Blounts disease is an important differential diagnosis because it causes knee deformities in a similar fashion to rickets namely bow legs or genu varum. Infants with rickets can have bone fractures. This sometimes leads to child abuse allegations. This issue appears to be more common for solely nursing infants of black mothers, in winter in temperate climates, suffering poor nutrition and no vitamin D supplementation. People with darker skin produce less vitamin D than those with lighter skin, for the same amount of sunlight. Treatment
Diet and sunlight
Treatment involves increasing dietary intake of calcium, phosphates and vitamin D. Exposure to ultraviolet B light (most easily obtained when the sun is highest in the sky), cod liver oil, halibut-liver oil, and viosterol are all sources of vitamin D.A sufficient amount of ultraviolet B light in sunlight each day and adequate supplies of calcium and phosphorus in the diet can prevent rickets. Darker-skinned people need to be exposed longer to the ultraviolet rays. The replacement of vitamin D has been proven to correct rickets using these methods of ultraviolet light therapy and medicine.Recommendations are for 400 international units (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance. Supplementation
Sufficient vitamin D levels can also be achieved through dietary supplementation and/or exposure to sunlight.
Diagnosis
Rickets may be diagnosed with the help of:

Blood tests:Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones. This can show enlarged limbs and joints. A bone density scan may be undertaken. Radiography typically show widening of the zones of provisional calcification of the metaphyses secondary to unmineralized osteoid. Cupping, fraying, and splaying of metaphyses typically appears with growth and continued weight bearing. These changes are seen predominantly at sites of rapid growth, including the proximal humerus, distal radius, distal femur and both the proximal and the distal tibia. Therefore, a skeletal survey for rickets can be accomplished with anteroposterior radiographs of the knees, wrists, and ankles. Types
Vitamin D-related ricketsVitamin D deficiency
Vitamin D-dependent rickets (VDDR)Type 1: insufficiency in activation
VDDR1A: 25-Hydroxyvitamin D3 1-alpha-hydroxylase deficiency
VDDR1B: CYP2R1 deficiency
Type 2: resistance to calcitriol
VDDR2A: calcitriol receptor mutation
VDDR2B: unknown nuclear ribonucleoprotein interfering with signal transduction
Type 3: excessive inactivation (CYP3A4 mutation, dominant)
Hypocalcemia-related rickets
Hypocalcemia
Chronic kidney failure (CKD-BMD)
Hypophosphatemia-related rickets
Congenital
Vitamin D-resistant rickets
Autosomal dominant hypophosphatemic rickets (ADHR)
Autosomal recessive hypophosphatemic rickets (ARHR)
Hypophosphatemia (typically secondary to malabsorption)
Fanconis syndrome
Secondary to other diseases
Tumor-induced osteomalacia
McCune-Albright syndrome
Epidermal nevus syndrome
Dents disease

Differential diagnosis
Osteochondrodysplasias, also known as genetic bone diseases, may mimic the clinical picture of rickets in regard to the features of bone deformities. The radiologic picture and the laboratory findings of serum calcium, phosphate and alkaline phosphatase are important differentiating factors.