Rickets and Osteomalacia: Consequences of Vitamin D Deficiency

Bones might feel like the most permanent part of the body, but they are actually living tissue that constantly rebuilds itself. When this rebuilding process runs short on a single fat-soluble vitamin, the consequences can reshape an entire skeleton. Rickets in children and osteomalacia in adults are two faces of the same underlying problem: a long-standing deficiency of vitamin D that prevents bones from mineralising properly. Despite plenty of sunshine across the subcontinent, both conditions remain surprisingly common, with studies reporting hypovitaminosis D in 84.9 to 100 per cent of school-going children and 30 to 91.2 per cent of adults across various Indian regions.

What are rickets and osteomalacia? 🔗

Rickets and osteomalacia describe the same biochemical failure occurring at two different stages of life. In both, bones are unable to absorb enough calcium and phosphorus to harden the protein scaffold that forms new bone tissue. The result is soft, weak, and easily deformed bone.

Rickets is the childhood form. It develops while bones are still growing, so the disease attacks the growth plates at the ends of long bones. Rickets results from deficient mineralisation at the cartilage of growth plates in children, leading to widened, irregular, and weakened bone ends.

Osteomalacia, on the other hand, is the adult version. Since adult bones have already finished growing, the disease shows up as bone softening rather than deformity. The condition involves defective mineralisation where the bone matrix is laid down but never properly hardened with minerals.

The vitamin D connection 🔗

Vitamin D acts like a key that unlocks calcium absorption in the gut. Without enough of it, even a calcium-rich diet cannot translate into strong bones. When vitamin D levels drop, the body responds by raising parathyroid hormone (PTH), which pulls calcium out of bones to keep blood levels normal. Over time, this process leads to weakened and brittle bones that break easily. About 40 to 60 per cent of total skeletal mass at maturity is built during childhood and adolescence, which is why deficiency during these years has lifelong consequences.

Why these conditions persist in a sunny country 🔗

It seems puzzling that vitamin D deficiency is widespread in a tropical country where sunlight is abundant for most of the year. Several factors explain the paradox.

Lifestyle and skin pigmentation 🔗

Darker skin contains more melanin, which acts like a natural sunscreen and reduces the skin’s ability to produce vitamin D from sunlight. Combined with urban lifestyles that keep people indoors, long working hours, full-body clothing for cultural or religious reasons, and routine sunscreen use, effective sun exposure becomes minimal. Indian skin typically requires more than 45 minutes of direct sun exposure daily on the face, arms, and legs to produce adequate vitamin D.

Poor dietary intake 🔗

Traditional vegetarian diets contain very few natural sources of vitamin D. Most rich sources are animal-based, such as fatty fish, egg yolks, and liver. Even non-vegetarians often do not consume these regularly. Worse, the high phytate content in cereal-heavy diets reduces calcium absorption further. National Nutrition Monitoring Bureau data from 1975 to 2017 showed that only 37 per cent of households consumed more than 70 per cent of the recommended daily allowance of calcium, while 44 per cent of households consumed less than 50 per cent of the RDA.

Air pollution and urbanisation 🔗

Heavy air pollution in many cities filters out ultraviolet B rays before they reach the skin. High-rise buildings, indoor schooling, and screen-based recreation all reduce children’s exposure to natural sunlight, making them more vulnerable to deficiency despite living in a sunny climate.

Symptoms of deficiency in children 🔗

Rickets often develops gradually, and early signs can be subtle. As the condition progresses, the skeletal changes become more visible and harder to ignore.

Bone deformities 🔗

The most recognisable signs of rickets affect the legs. Common skeletal symptoms include bowed legs or knock-knees, thickened wrists and ankles, and breastbone projection. Bowlegs (genu varum) occur when softened leg bones bend outward under the child’s body weight as they start walking. Knock-knees (genu valgum) are the opposite curvature, where the knees touch but the ankles spread apart. While both can occur normally in young children, persistence beyond two years of age or worsening curvature is a red flag.

Growth and developmental issues 🔗

Children with rickets often show delayed growth, short stature, and difficulty walking or running. The softened skull bones may delay the closure of the soft spots (fontanelles), and the rib cage may develop a characteristic beaded appearance known as the “rachitic rosary.” Teeth may erupt late and develop poor enamel, leading to frequent cavities.

Pain and weakness 🔗

Bone pain in the legs, spine, and pelvis is common, along with muscle weakness that contributes to delayed motor milestones. Severe cases can present with seizures, arrhythmias, or muscle cramps caused by very low blood calcium levels, requiring urgent medical attention.

Symptoms of deficiency in adults 🔗

Because adult bones are no longer growing, osteomalacia does not produce the dramatic deformities seen in rickets. Instead, the symptoms are often vague and easy to dismiss, which is why the condition frequently goes undiagnosed for years.

Diffuse bone pain 🔗

The hallmark of osteomalacia is dull, aching bone pain that worsens with weight-bearing activity. It typically affects the lower back, hips, pelvis, and legs. Many patients describe it as “feeling old before their time.” Unlike joint pain from arthritis, this discomfort comes from the bones themselves.

Muscle weakness and gait changes 🔗

Vitamin D plays a direct role in muscle function. Adults with osteomalacia often develop proximal muscle weakness, particularly in the thigh and shoulder muscles. The main symptoms include bone pain, fatigue fractures, muscular cramps, muscle pain, and gait disorders, with an increased incidence of falls in the elderly. A characteristic “waddling gait” may develop, where the person rocks from side to side while walking because the hip muscles cannot stabilise the pelvis.

Fractures and pseudofractures 🔗

Softened bones fracture under stresses that healthy bones would easily withstand. Pseudofractures, also called Looser’s zones, are narrow bands of unmineralised bone visible on X-rays. Women, especially those who have had multiple pregnancies and prolonged breastfeeding, are particularly vulnerable because pregnancy depletes calcium and vitamin D stores.

Diagnosis and biochemistry 🔗

Diagnosing rickets and osteomalacia involves a combination of clinical examination, blood tests, and imaging. The key blood markers include low serum 25-hydroxyvitamin D, low or normal calcium, low phosphorus, and elevated alkaline phosphatase. Parathyroid hormone is usually elevated as the body tries to compensate. X-rays show characteristic changes: cupped, frayed growth plates in children, and pseudofractures in adults.

Prevention and treatment 🔗

The good news is that both rickets and osteomalacia are largely preventable and, in most cases, fully reversible with timely treatment. The strategy rests on three pillars: sunlight, diet, and supplementation.

Safe sun exposure 🔗

Sunlight remains the cheapest and most efficient source of vitamin D. Aiming for 20 to 30 minutes of midday sun exposure on the arms, legs, and face several times a week is generally sufficient for most people. People with darker skin or limited mobility may need longer exposure. The trade-off with skin cancer risk is real, but in populations where deficiency is widespread, moderate, unprotected sun exposure during non-peak hours offers more benefit than harm.

Dietary sources 🔗

Few foods naturally contain meaningful amounts of vitamin D. The best dietary sources include fatty fish like salmon, sardines, and mackerel, egg yolks, and liver. Sun-dried mushrooms are one of the few plant-based options, since their ergosterol converts to vitamin D2 when exposed to ultraviolet light. Fortified foods such as milk, cereals, and edible oils are increasingly available and help close the dietary gap. Calcium-rich foods, including dairy products, ragi, sesame seeds, green leafy vegetables, and small fish eaten with bones, complete the picture.

Supplementation 🔗

For people who cannot get enough vitamin D from sun and diet, supplements are essential. Treatment for osteomalacia includes vitamin D, calcium, and sometimes phosphorus supplements, with most patients showing improvement within weeks, although full bone healing can take several months. For nutritional rickets, oral vitamin D in adequate doses combined with calcium supplements is the standard approach. Pregnant and lactating women, exclusively breastfed infants, and the elderly should be considered priority groups for routine supplementation under medical guidance.

Public health measures 🔗

Beyond individual action, food fortification is considered the most viable population-level strategy. Several states have begun fortifying milk and edible oils with vitamin D. Maternal nutrition programmes, school health initiatives, and awareness campaigns about safe sun exposure all play roles in tackling this silent epidemic.

What do you think? If sunlight is free and abundant, why do you think so many people still develop vitamin D deficiency? Could a simple change in daily routine, like a morning walk or a midday break outdoors, meaningfully shift the bone health of an entire generation?

References

1. https://pubmed.ncbi.nlm.nih.gov/30666982/
2. https://www.ncbi.nlm.nih.gov/books/NBK551616/
3. https://my.clevelandclinic.org/health/diseases/13017-osteomalacia
4. https://pmc.ncbi.nlm.nih.gov/articles/PMC3942730/
5. https://www.1mg.com/articles/know-your-food-vitamin-d-sources-sun-diet-and-supplements
6. https://wjwch.com/nutritional-vitamin-d-deficiency-rickets-in-children-challenges-in-diagnosis-management-and-prevention/
7. https://www.mayoclinic.org/diseases-conditions/rickets/symptoms-causes/syc-20351943
8. https://pubmed.ncbi.nlm.nih.gov/26205357/