Niekoľko slov na úvod

Clin Osteol 2024; 29(3): 53

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.

Růžičková Olga

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

The EGFR signaling pathway is involved in the regulation of cellular functions of osteoclasts and osteoblasts. Suppression of signaling in this pathway by administration of EGFR-TKIs has been used as an option for anticancer therapy in NSCLC patients with activating mutations of the EGFR gene. We describe the case of an NSCLC patient treated with afacitinib in whom we observed a significant suppression of bone remodeling accompanied by an increase in BMD, which was further potentiated by downstream administration of denosumab. The effect of EGFR-TKI inhibition on bone metabolism has not been sufficiently studied. In vitro data show that EGFR inhibition leads to attenuation of osteoblast and osteoclast activity. Further research is also desirable in view of important overlaps into clinical practice (bone metastases, Skeletal-Related Events, OsteoNecrosis of the Jaw).

Rosa Jan, Fabrik Ivo, Soukup Ondřej, Palička Vladimír

Clin Osteol 2024; 29(3): 80-83

27. kongres slovenských a českých osteológov

Clin Osteol 2024; 29(3): 87-113

Kardiovaskulární riziko při léčbě romosozumabem

Vrablík Michal

Clin Osteol 2024; 29(3): 77-79

Výber z najnovších vedeckých informácií v osteológii

Šteňová Ke Em

Clin Osteol 2024; 29(3): 84-86