Rickets is defined as the failure to mineralize growing bone.  The two principle substances necessary for bone mineralization are calcium and phosphate, both of which are influenced by Vitamin D. 

Vitamin D2, (ergocalciferol) is found in some plants and fish. Vitamin D3, (cholecalcifereol) is consumed in milk and formed in sun-exposed skin from 7-dehydrocholesterol.  90% of our vitamin D comes from sun exposure. It is activated by ultraviolet rays to cholecalciferol and transferred to the liver. 

The liver hydoxylates Vit D2 and Vit D3  to 25-OH-cholecalciferol and the kidneys convert it to 1,25- dihydroxycholecalciferol, the most potent active agent. 

Vitamin D facilitates absorption of calcium and phosphorus from the upper small intestine, enhances the renal reabsorption of phosphorous, and aids in the mineralization of bone.  Along with parathyroid hormone and calcitonin, it plays a major part in the homeostasis of calcium and phosphorus.

Vitamin D deficiency rickets is still prevalent in the United States.  The majority of cases occur in strictly breastfed infants who are not being supplemented with vitamin D. The AAP recommends supplementation but a recent survey demonstrated that approximately 30% of breastfed infants were not receiving any.  Other susceptible individuals include dark skinned individuals and those living in northern latitudes that do not come in contact with sunlight. Strict vegans are also susceptible to rickets because they do not eat dairy products. 

Decreased vitamin D leads to a reduced absorption of calcium. This stimulates the release of PTH and the resorption of calcium from bone and decreased reabsorption of P in the kidney.

Common Presentations
1. Clinical findings on a routine physical examination. 
2. Seizures associated with hypocalcemia  and tetany
3. Developmental delay
4. Multiple fractures
5. Pulmonary infections
6. Incidental finding on a radiograph 

Clinical Manifestations
1. Decreased linear growth
2. Bowing of lower extremities
3. Failure to thrive
4. Craniotabes- Ping Pong skull.  Usually in the first year of life
5. Hypotonia
6. Widened ankles and wrist
7. Frontal bossing 
8. Rachitic rosary and chest deformities 

Laboratory Findings
1. Low or normal Ca++( PTH tries to normalize serum levels)
2. Low phosphorus
3. Elevated alkaline phosphatase
4. Low 25-OH-Vit D and normal or increased 1,25-dihydroxy Vit D
5. Increased PTH

Radiograph Findings
1. Osteopenia
2. Metaphysis widening, cupping, and fraying
3. Fractures of different ages

Differential diagnosis
1. Vitamin D resistant rickets-hypophosphatemia.  Kidney disease leads to phosphate wasting and disruption of calcium and phosphate homeostasis.
2. Vitamin D dependent rickets- failure to convert 25 OH to 1,25 diOH.  Autosomal recessive
3. Renal osteodystrophy- decrease 1 alpha hydroxlase activity in the kidney
4. Renal tubular acidosis
5. Malabsorption syndromes
6. Prematurity

Treatment
1. If the serum Ca++ is low, need to give to bring levels up to normal
2. Vitamin D - 300,000 units IM This is a safe and effective method of treating Vit D deficiency and overcomes any issues of compliance. 
3. 400 units daily orally of Vit D.