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.
History
Greek physician Soranus of Ephesus, one of the chief representatives of the Methodic school of medicine who practiced in Alexandria and subsequently in Rome, reported deformation of the bones in infants as early as the first and second centuries AD. Rickets was not defined as a specific medical condition until 1645, when an English physician Daniel Whistler gave the earliest known description of the disease. In 1650 a treatise on rickets was published by Francis Glisson, a physician at Caius College, Cambridge, who said it had first appeared about 30 years previously in the counties of Dorset and Somerset. In 1857, John Snow suggested rickets, then widespread in Britain, was being caused by the adulteration of bakers bread with alum. German pediatrician Kurt Huldschinsky successfully demonstrated in the winter of 1918–1919 how rickets could be treated with ultraviolet lamps. The role of diet in the development of rickets was determined by Edward Mellanby between 1918 and 1920. In 1923, American physician Harry Steenbock demonstrated that irradiation by ultraviolet light increased the vitamin D content of foods and other organic materials. Steenbocks irradiation technique was used for foodstuffs, but most memorably for milk. By 1945, rickets had all but been eliminated in the United States. Etymology
The word rickets may be from the Old English word wrickken (to twist), although because this is conjectured, several major dictionaries simply say "origin unknown". The name rickets is plural in form but usually singular in construction.