Populations and Risk Factors
- Children before epiphyseal plate fusion
- Inadequate sunlight exposure or poor dietary vitamin D/calcium intake
- Darker skin pigmentation (melanin reduces cutaneous vitamin D synthesis)
- Malabsorption syndromes: celiac disease, cystic fibrosis, Crohn disease
- Chronic kidney disease (renal rickets: kidneys cannot activate vitamin D)
- Rare genetic forms: X-linked hypophosphatemic rickets (renal phosphate wasting)
- Anticonvulsant medication use (accelerates vitamin D catabolism)
- Exclusively breastfed infants without vitamin D supplementation
Causes and Pathophysiology
- Primary defect: Inadequate or delayed calcification of extracellular bone matrix due to insufficient vitamin D, calcium, or phosphorus
- Growth plate disruption: New bone at epiphyseal growth plates fails to ossify properly. Cartilage overgrows, making plates wide and irregular — this is the radiographic hallmark
- Soft bone deformation: Unmineralized bone remains "rubbery" and deforms under weight-bearing stress, producing characteristic skeletal deformities
- Site-specific deformation: Infants develop head and chest deformities first (gravitational stress). Weight-bearing children develop limb bowing
- Muscular involvement: Children often have hypotonic muscles (low muscle tone), further destabilizing fragile joints and delaying motor milestones
Signs and Symptoms
- Bowed legs (genu varum) or knock-knees (genu valgum)
- Rachitic rosary: visible/palpable beads at costochondral junctions
- Rachitic potbelly: prominently protruding abdomen
- Enlarged, soft skull with delayed closure of fontanels (craniotabes)
- Stunted growth (height far below normal range)
- Slow tooth development and dental enamel defects
- Deep bone pain and tenderness
- Difficulty standing or walking. Waddling gait
- Red flags: Pathologically weak bones with extreme fracture risk; sudden unexplained limb pain may indicate pathologic fracture requiring imaging
CMTO Exam Relevance
- Category A7 Systemic Conditions (Endocrine/Metabolic)
- Rickets is the childhood counterpart to osteomalacia — both involve defective mineralization, distinguished by whether growth plates are open (rickets) or closed (osteomalacia)
- Pathologically weak bones with extreme fracture risk — massage pressure modification is essential
- Recognize classic triad: bowed legs, rachitic rosary, rachitic potbelly
- Renal rickets from chronic kidney disease is an important secondary cause
Massage Therapy Considerations
- Contraindications: Rigorous or deep massage and vigorous stretching are contraindicated due to extreme bone fragility and pathological fracture risk
- Indications: Gentle, non-intrusive massage may help address deep bone pain, muscle weakness, and provide comfort
- Pressure: Significantly reduced to respect pathological bone weakness — lighter than standard pediatric pressure
- Pediatric approach: Parental consent and presence required. Sessions should be brief and age-appropriate
- Referral: Sudden unexplained limb pain should prompt referral for medical imaging (suspect pathologic fracture)
Key Takeaways
- Rickets is a childhood metabolic bone disease caused primarily by vitamin D deficiency, leading to inadequate calcification and soft, deformable bones
- Rigorous or deep massage and vigorous stretching are contraindicated due to extreme bone fragility and pathological fracture risk
- Classic signs include bowed legs, rachitic rosary (beads at costochondral junctions), rachitic potbelly, and delayed fontanel closure
- Sudden unexplained limb pain should prompt referral for medical imaging to rule out pathologic fracture
- Rickets is the childhood counterpart to osteomalacia. It occurs before epiphyseal plates have fused