A brief history of rickets
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EDUCATIONAL REVIEW
A brief history of rickets Aaron Friedman 1,2 Received: 13 August 2019 / Accepted: 12 September 2019 # IPNA 2019
Abstract The review provides a historical perspective on the convergence of our understanding of the physiology and pathophysiology of bone, calcium, phosphorus, vitamin D, parathyroid hormone, and FGF-23 their impact on rickets. Keywords Rickets . Parathyroid hormone . Vitamin D . Calcium . Phosphate . FGF-23
Introduction
Bone
This review is based on a presentation at the Pediatric Academic Societies Annual Meeting in 2019. The presentation was part of a symposium honoring the memory of Dr. Russell W Chesney (1941–2015) and his contributions to our understanding of the treatment of bone disease in children, especially those with chronic kidney disease. Rickets is a deficiency disease that affects the young during the period of skeletal growth, is characterized especially by soft and deformed bones, and is caused by failure to assimilate and use calcium and phosphorus normally. Rickets is a clinical/radiologic condition, manifest in children most typically by deformed lower extremities, usually bowing of the legs; by widening of wrist bones; and by protuberant ends of the ribs at the sternum (rachitic rosary). Pain with standing and walking is also a feature of rickets. For most of history, rickets referred to a nutritional/environmental deficiency in vitamin D, calcium, and/or phosphorus. We know that some forms of rickets are more complicated, such as chronic renal failure or excessive phosphate loss and a diminution in production of the active form of vitamin D as seen in hypophosphatemic rickets. In this review, I will briefly touch on the HISTORY surrounding different physiologic “players” in bone physiology and how their roles unfolded to enhance our understanding of rickets (Fig. 1).
Bone growth is dependent on a carefully orchestrated interplay between bone cells (osteoblasts, osteocytes, and osteoclasts) which help build and remodel bone, extracellular matrix, and minerals (especially calcium and phosphorus) that are needed to provide structural integrity and sound scaffolding. The description and function of cells in bone are relatively new. Osteoclasts were first described by Albert von Kollicker in 1873 [1]. He theorized (mostly correctly) that these cells, he called osteoclasts, were necessary for the resorption of bone. Gegenbauer, in 1864, described osteoblasts and speculated on the evolution of osteoblasts to osteocytes [2]. Osteocytes were long considered inert, but Harold Frost, in 1960, opened up study into osteocytes and their role in matrix formation and bone mechanics [3]. From then on, more and more has been learned about the complex involvement of cells, matrix, mineralization, and their roles in bone formation and resorption. Strikingly, more than 100 years passed before significant study of cellular activity in bone health yielded greater understanding of bone as an endocrine organ.
* Aaron Friedman [email protected] 1
University of Minnesota, Minneapoli
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