Abstract
Osteoporosis is an unavoidable public health problem in an aging or aged society. Anti-resorptive agents (calcitonin, estrogen, and selective estrogen-receptor modulators, bisphosphonates, anti-receptor activator of nuclear factor κB ligand antibody along with calcium and vitamin D supplementations) and anabolic agents (parathyroid hormone and related peptide analogs, sclerostin inhibitors) have major roles in current treatment regimens and are used alone or in combination based on the pathological condition. Recent advancements in the molecular understanding of bone metabolism and in bioengineering will open the door to future treatment paradigms for osteoporosis, including antibody agents, stem cells, and gene therapies. This review provides an overview of the molecular mechanisms, clinical evidence, and potential adverse effects of drugs that are currently used or under development for the treatment of osteoporosis to aid clinicians in deciding how to select the best treatment option.
Highlights
At the Consensus Development Conference in 1993, osteoporosis was defined as a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture [1]
EspecTiraelalytm, tehnetys feoxrcolussteivoeployrosescisreatree sdcilveirdoesdtinin[t1o3s]e.veral groups, including therapies based on essential nutriTenretsa,tmanetni-trsesfoorrptoisotneodprourgoss,iasnaarbeoldicivdirduegds,ianntod csoemvebrianlagtiroonusposf, tihnecsleu.dMinagjotrheesrsaepniteisalbnausterdienotns efossretnhteiatlrenauttmrieennttso, faonstit-eroepsoorrpotsiiosnarderucaglsc,iaunma,bvoiltiacmdriungDs, aanndd cvoimtambininatKio2n, salolfotfhweshei.cMh aajroeriensvsoenlvtieadl nutrients for the treatment of osteoporosis are calcium, vitamin D, and vitamin K2, all of which are involved in bone metabolism
This review summarized the mechanisms of action, major clinical trials, and side effects for current therapeutics for osteoporosis
Summary
At the Consensus Development Conference in 1993, osteoporosis was defined as a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture [1]. EspecTiraelalytm, tehnetys feoxrcolussteivoeployrosescisreatree sdcilveirdoesdtinin[t1o3s]e.veral groups, including therapies based on essential nutriTenretsa,tmanetni-trsesfoorrptoisotneodprourgoss,iasnaarbeoldicivdirduegds,ianntod csoemvebrianlagtiroonusposf, tihnecsleu.dMinagjotrheesrsaepniteisalbnausterdienotns efossretnhteiatlrenauttmrieennttso, faonstit-eroepsoorrpotsiiosnarderucaglsc,iaunma,bvoiltiacmdriungDs,, aanndd cvoimtambininatKio2n, salolfotfhweshei.cMh aajroeriensvsoenlvtieadl nutrients for the treatment of osteoporosis are calcium, vitamin D, and vitamin K2, all of which are involved in bone metabolism. Anti-resorptive drugs, which suppress bone resorption, include calcitonin, estrogen and selective estrogen receptor modulators (SERMs), bisphosphonates (BPs), and anti-RANKL antibody. Stem cell therapies for osteoporosis have been receiving increased attention in recent years. These therapies are helpful for the treatment of osteoporosis as evidenced by numerous clinical trials. We summarize the mechanisms of action of current and anticipated drugs in terms of basic bone biology, major clinical trials, and side effects, to aid clinicians in deciding how to select the best treatment option (Table 1). PTH, parathyroid hormone; SERMs, selective estrogen receptor modulators; RANKL, receptor activator of nuclear factor κB ligand; OPG, osteoprotegerin; N/A, not available; BMP, bone morphogenetic protein
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