About this Research Topic
An adequate supply of calcium and phosphate is required for successful mineralisation of osteoid tissue in bone. Failure of this mineral supply, no matter the reason, results in a mineralisation defect. In adults this leads to osteomalacia (impaired mineralisation of bone matrix) and osteoporosis (overall low bone mass). In children, this failure leads to rickets.
Rickets comprises a group of bone disorders specific to the growing child. As in adults, it causes generalized osteomalacia, but as children have open growth plates, there is a failure of mineralisation at the metaphysis. This lead to the classic bony features of rickets, including: weakening of long bones, particularly those involved in weight bearing, leading to lower limb bowing; poor growth; delayed dentition; slowed motor development, and rarely, pathological fracture. The growth plate defect leads to the other stigmata of rickets, including swelling at the ends of long bones, particularly wrists and knees, costo-chondral abnormalities known as “rachitic rosary”, and frontal bossing of the skull. While usually most attention is focused on calcium and vitamin D, phosphate plays a crucial role in the pathogenesis of rickets and the appearance of the classic clinical and biochemical features of rickets.
The pathogenic mechanisms, briefly outlined above, are common to all forms of rickets, both acquired and genetic, and can be used to classify rickets i.e. as PTH dependant (e.g. VDDR/nutritional rickets, VDR and post-receptor mutations); FGF23 dependant (e.g. X-linked or autosomally inherited forms of hypophosphatemic rickets); or renal (Fanconi syndrome).
There remains a need to better understand all forms of rickets, from common causes such as classic vitamin D deficiency rickets to the rarer forms. With this Research Topic, we aim to provide a platform for researchers interested in this area to contribute original research studies and review articles on, but not limited to, new developments in not only epidemiology of all forms of childhood rickets, but also exploring pathogenic mechanisms, as well as prevention and treatment.
Rickets comprises a group of bone disorders specific to the growing child. As in adults, it causes generalized osteomalacia, but as children have open growth plates, there is a failure of mineralisation at the metaphysis. This lead to the classic bony features of rickets, including: weakening of long bones, particularly those involved in weight bearing, leading to lower limb bowing; poor growth; delayed dentition; slowed motor development, and rarely, pathological fracture. The growth plate defect leads to the other stigmata of rickets, including swelling at the ends of long bones, particularly wrists and knees, costo-chondral abnormalities known as “rachitic rosary”, and frontal bossing of the skull. While usually most attention is focused on calcium and vitamin D, phosphate plays a crucial role in the pathogenesis of rickets and the appearance of the classic clinical and biochemical features of rickets.
The pathogenic mechanisms, briefly outlined above, are common to all forms of rickets, both acquired and genetic, and can be used to classify rickets i.e. as PTH dependant (e.g. VDDR/nutritional rickets, VDR and post-receptor mutations); FGF23 dependant (e.g. X-linked or autosomally inherited forms of hypophosphatemic rickets); or renal (Fanconi syndrome).
There remains a need to better understand all forms of rickets, from common causes such as classic vitamin D deficiency rickets to the rarer forms. With this Research Topic, we aim to provide a platform for researchers interested in this area to contribute original research studies and review articles on, but not limited to, new developments in not only epidemiology of all forms of childhood rickets, but also exploring pathogenic mechanisms, as well as prevention and treatment.
Keywords: Rickets, Vitamin D, Bone Health, Epidemiology, Prevention
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