Rickets in children is basically due to deficiency of vitamin D or lack of exposure to sunlight. Lack of vitamin D or calcium in elder women is called as Osteomalacia, while deficiency if this mineral in children is known as Rickets. Males and females are equally effective from rickets. Such mothers who don’t take vitamin D in their diet or don’t exposed to sunlight, their children are at higher risk of suffering from rickets. Rickets is actually a failure of mineralization of growing ends of bones that results in defective growth of the bones and bones are weaker, unable to bear the body weight.
Bones become soft and children may have bone pain or muscular pain. Ideally, a child requires 30 minutes of the total body exposure to sunlight weekly or a child required 2 hours of exposure of the total head per week. The lack of exposure and vitamin D deficiency is the main leading cause of rickets.
How Vitamin D Affects The Body?
Vitamin D is required to maintain the plasma level of calcium and phosphorus and also involved in bone growth and bone health. It maintains the calcium and phosphorus level by three ways
- Increases the absorption of calcium and phosphorus from the intestine
- They Increase the mobilization of calcium from bone.
- Increases the reabsorption of phosphorus from the kidneys
These three ways are sufficient to balance their concentration in blood. Vitamin D exists in the three forms. Vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). There is no vitamin D1 and the active form is D3.
Bones Growth and Development a Complete Guide
Our skin cells have 7- hyrocholestrol which is converted to vitamin D3 when ultraviolet rays fall on our skin. This vitamin D3 absorbed in the blood binds with the Alpha 1-globulin and transported to the liver. In the liver, hydroxylation takes place and cholecalciferol is converted into 25- hydroxycholecalciferol. In the kidney, alpha 1-hydroxylase convert the 25, OH cholecalciferol into the 1,25 (OH)2 D3. This is the active form of vitamin D which actually works and regarded as the best steroid hormones.
Deficiency of Vitamin D
As we have discussed, vitamin D maintains the level of calcium and phosphorus. Therefore it’s deficiency impaired the ions absorption. Vitamin D lacking causes the following.
Decreased absorption of calcium and phosphorus from the intestine that may result in hypocalcemia.
Therefore, to maintain the balance of plasma calcium, more calcium is released from bones and restore the plasma calcium concentration.
Due to vitamin D deficiency, phosphorus will not reabsorb from the kidney and more phosphorus will excrete out by urine that results in hypophosphatemia.
Due to increase calcium mobilization of calcium from bones, leaves the bones weak and bone density will decrease.
In infants, growing ends of bones are failed to mineralize. Epiphyseal cartilage will not grow, ossification is delayed and fusion not occur.
Types of Rickets in Children
There are four main types of rickets.
1- Vitamin D dependent rickets
This is the Type 1 rickets which is an autosomal disease due to mutation in the vitamin D receptor gene. This mutated vitamin D gene leads to end-organ resistance to 1,25(OH) 2 vitamin D3, though the body has a sufficient amount of vitamin D3 in the body. This type of patient presents retarded growth and refractory rickets in the first year of life.
2- Defect in alpha-1 hydroxylase kidney like is osteodystrophy.
This enzyme (alpha-1 hydroxylase) is present in proximal tubules of the kidney, skin cells, bone cells, and immune cells. This enzyme is particularly involved in the conversion of 25-hydroxy vitamin D2 to 1,25-hydroxyvitamin D3 in the kidney. Lack of defect in this enzyme leads to improper conversion of vitamin D activated form and causes rickets.
3- Vitamin D deficiency rickets
Due to less intake of vitamin D or lack of exposure to sunlight.
4- Vitamin D resistant rickets
Due to X-linked autosomal dominant disorders that mainly affect males. There is an impairment in vitamin D activation and renal tubular absorption.
Classic Signs of Rickets in Children
Rickets in children presents with some classical signs which are exclusively characteristics of rickets. Children suffering from rickets are easily diagnosed clinically due to their characteristic features. Rickets occurs mostly in the infants of 6 months to 2 years and mostly affects the large bones like ankle, elbow, knees, or wrist. Common features of rickets in children are
- Frontal bossing of head
- Delayed closure of anterior fontanale
- Ping pong sensation on the occipital region that’s known as Craniotabes.
- The square shape of the head
- Legs are bowing in shape
- Greenstick deformity present.
- Ends of long bones are flaring and rough.
- Widening of wrist joint, ankles, knees
- Defective spinal growth causes Kyphosis and
- Sclerosis (hump shape back)
Their thorax is like Rachitic Rosary (which have prominent costochondral junction),
Pigeon chest deformity and Harrison Sulcus ( depression above the costal margin at the level of attachment of the diaphragm
They also may have Delayed eruption of temporary teeth, Delayed or impaired growth of permanent teeth, Defective enamel, and caries.
How to Diagnose the Rickets in Children?
Rickets is diagnosed on a clinical basis. Mean clinical features are suggestive of rickets. Other findings include
Widening of the wrist joint. There is fraying, flaring, and cupping of long bones. Distance increased between epiphyses and diaphysis. Bone density is reduced.
- The serum level of calcium, phosphorus, and alkaline phosphatase are monitored.
- The calcium level is decreased.
- The phosphorus level is also slightly decreased.
- The alkaline phosphatase level is raised.
Treatment of Rickets
- Vitamin D orally 2000-6000 IU daily for 4 weeks is advised.
- Ask the mother to give the children milk and fortified milk.
- Daily exposed your child to sun rays.