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Rickets and Metabolic Bone Disorders

We begin by understanding rickets as a disorder of bone mineralization in the growing skeleton, reviewing its clinical presentation: bowed legs, genu varum and valgum, widened wrists, delayed milestones, rachitic rosary, Harrison sulcus, skull bossing, delayed dentition, muscle weakness, hypocalcemic seizures, and systemic complications. From there, we analyze the radiographic hallmarks—widened and cupped growth plates, metaphyseal splaying, Looser zones, pseudofractures, short stature, and deformities affecting every physis. Next, we explore the classification of rickets, structured around what is lacking at the osteoblast–bone interface: calcium, phosphate, or alkaline phosphatase. Nutritional rickets, gastrointestinal malabsorption, vitamin D–dependent rickets types I and II, renal tubular disorders, renal osteodystrophy, and hypophosphatasia are all examined in detail. The lecture emphasizes pathophysiology, clinical features, and the biochemical findings that differentiate these disorders. Particular attention is given to nutritional rickets, once endemic in industrialized societies and still prevalent in developing regions. We discuss the role of vitamin D deficiency, low-calcium diets, sunlight exposure, and prevention strategies with supplementation. X-linked hypophosphatemia is explained as the most common inherited rickets, including its PHEX gene defect, phosphate wasting, inappropriately low calcitriol, dental abscesses, and orthopedic deformities. Rare conditions such as 1-alpha hydroxylase deficiency (type I) and end-organ resistance to vitamin D (type II) are reviewed, including their clinical signs and therapeutic challenges. We then transition to renal osteodystrophy, where chronic kidney disease disrupts phosphate and calcium balance, driving secondary hyperparathyroidism. Students will see the radiographic images of brown tumors, subperiosteal resorption, rickets-like deformities, Looser zones, slipped capital femoral epiphysis, and soft bone complications that require medical and orthopedic management. Treatment principles include calcitriol supplementation, phosphate binders, dialysis, transplantation, parathyroid management, and orthopedic stabilization. Finally, the lecture concludes with a clinical approach: how to evaluate a child presenting with suspected rickets—history taking, physical examination, lab investigations (calcium, phosphate, alkaline phosphatase, vitamin D metabolites, PTH), and radiographic interpretation—leading to a differential diagnosis and targeted therapy. This video is designed as a complete, immersive medical classroom experience. Whether you are preparing for exams, working in pediatrics, orthopedics, or nephrology, or simply interested in the intersection of bone biology and clinical disease, this lecture will provide clarity, depth, and memorable explanations that bridge anatomy, physiology, pathology, and clinical medicine.