Clin Osteol 2024; 29(3): 55-76

Osteoporosis (OP) is a systemic metabolic disease characterized by reduced bone mass and disturbed bone microarchitecture, which causes increased bone fragility and thus increased risk of fractures even with minimal trauma. The goal of osteoporosis treatment is restitution of thinned bone tissue. The ultimate and main goal is fracture prevention. The effectiveness of treatment can also be judged accordingly. An early, indirect indicator of the success of treatment is an increase in bone density, or at least a slowing of bone loss to the physiological limit. Sclerostin is a protein that in humans is encoded by the SOST gene. Sclerostin is produced mainly by osteocytes and has antianabolic effects on bone formation. Romosozumab is a humanized IgG2 monoclonal antibody against sclerostin. The development of an antibody against sclerostin seemed ideal to affect bone formation precisely because of the almost exclusive expression of the SOST gene in bone. Romosozumab has proven to be extremely effective in increasing bone mineral density (BMD), modulating markers of bone turnover and reducing fracture risk. Treatment with romosozumab results in a rapid and effective reduction in fracture risk in postmenopausal women with osteoporosis. The dual mechanism of action makes romosozumab a unique and effective treatment option for osteoporosis, particularly in cases where rapid increases in bone density are desired. The significant reduction in fracture risk represents a substantial clinical benefit.Review articles

Růžičková Olga
Osteologické centrum, Revmatologický ústav, Praha

Osteoporóza (OP) je systémové metabolické onemocnění charakterizované sníženým obsahem kostní hmoty a narušením mikroarchitektury kosti, což je příčinou zvýšené fragility kosti, a tím zvýšeného rizika zlomenin již při minimálním traumatu. Cílem léčby osteoporózy je restituce prořídlé kostní tkáně. Konečným a hlavním cílem je prevence zlomenin. Podle toho je možno také posuzovat účinnost léčby. Časnějším, nepřímým ukazatelem úspěšnosti léčby je zvýšení kostní denzity, nebo alespoň zpomalení jejího úbytku na fyziologickou hranici. Sklerostin je protein, který je u lidí kódován genem SOST. Sklerostin je produkován především osteocyty, má antianabolické účinky na novotvorbu kostí. Romosozumab je humanizovaná monoklonální protilátka IgG2 proti sklerostinu. Vývoj protilátky proti sklerostinu se jevil ideálním k ovlivnění novotvorby kosti právě pro téměř výhradní expresi genu SOST v kosti. Romosozumab se ukázal jako mimořádně účinný při zvyšování denzity kostního minerálu (BMD), modulaci markerů kostního obratu a redukci rizika fraktur. Při léčbě romosozumabem dochází k rychlému a účinnému snížení rizika zlomenin u postmenopauzálních žen s osteoporózou. Dvojí mechanizmus účinku činí z romosozumabu jedinečnou a účinnou možnost léčby osteoporózy, zejména v případech, v nichž je žádoucí rychlé navýšení denzity kostí. Významné snížení rizika zlomenin představuje podstatný klinický přínos.

Keywords: osteoporosis; osteoporotic fracture; romosozumab; sclerostin

Published: December 11, 2024  Show citation

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Růžičková O. Osteoporosis (OP) is a systemic metabolic disease characterized by reduced bone mass and disturbed bone microarchitecture, which causes increased bone fragility and thus increased risk of fractures even with minimal trauma. The goal of osteoporosis treatment is restitution of thinned bone tissue. The ultimate and main goal is fracture prevention. The effectiveness of treatment can also be judged accordingly. An early, indirect indicator of the success of treatment is an increase in bone density, or at least a slowing of bone loss to the physiological limit. Sclerostin is a protein that in humans is encoded by the SOST gene. Sclerostin is produced mainly by osteocytes and has antianabolic effects on bone formation. Romosozumab is a humanized IgG2 monoclonal antibody against sclerostin. The development of an antibody against sclerostin seemed ideal to affect bone formation precisely because of the almost exclusive expression of the SOST gene in bone. Romosozumab has proven to be extremely effective in increasing bone mineral density (BMD), modulating markers of bone turnover and reducing fracture risk. Treatment with romosozumab results in a rapid and effective reduction in fracture risk in postmenopausal women with osteoporosis. The dual mechanism of action makes romosozumab a unique and effective treatment option for osteoporosis, particularly in cases where rapid increases in bone density are desired. The significant reduction in fracture risk represents a substantial clinical benefit. Clinical Osteology. 2024;29(3):55-76.
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