted osteoclasts apoptosis, suppressed osteoclasts differentiation and function. Experiments in vivo validated that FHA participation brought about an inhibitory effect on osteoclasts hyperfunction and less bone absorption.ConclusionThe results indicated that FHA served as an efficient regulator to attenuate osteoclasts formation and function and was proposed as a candidature for bone tissue engineering applications.
Highlights
The dynamic process of bone remodelling is maintained through tight intercoordination between bone formation and bone absorption owing to the activities of osteoblasts and osteoclasts.[1,2]
Hydroxyapatite is vulnerable when exposed to hyperfunction of osteoclasts.[22]
A convincing evidence was provided that FHA had an inhibitory effect on osteoclastic activity and suppressed bone resorption in OVX rats via comparison to pure HA
Summary
The dynamic process of bone remodelling is maintained through tight intercoordination between bone formation and bone absorption owing to the activities of osteoblasts and osteoclasts.[1,2] The exquisite balance can be interrupted result from osteoclasts hyperfunction triggered by various pathologic conditions, including inflammation, metabolic and endocrine disorders.[3,4] Patients with osteoporosis, diabetes and Paget's disease suffer from accelerated bone destruction and pathological bone loss.[5,6,7] Osteoclasts are multinucleated giant cells exactly verified to degrade bone solely and essential for maintaining mineral homeostasis.[8,9] Increased number or function of osteoclasts cause bone absorption to prevail over formation, leading to bone microstructural deterioration and increased bone frailty, and biomaterial implants failure.[10,11,12]. Fluorine exerts positive actions on maintaining bone structure and function.[18] Fluorine bounds to a mitogenic stimulus for osteoblasts and possesses the capability to promote osteoblasts proliferation, enhance bone formation.[19] studies have shed light on the preventive effects of fluorine on osteoclastogenesis through restraining osteoclasts formation and decreasing expressions of matrix metalloproteinase 9 and tartrate‐resistant acid phosphatase.[20] Titanium surface modified with fluoride could increase the synthesis of osteoprotegerin, and impeded osteoclasts activation and differentiation were followed.[21]. Its effects on regulating bone metabolism in osteoporotic rat model in vivo were explored, expecting to provide a therapeutic agent for more stable implants under osteoclasts hyperfunction conditions
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