Emerging concepts on the FGF23 regulation and activity.

Fibroblast growth factor 23 (FGF23) discovery has provided new insights into the regulation of Pi and Ca homeostasis. It is secreted by osteoblasts and osteocytes, and acts mainly in the kidney, parathyroid, heart, and bone. The aim of this review is to highlight the current knowledge on the factors modulating the synthesis of FGF23, the canonical and non-canonical signaling pathways of the hormone, the role of FGF23 in different pathophysiological conditions, and the anti-FGF23 therapy. This is a narrative review based on the search of PubMed database in the range of years 2000-2023 using the keywords local and systemic regulators of FGF23 synthesis, FGF23 receptors, canonical and non-canonical pathways, pathophysiological conditions and FGF23, and anti-FGF23 therapy, focusing the data on the molecular mechanisms. The regulation of FGF23 synthesis is complex and multifactorial. It is regulated by local factors and systemic regulators mainly involved in bone mineralization. The excessive FGF23 production is associated with different congenital diseases and with diseases occurring with a secondary high FGF23 production such as in chronic disease kidney and tumor-induced osteomalacia (TIO). The anti-FGF23 therapy appears to be useful to treat chromosome X-linked hypophosphatemia and TIO, but there are doubts about the handle of excessive FGF23 production in CKD. FGF23 biochemistry and pathophysiology are generating a plethora of knowledge to reduce FGF23 bioactivity at many levels that might be useful for future therapeutics of diseases associated with high-serum FGF23 levels.

Melatonin and periodontal tissues: Molecular and clinical perspectives.

Periodontal disease is a frequent chronic inflammatory pathology that implies the destruction of the tissues supporting the teeth, which represents a high sanitary cost. It usually appears associated with other systemic conditions such as diabetes, metabolic syndrome, depression and Alzheimer disease among others. The presence of melatonin and its receptors in the oral cavity supports the hypothesis that this hormone could play a role in homeostasis of periodontal tissues. In the present review we will discuss the potential role of melatonin, a circadian synchronizing hormone, with proved antiinflammatory and antioxidant profile, in the pathogenesis and treatment of periodontitis. Particular emphasis will be placed on the role of the indolamine in the treatment of periodontal disease when this oral condition is comorbid with other pathologies that would also benefit from the therapeutic potential of melatonin and its analogs through diverse mechanisms.

El hueso en el síndrome de Turner / The bone in Turner syndrome

Las pacientes con síndrome de Turner presentan retardo en el crecimiento óseo, que determina una talla final muy inferior a la normal. Muestran anomalías óseas tales como metacarpianos cortos, cubitus valgus, genu valgum, deformidad de Madelung, micrognatia y paladar ojival, cuya etiología se atribuye a la deleción heterocigota del gen SHOX debido a la ausencia total o parcial del cromosoma X. Esta haploinsuficiencia de SHOX podría también contribuir, junto con otros genes, a la hipomineralización ósea predominantemente cortical que presentan estas niñas, la cual se agudiza en la adolescencia y en la vida adulta, etapa en la que se añade hipomineralización del hueso trabecular, producto de la deficiencia estrogénica crónica. Estas alteraciones conducen a un incremento en el riesgo de fracturas. La administración de hormona de crecimiento mejora sustancialmente la talla final, mientras que la terapia de reemplazo hormonal es fundamental para la adquisición y el mantenimiento de la densidad mineral ósea.