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My child has bowed legs should I be worried?

My child has bowed legs should I be worried?


Parents of children who have bowed legs often want to know if the child’s legs are abnormal. To help answer that question, here are some basic facts about bowing. This section will give you an idea of what the physician is thinking about when he or she is examining your child.{{more}}

First, bowing or the technical term genu varum (genu = knee, varus/varum = angles in) is a part of the normal development of a child. The role of the physician is to determine if the bowing is physiologic (part of normal development) or pathologic (due to some disease process). Physiologic bowing will improve as the child grows without treatment, while pathologic bowing will tend to worsen over time without treatment. The bowing can arise from the lower portion of the femur near the knee, the knee joint itself, the upper shin bone near the knee, or a combination of these areas.

Normally, an infant is born with bowed legs. Over time, the leg alignment will correct and usually straightens out by about eighteen months of age. By the time the child is three to four years old, he or she will normally develop a knock-kneed alignment. The technical term for this is genu valgum (valgus/valgum = angles out). This genu valgum will then correct somewhat by the age of five to six years old, leaving the normal adult alignment of slight genu valgum (slight knock-kneed).

Listed above are the main ages for these changes to occur so half of the children will correct their bowing earlier and half will correct it later.

Occasionally, the bowing never fully corrects. That is why some adults have bowed legs. So you can see, there is a wide range of normal when looking at bowed legs. Physiologic bowing does not require any treatment other than observation for correction as the child grows.

Internal tibial torsion (inward twist of the tibia caused by intrauterine positioning), also called medial tibial torsion, can complicate matters by making the bowing appear worse than it really is, as we see the side of the knee relative to the foot rather than the front. Correction of the torsion will make the legs appear straighter. Fortunately, internal tibial torsion tends to correct itself without treatment up until the age of four to six years, thereby correcting the visual bowing also.

Many disease processes effecting bone growth cause pathologic bowing. Two of the more common diseases known to cause bowing are Rickets and Blount’s disease.


Rickets is a generalized skeletal disease involving Vitamin D metabolism. Vitamin D is vital for bone mineralization. Although this vitamin is important it does not act alone. The term ‘rickets’ predates the later and current notions of the actual causal chemistry. So older usages run counter to current more precise etiologic (based on cause) uses of the term. In the older sense, a child with bowing of bones, with thickened ends of bones (including ribs), often irritable, and eventually (when x-ray allowed) noted to be associated with widened growth plates which did not fully calcify – that was called rickets. Calcium as Ca++ interacts with Phosphate as PO4= such that at a certain concentration, the calcium can precipitate. The body uses several mechanisms to keep the two at a certain level. When that is off – either by the Ca++ or by the PO4= then the syndrome may manifest.

Dietary deficiency of Vitamin D is the most familiar (to the public) form of rickets. Dietary supplementation of Vitamin D has gone a long way toward abolishing dietary rickets, but it is still occasionally seen in less developed countries and in circumstances of dietary peculiarity. Because of this, the hereditary forms of rickets are more commonly seen. Rickets causes a distinctive cupping and widening of the growth plates which can be recognized on a plain x-ray along with other characteristic findings.

A precursor

However, rickets, in today’s terminology, is really a family of entities. Vitamin D in the diet isn’t really an active agent, but rather a precursor, a build it yourself kit for what is often called “active vitamin-D”. The substance in the diet must first be absorbed, altered by the liver, then altered further by the kidney, then changed again in the skin by sunlight before it is in the active form. If any of those steps is faulty, then dietary vitamin D will be no more active than sand or jelly beans.

Therefore, even with a normal intake of “vitamin-D”, if any of the needed bodily steps are not functional, a rickets syndrome may be seen. Caught early, while there is lots of growth remaining, corrected growth can undo deformations which have not gone too far. Correction by supplements is from corrected growth. No growth, no correction. Adults will not correct bowed bones by diet.

A little girl has a genetic form of rickets seen only in the females of her family (four generations). A dominant defective gene disabled her ability to activate the vitamin D form found in food. Dietary change would do little.

At an early time, by giving her a processed already activated form of vitamin D which gets around her inherited bodily inability to activate it, her deformities went away. Her younger sister with similar findings behaved in exactly the same manner. Although boys in alternate generations could also land this particular gene defect, four generations in this girl bearing family managed to dodge this outcome. The girls treated early have statures greater than their mother, grandmother and great grandmother by age eight.

Active vitamin supplementation will not undo deformities if they are addressed too late for remaining corrective growth to get the job done. If the activated form of the vitamin fails to alter the course of things then rather than blame the key (vitamin D) we need to suspect the lock. Hormones or vitamins work like keys by fitting into something that responds. If that something is defective, then it gets even more difficult to get around.