Rickets, strictly speaking, is a childhood disease. Once your growth plates have fused, usually by your late teens, rickets in its classic form can no longer develop. But the same underlying problem, defective mineralization of bone, absolutely does occur in adults. When it does, it goes by a different name: osteomalacia. The distinction is anatomical rather than philosophical, and for practical purposes, an adult searching for “rickets” is looking at osteomalacia. The causes overlap heavily with childhood rickets, the symptoms can be debilitating, and the condition is more common than most people realize.
Why the Name Changes After Childhood
In children, bones are still growing. The growth plates at the ends of long bones are active, and when the body cannot properly mineralize new bone tissue, those growth plates widen and deform. That produces the bowed legs and swollen joints people associate with rickets. In adults, growth plates have fused, so that particular deformity cannot happen. Instead, the mineralization defect hits existing bone: new bone tissue (called osteoid) is laid down but never hardens properly, leaving bones soft, painful, and prone to fractures.1Medicine. Rickets and osteomalacia The underlying chemistry is the same in both cases. The body needs adequate calcium, phosphate, and vitamin D to harden bone. When any of those are missing or disrupted, mineralization fails, whether you are five or fifty.
The Most Common Cause: Vitamin D Deficiency
Severe, prolonged vitamin D deficiency is the single most frequent driver of osteomalacia in adults.2PubMed. Osteomalacia as a result of vitamin D deficiency Your body needs vitamin D to absorb calcium from food. Without enough of it, calcium levels drop, phosphate handling goes awry, and the machinery that hardens bone grinds to a halt. The people most at risk tend to share some combination of limited sun exposure, darker skin pigmentation at higher latitudes, restrictive diets, and indoor lifestyles. Older adults living in care facilities are a classic high-risk group, but younger adults who cover most of their skin, work night shifts, or live in northern climates are also vulnerable. Vitamin D deficiency severe enough to cause osteomalacia is not a brief dip in blood levels; it represents chronic, deep depletion sustained over months or years.
Gut Conditions That Starve Your Bones
Even if your diet contains plenty of vitamin D and calcium, your bones can still soften if your gut cannot absorb those nutrients properly. Celiac disease is a well-documented example. The chronic intestinal inflammation and damage to the absorptive lining of the small intestine can slash calcium and vitamin D uptake enough to trigger osteomalacia.3PubMed Central. Management of bone health in patients with celiac disease: Practical guide for clinicians In some cases, osteomalacia has been the first symptom that led doctors to suspect celiac disease in adults who had no obvious digestive complaints.4PubMed Central. Osteomalacia can still be a point of attention to celiac disease Two mechanisms seem to work together: direct malabsorption and the chronic inflammatory process itself, which disrupts bone and mineral metabolism through both local and systemic pathways.5PubMed. Bone in celiac disease
Other inflammatory bowel conditions, Crohn’s disease in particular, can do the same thing. Any condition that damages or removes a significant stretch of small intestine puts you at risk, because that is where the bulk of calcium and fat-soluble vitamin absorption takes place.
Bariatric Surgery and Bone Health
Weight-loss surgeries that reroute or bypass portions of the small intestine create a lasting reduction in nutrient absorption by design. That is how they work: food moves through the gut faster and bypasses absorptive segments, limiting calorie uptake. The trade-off is that calcium and vitamin D absorption is also compromised, sometimes severely.6PubMed Central. Hypocalcemia and osteomalacia after bariatric surgery In a case series of patients who had undergone gastric bypass or biliopancreatic diversion, all developed low or undetectable vitamin D levels, low calcium, and elevated markers of bone breakdown. Symptoms of fatigue, muscle pain, and joint pain had persisted for months or years before anyone connected them to bone disease.7PubMed. Metabolic bone disease after gastric bypass surgery for obesity The problem tends to emerge years after surgery rather than immediately, which makes it easy to miss. Anyone who has had bariatric surgery needs lifelong monitoring of vitamin D, calcium, and bone density.
Kidney Disease and Bone Mineralization
Your kidneys do more than filter waste. They convert vitamin D into its active form, and they regulate how much phosphate your body retains versus excretes. As kidney function declines, both of those jobs suffer. Mineral and bone disorders begin showing up even in the early stages of chronic kidney disease and progressively worsen as kidney function drops further.8PubMed Central. Vitamin D and chronic kidney disease-mineral bone disease (CKD-MBD) The result is a spectrum of bone abnormalities, collectively referred to as renal osteodystrophy, that can include osteomalacia as one component. Because chronic kidney disease affects tens of millions of adults worldwide, this is a numerically significant source of adult bone softening that rarely gets framed in terms of “rickets,” even though the mechanism is related.
Phosphate-Wasting Disorders and Tumor-Induced Osteomalacia
Not every case of adult osteomalacia traces back to vitamin D. Some of the most puzzling cases involve phosphate, the other essential mineral for bone hardening. In tumor-induced osteomalacia, a small, usually benign, mesenchymal tumor secretes excessive amounts of a hormone called FGF23. That hormone signals the kidneys to dump phosphate into the urine and simultaneously suppresses the activation of vitamin D, creating a double hit: phosphate plummets and the body loses its ability to compensate through vitamin D-driven intestinal absorption.9PubMed Central. Tumor-induced osteomalacia 10Journal of the Endocrine Society. Diagnosis and Management of Tumor-induced Osteomalacia: Perspectives From Clinical Experience
These tumors are notoriously hard to find. They tend to be tiny, can hide anywhere in the body, and may take years of investigation to locate. In the meantime, patients often suffer profoundly. A literature review documented that people living with tumor-induced osteomalacia experience impaired walking, difficulty climbing stairs, trouble standing up, and sometimes need mobility aids or become bedridden.11PubMed Central. A literature review to understand the burden of disease in people living with tumour-induced osteomalacia When the tumor is found and removed, phosphate levels typically normalize and bone begins healing. When surgery is not possible, a targeted medication called burosumab can block FGF23’s effects and allow phosphate levels to recover. In a trial of patients with tumor-induced osteomalacia, burosumab raised phosphate levels within the first week and maintained that improvement through nearly three years of treatment, with bone biopsy measures of osteomalacia improving as well.12Journal of Bone and Mineral Research. Burosumab for the Treatment of Tumor‐Induced Osteomalacia
Burosumab was originally developed for X-linked hypophosphatemia, a genetic condition that causes lifelong phosphate wasting and osteomalacia persisting into adulthood. In a phase 3 trial of adults with that condition, 48 weeks of burosumab cut bone biopsy measures of excess unmineralized bone by roughly half and reduced the osteoid thickness from abnormal to near-normal levels.13PubMed Central. Burosumab Improved Histomorphometric Measures of Osteomalacia in Adults with X‐Linked Hypophosphatemia: A Phase 3, Single‐Arm, International Trial
Medications That Can Soften Bones
Certain drugs cause osteomalacia as a side effect, usually by interfering with phosphate handling in the kidneys. Tenofovir, a widely used antiviral in HIV and hepatitis B treatment, is one of the best-recognized culprits. It can damage the proximal tubules of the kidneys, causing them to leak phosphate into the urine. In people on prolonged tenofovir therapy, this can gradually produce full-blown osteomalacia.14PubMed Central. Tenofovir-induced hypophosphatemic osteomalacia: how do bone mineral density, trabecular bone score and proximal hip geometry change with treatment? A large pharmacovigilance analysis of adverse-event reporting databases found that tenofovir-containing regimens had some of the strongest statistical signals for bone metabolism disorders among all reported drugs.15PubMed Central. Real-world pharmacovigilance of drug-related bone metabolism disorders: integrating FAERS and VigiAccess with a Bradford Hill-based causal plausibility assessment The risk tends to rise with years of use, and symptoms often develop insidiously. Newer versions of the drug (tenofovir alafenamide rather than tenofovir disoproxil fumarate) were designed partly to reduce this kidney and bone toxicity.
Other drugs occasionally linked to osteomalacia include certain anticonvulsants, which accelerate the breakdown of vitamin D in the liver, and long-term high-dose proton pump inhibitors, which can impair calcium absorption.
What It Feels Like
Adult osteomalacia is easy to miss in its early stages because the symptoms are vague and overlap with dozens of other conditions. The most common complaint is a deep, diffuse bone ache, often worst in the hips, lower back, pelvis, and legs. It tends to be worse with activity and at night. Muscle weakness, especially in the thighs and upper arms, is another hallmark. People notice they have trouble getting out of a chair, climbing stairs, or walking without a waddling gait. Fatigue is almost universal.
Because these symptoms sound like so many other things, from fibromyalgia to depression to normal aging, the correct diagnosis is often delayed by months or years. The bariatric-surgery patients described earlier had symptoms for extended periods before anyone connected them to metabolic bone disease.16PubMed. Metabolic bone disease after gastric bypass surgery for obesity A similar delay is common in tumor-induced osteomalacia, where the average time from symptom onset to diagnosis can stretch well beyond five years.
In advanced cases, bones can develop stress fractures, sometimes called pseudo-fractures or Looser zones, particularly in the pelvis, ribs, and femur. These are partial cracks in undermineralized bone that appear on X-rays as thin, translucent lines. They can be intensely painful and can progress to complete fractures with minimal trauma.
How Doctors Confirm the Diagnosis
Blood tests usually provide the first clues, though they are not always straightforward. In one study of biopsy-proven osteomalacia, about 94% of patients had elevated alkaline phosphatase, which reflects increased bone turnover. But only about half had low calcium or low phosphate, and just 29% had low vitamin D levels on standard blood tests.17The American Journal of Medicine. Noninvasive testing in the diagnosis of osteomalacia That means a substantial number of people with genuine osteomalacia can have normal-looking routine blood work. Parathyroid hormone is often elevated because the body raises it in response to low calcium, trying to pull more from bone stores.
A typical pattern in nutritional osteomalacia includes low vitamin D, low-normal calcium, elevated alkaline phosphatase, and elevated parathyroid hormone, sometimes paired with pseudo-fractures on imaging.18PubMed. Changes in bone mineral density following treatment of osteomalacia But in phosphate-wasting forms, calcium and vitamin D may be normal while phosphate is conspicuously low. The blood test pattern depends heavily on the cause, which is part of why the condition is underdiagnosed.
The definitive confirmation comes from a bone biopsy, though it is rarely needed in routine practice. Histomorphometry, the microscopic measurement of bone tissue, shows increased thickness of the unmineralized layer of bone and a prolonged mineralization lag time. A lag time greater than 100 days, meaning newly laid-down bone takes more than 100 days to start hardening, is considered diagnostic of osteomalacia.19Bone Reports. Bone histomorphometry in the evaluation of osteomalacia Most clinicians treat based on clinical and laboratory findings without a biopsy, reserving it for cases where the cause is unclear or the patient does not respond to treatment as expected.
How Osteomalacia Differs From Osteoporosis
People frequently confuse osteomalacia with osteoporosis, and it is true that both show up as low bone density on a DEXA scan. But the two conditions are fundamentally different. Osteoporosis means there is less bone than normal, but the bone that remains is properly mineralized. Osteomalacia means there may be a normal amount of bone tissue, but it is soft because it has not been hardened with minerals.20PubMed Central. Introduction to Osteoporosis, Osteomalacia, and Fragility Fractures The distinction matters for treatment. Osteoporosis is managed with medications that slow bone breakdown or stimulate new bone formation. Osteomalacia is managed by correcting the underlying mineral or vitamin deficiency. Treating osteomalacia with osteoporosis drugs alone would miss the point entirely, and some osteoporosis medications can actually cause harm in the presence of unresolved vitamin D deficiency.
Complicating things further, the two conditions can coexist. An older adult with chronically low vitamin D may have both thin bones (osteoporosis) and poorly mineralized bones (osteomalacia) at the same time. The DEXA scan cannot distinguish between them, which is another reason blood tests and clinical context are so important.
Treatment for Nutritional Osteomalacia
When vitamin D deficiency is the cause, treatment is straightforward in principle: replace what is missing. A common approach is high-dose vitamin D taken weekly for about eight to twelve weeks, followed by a daily maintenance dose of around 1,000 to 2,000 IU long-term. Calcium supplements, typically around 1,000 mg daily split into multiple doses, are given alongside vitamin D, because you need both raw materials to remineralize bone.21JBMR Plus. Osteomalacia and Vitamin D Status: A Clinical Update 2020 In people with malabsorption or after bariatric surgery, much higher doses may be necessary, sometimes tens of thousands of IU daily, because the gut simply cannot absorb standard doses efficiently. Calcium requirements in those patients can also rise to two or three times the usual amount.22JBMR Plus. Osteomalacia and Vitamin D Status: A Clinical Update 2020
After treatment begins, blood calcium often normalizes within a few weeks, but full biochemical recovery takes much longer. A two-year follow-up study of elderly patients with biopsy-proven osteomalacia found that while calcium reached normal range within about four weeks, phosphate and alkaline phosphatase levels took at least a year to stabilize, with a continuing trend toward improvement through the full two years of monitoring.23PubMed Central. Biochemical recovery time scales in elderly patients with osteomalacia This means patience is required. Bone pain and muscle weakness often improve within the first few months, but complete bone remineralization is measured in seasons, not weeks. Lifelong maintenance supplementation is typically recommended to prevent relapse.24PubMed Central. Nutritional rickets & osteomalacia: A practical approach to management
Rare Genetic Forms That Persist Into Adulthood
A small number of adults have osteomalacia caused not by deficiency but by inherited metabolic conditions. X-linked hypophosphatemia, mentioned earlier in the context of burosumab treatment, is the most common genetic form. People with this condition leak phosphate through their kidneys from birth and often carry the skeletal consequences of childhood rickets into adult life, with ongoing osteomalacia, bone pain, dental problems, and joint stiffness.
Hypophosphatasia is another rare inherited condition worth knowing about. It results from mutations in the gene for tissue-nonspecific alkaline phosphatase, the enzyme that plays a central role in bone mineralization. Adults with mild forms may go undiagnosed for years, presenting with recurrent stress fractures, early loss of teeth, muscle weakness, and joint pain.25PubMed. Hypophosphatasia in Adults: Clinical Spectrum and Its Association With Genetics and Metabolic Substrates The key lab finding in hypophosphatasia is paradoxically low alkaline phosphatase, the opposite of what you see in nearly every other form of osteomalacia. Diagnosis remains a challenge in adults because symptoms can be subtle and nonspecific, and clinicians may not think to check for it.26PubMed. The challenge of hypophosphatasia diagnosis in adults: results from the HPP International Working Group Literature Surveillance One clue is persistently low alkaline phosphatase on routine blood work, especially in someone with unexplained fractures or early tooth loss.27Modern Rheumatology Case Reports. Adult hypophosphatasia with a single heterozygous c.572A > G p.Glu191Gly mutation in the ALPL gene: Case report
Who Should Be Thinking About This
Most adults will never develop osteomalacia, but certain groups should be aware of their risk. You are at higher risk if you have had bariatric surgery, live with celiac disease or inflammatory bowel disease, have chronic kidney disease, take medications like tenofovir or certain anticonvulsants long-term, or get very little sunlight and eat a diet low in fortified dairy or fatty fish. Older adults, especially those who are housebound or institutionalized, are also at particular risk. Pregnancy and lactation increase calcium and vitamin D demands and can unmask borderline deficiency.
If you fall into one of these categories and experience persistent bone pain, muscle weakness, or unusual fatigue, it is worth raising the possibility with your doctor explicitly, because the condition is underdiagnosed. A simple blood panel checking vitamin D, calcium, phosphate, alkaline phosphatase, and parathyroid hormone can usually point in the right direction. The good news is that nutritional osteomalacia is one of the most treatable metabolic bone diseases. When caught and treated properly, bone can fully remineralize and symptoms can resolve, though recovery takes time and requires staying on maintenance supplementation indefinitely.