What is osteomalacia

Osteomalacia (soft bones) is a disease that is characterized by a weakening of the bone, often due to a deficiency of vitamin D. Osteomalacia is the adult counterpart of rickets in children. Both of these conditions are caused by a defect in vitamin D availability or metabolism. Vitamin D supports the development of the bones of the body, so when there are low levels of vitamin D, the bones are not strong enough (see Vitamin D section below). Osteomalacia is characterized by poor bone formation, resulting in abnormal bone formation with weakened bone. Symptoms of osteomalacia can include muscle weakness, bone pain, and walking with a waddling gait. Pain is especially likely to occur in the lower back, hips, and legs. The weakening of the bones may also cause them to easily fracture, which tend to affect the vertebral bodies in the spine and the neck of femur. If osteomalacia persists, it may result in lower density bone and subsequently osteoporosis.

The incidence of osteomalacia is approximately 1 in 1000 people. Osteomalacia develops most commonly due to lack of vitamin D (often from not getting enough sunlight), or less frequently, due to a digestive or kidney disorder. These disorders can interfere with the body’s ability to absorb vitamins. There are also rare genetic conditions that can cause osteomalacia.

When osteomalacia is in its early stages, you might not have any symptoms, although signs of osteomalacia may be apparent on an X-ray or other diagnostic tests. As osteomalacia progresses, you might develop bone pain and muscle weakness.

The dull, aching pain associated with osteomalacia most commonly affects the lower back, pelvis, hips, legs and ribs. The pain might be worse at night, or when you put pressure on the bones, and are rarely relieved completely by rest.

Decreased muscle tone and leg weakness can cause a waddling gait and make walking slower and more difficult.

Osetomalacia can be caused by having a low level of vitamin D in the diet or lack of sun exposure. The condition may also be the result of an underlying disease such as celiac disease, or kidney or liver disorders.

Diagnosis of osteomalacia is possible through blood or urine tests to check for vitamin D levels or a bone biopsy.

Treatment should be aimed at correcting any underlying cause where possible. Osteomalacia due to poor intake is reversed by ensuring adequate diet, sunlight exposure and vitamin D and calcium supplements if necessary (see Treatment below).

Osteomalacia vs Rickets

Rickets is a condition that causes children to have soft, weak bones. Rickets usually occurs when children do not get enough vitamin D. Rickets can also happen when calcium or phosphorus levels are too low.

What population group is at highest risk for osteomalacia?

• People with inadequate dietary intake of vitamin D:
  • Follow a vegetarian diet
  • Are lactose intolerant (have trouble digesting milk products)
  • Do not eat or drink milk products (more common in older adults)
• People with inadequate exposure to sunlight (ultraviolet radiation), which produces vitamin D in the body (increased risk in elderly people who are housebound)
• People with malabsorption of vitamin D due to gastrointestinal problems e.g. Celiac disease, lactose intolerance
• People who’ve had surgery to remove part of the stomach or bypass their small intestine also can lead to vitamin D and calcium deficiency. Normally, the stomach breaks down food to release vitamin D and other minerals that are absorbed in the intestine. This process is disrupted if you have surgery to remove part or all of your stomach, and can result in vitamin D and calcium deficiency. Surgery to remove or bypass your small intestine also can lead to vitamin D and calcium deficiency.
• Inherited or acquired disorders of vitamin D metabolism
• People with advanced kidney disease
• People with liver failure
• People with cancer
• Phosphate depletion associated with low dietary intake of phosphates
• People who use certain medications such as those used to treat epilepsy e.g. phenytoin (Dilantin, Phenytek) and phenobarbital

Osteomalacia prognosis

Prognosis is good if underlying causes of vitamin D deficiency are addressed. Patients should be encouraged to eat a balanced diet and ensure adequate sun exposure.

Some people with vitamin D deficiency disorders will get better within a few weeks. With treatment, healing should happen within 6 months.

What is Vitamin D

Vitamin D (calciferol) is a fat-soluble vitamin that is naturally present in very few foods, added to others, and available as a dietary supplement. Vitamin D is also produced endogenously when ultraviolet rays from sunlight strike the skin and trigger vitamin D synthesis. Vitamin D obtained from sun exposure, food, and supplements is biologically inert and must undergo two hydroxylations in the body for activation ¹⁾. The first occurs in the liver and converts vitamin D to 25-hydroxyvitamin D [25(OH)D], also known as calcidiol. The second occurs primarily in the kidney and forms the physiologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol ²⁾.

The plasma calcitriol (1,25-dihydroxyvitamin D or 1,25(OH)2D) concentration depends on the availability of calcidiol (25-hydroxyvitamin D or 25(OH)D) and the activities of the renal enzymes 1-α-hydroxylase and 24-α-hydroxylase ³⁾. The renal 1-α-hydroxylase enzyme is primarily regulated by parathyroid hormone (PTH), serum calcium and phosphate concentrations, and fibroblast growth factor 23 (FGF23) ⁴⁾. Increased parathyroid hormone (PTH), calcitonin, and hypophosphatemia (low blood phosphate) stimulate the renal enzymes 1-α-hydroxylase and enhance calcitriol [1,25(OH)2D] production, while high calcium, hyperphosphatemia (high blood phosphate) and calcitriol [1,25(OH)2D] inhibit the renal enzymes 1-α-hydroxylase ⁵⁾. Calcitriol [1,25-dihydroxyvitamin D or 1,25(OH)2D] inhibits the synthesis and secretion of parathyroid hormone (PTH), providing negative feedback regulation of calcitriol production. Calcitriol [1,25-dihydroxyvitamin D or 1,25(OH)2D] synthesis may also be modulated by vitamin D receptors on the cell surface; downregulation of these receptors may play an important role in regulating vitamin D activation ⁶⁾. Fibroblast growth factor 23 (FGF23), a newly described phosphaturic hormone, inhibits renal production of Calcitriol [1,25-dihydroxyvitamin D or 1,25(OH)2D] by inhibiting 1-α-hydroxylase in the renal proximal tubule and by simultaneously increasing the expression of 24-α-hydroxylase and production of 24,25(OH)2D (an inactive metabolite) ⁷⁾. Calcitriol [1,25-dihydroxyvitamin D or 1,25(OH)2D] stimulates fibroblast growth factor 23 (FGF23), creating a feedback loop. Fibroblast growth factor 23 (FGF23) decreases renal reabsorption of phosphate, and thereby counteracts the increased gastrointestinal phosphate reabsorption induced by Calcitriol, maintaining phosphate homeostasis ⁸⁾.

When hypocalcemia (low blood calcium) occurs, serum parathyroid hormone (PTH) concentration increases and enhances renal tubular reabsorption of calcium, as well as the activity of 1-α-hydroxylase in the kidney. This results in increased Calcitriol [1,25-dihydroxyvitamin D or 1,25(OH)2D] production, and in turn, intestinal calcium absorption. Parathyroid hormone (PTH) also stimulates bone osteoclast activity to mobilize bone calcium stores, thereby increasing serum calcium. Both Calcitriol and Calcidiol [25-hydroxyvitamin D or 25(OH)D] are degraded in part by being hydroxylated at the 24 position by a 24-hydroxylase. The activity of the 24-hydroxylase gene is increased by calcitriol (which therefore promotes its own inactivation) and reduced by parathyroid hormone (thereby allowing more active hormone to be formed) ⁹⁾. Estrogen, placental growth hormone, and prolactin may also regulate vitamin D metabolism, playing a role during pregnancy to meet increased calcium demands. Calcitriol is also formed in some other tissues, but is used only within the tissues and not circulated. Parathyroid hormone (PTH)- independent extrarenal production of Calcitriol from Calcidiol is by activated macrophages in the lung and lymph nodes. The 1-α-hydroxylase enzyme is also expressed at other extrarenal sites, including the gastrointestinal tract, skin, vasculature, mammary epithelial cells, and in osteoblasts and osteoclasts ¹⁰⁾.

Vitamin D is a nutrient found in some foods that is needed for health and to maintain strong bones. It does so by helping the body absorb calcium (one of bone’s main building blocks) from food and supplements. People who get too little vitamin D may develop soft, thin, and brittle bones, a condition known as rickets in children and osteomalacia in adults.

Vitamin D is important to the body in many other ways as well. Muscles need it to move, for example, nerves need it to carry messages between the brain and every body part, and the immune system needs vitamin D to fight off invading bacteria and viruses. Together with calcium, vitamin D also helps protect older adults from osteoporosis. Vitamin D is found in cells throughout the body.

Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone and to prevent hypocalcemic tetany. It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts ¹¹⁾, ¹²⁾. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults ¹³⁾. Together with calcium, vitamin D also helps protect older adults from osteoporosis.

Figure 1. Vitamin D synthesis and function in your body for maintaining Calcium and Phosphate homeostasis

Figure 2. Vitamin D synthesis and function in your body including its anti-cancer effect

Figure 3. Microscopic Structure of a Typical Bone

Figure 4. Internal organization of bones

Vitamin D has other roles in the body, including modulation of cell growth, neuromuscular and immune function, and reduction of inflammation ¹⁴⁾, ¹⁵⁾, ¹⁶⁾. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D ¹⁷⁾. Many cells have vitamin D receptors, and some convert 25(OH)D to 1,25(OH)2D.

Serum concentration of 25(OH)D is the best indicator of vitamin D status. It reflects vitamin D produced cutaneously and that obtained from food and supplements ¹⁸⁾ and has a fairly long circulating half-life of 15 days ¹⁹⁾. 25(OH)D functions as a biomarker of exposure, but it is not clear to what extent 25(OH)D levels also serve as a biomarker of effect (i.e., relating to health status or outcomes) ²⁰⁾. Serum 25(OH)D levels do not indicate the amount of vitamin D stored in body tissues.

In contrast to 25(OH)D, circulating 1,25(OH)2D is generally not a good indicator of vitamin D status because it has a short half-life of 15 hours and serum concentrations are closely regulated by parathyroid hormone, calcium, and phosphate ²¹⁾. Levels of 1,25(OH)2D do not typically decrease until vitamin D deficiency is severe ²²⁾, ²³⁾.

Table 1 : The amount of vitamin D you need each day depends on your age. Average daily recommended amounts from the Food and Nutrition Board (a national group of experts) for different ages are listed below in International Units (IU) or microgram (mcg):

Life Stage	Recommended Amount
Birth to 12 months	400 IU [10 mcg]
Children 1–13 years	600 IU [15 mcg]
Teens 14–18 years	600 IU [15 mcg]
Adults 19–70 years	600 IU [15 mcg]
Adults 71 years and older	800 IU [20 mcg]
Pregnant and breastfeeding women	600 IU [15 mcg]

Note: The amount of vitamin D contained in supplements is sometimes expressed in international units (IU) where 40 IU is equal to one microgram (1 mcg) of vitamin D.

Table 2: Selected Food Sources of Vitamin D

Food	IUs per serving*	Percent DV**
Cod liver oil, 1 tablespoon	1,360	340
Swordfish, cooked, 3 ounces	566	142
Salmon (sockeye), cooked, 3 ounces	447	112
Tuna fish, canned in water, drained, 3 ounces	154	39
Orange juice fortified with vitamin D, 1 cup (check product labels, as amount of added vitamin D varies)	137	34
Milk, nonfat, reduced fat, and whole, vitamin D-fortified, 1 cup	115-124	29-31
Yogurt, fortified with 20% of the DV for vitamin D, 6 ounces (more heavily fortified yogurts provide more of the DV)	80	20
Margarine, fortified, 1 tablespoon	60	15
Sardines, canned in oil, drained, 2 sardines	46	12
Liver, beef, cooked, 3 ounces	42	11
Egg, 1 large (vitamin D is found in yolk)	41	10
Ready-to-eat cereal, fortified with 10% of the DV for vitamin D, 0.75-1 cup (more heavily fortified cereals might provide more of the DV)	40	10
Cheese, Swiss, 1 ounce	6	2

* IUs = International Units.
** DV = Daily Value. DVs were developed by the U.S. Food and Drug Administration to help consumers compare the nutrient contents among products within the context of a total daily diet. The DV for vitamin D is currently set at 400 IU for adults and children age 4 and older. Food labels, however, are not required to list vitamin D content unless a food has been fortified with this nutrient. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

Note: The amount of vitamin D contained in supplements is sometimes expressed in international units (IU) where 40 IU is equal to one microgram (1 mcg) of vitamin D.

[Source ²⁴⁾]

Calcium

People should get most of their nutrients from food, advises the federal government’s Dietary Guidelines for Americans. Foods contain vitamins, minerals, dietary fiber and other substances that benefit health. In some cases, fortified foods and dietary supplements may provide nutrients that otherwise may be consumed in less-than-recommended amounts. For more information about building a healthy diet, refer to the Dietary Guidelines for Americans ²⁵⁾ and the U.S. Department of Agriculture’s MyPlate ²⁶⁾.

Table 3: Average calcium daily recommended amounts are listed below in milligrams (mg):

Life Stage	Recommended Dietary Allowances (RDAs) for Calcium Amount
Birth to 6 months	200 mg
Infants 7–12 months	260 mg
Children 1–3 years	700 mg
Children 4–8 years	1,000 mg
Children 9–13 years	1,300 mg
Teens 14–18 years	1,300 mg
Adults 19–50 years	1,000 mg
Adult men 51–70 years	1,000 mg
Adult women 51–70 years	1,200 mg
Adults 71 years and older	1,200 mg
Pregnant and breastfeeding teens	1,300 mg
Pregnant and breastfeeding adults	1,000 mg

Table 4: Selected Food Sources of Calcium

Food	Milligrams (mg) per serving	Percent DV*
Yogurt, plain, low fat, 8 ounces	415	42
Mozzarella, part skim, 1.5 ounces	333	33
Sardines, canned in oil, with bones, 3 ounces	325	33
Yogurt, fruit, low fat, 8 ounces	313–384	31–38
Cheddar cheese, 1.5 ounces	307	31
Milk, nonfat, 8 ounces**	299	30
Soymilk, calcium-fortified, 8 ounces	299	30
Milk, reduced-fat (2% milk fat), 8 ounces	293	29
Milk, buttermilk, lowfat, 8 ounces	284	28
Milk, whole (3.25% milk fat), 8 ounces	276	28
Orange juice, calcium-fortified, 6 ounces	261	26
Tofu, firm, made with calcium sulfate, ½ cup***	253	25
Salmon, pink, canned, solids with bone, 3 ounces	181	18
Cottage cheese, 1% milk fat, 1 cup	138	14
Tofu, soft, made with calcium sulfate, ½ cup***	138	14
Ready-to-eat cereal, calcium-fortified, 1 cup	100–1,000	10–100
Frozen yogurt, vanilla, soft serve, ½ cup	103	10
Turnip greens, fresh, boiled, ½ cup	99	10
Kale, fresh, cooked, 1 cup	94	9
Ice cream, vanilla, ½ cup	84	8
Chinese cabbage, bok choi, raw, shredded, 1 cup	74	7
Bread, white, 1 slice	73	7
Pudding, chocolate, ready to eat, refrigerated, 4 ounces	55	6
Tortilla, corn, ready-to-bake/fry, one 6” diameter	46	5
Tortilla, flour, ready-to-bake/fry, one 6” diameter	32	3
Sour cream, reduced fat, cultured, 2 tablespoons	31	3
Bread, whole-wheat, 1 slice	30	3
Kale, raw, chopped, 1 cup	24	2
Broccoli, raw, ½ cup	21	2
Cheese, cream, regular, 1 tablespoon	14	1

* DV = Daily Value. DVs were developed by the U.S. Food and Drug Administration to help consumers compare the nutrient contents among products within the context of a total daily diet. The DV for calcium is 1,000 mg for adults and children aged 4 years and older. Foods providing 20% of more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

[Source ²⁷⁾]

Osteomalacia vs Osteoporosis

Osteoporosis literally means “porous bone.” Having osteoporosis raises the risk of experiencing fractures ²⁸⁾, ²⁹⁾. Osteoporosis is characterized by too little bone formation, excessive bone loss, or a combination of both, leading to bone fragility and an increased risk of fractures of the hip, spine and wrist ³⁰⁾.

Bone is continually being formed and resorbed. Normally, bone formation and resorption are closely balanced.

Osteoporosis causes bones to become less dense and more fragile. Some people are more at risk than others.

Bones are at their thickest and strongest in your early adult life and their density increases until your late 20s. You gradually start losing bone density from around the age of 35.

This happens to everyone, but some people develop osteoporosis and lose bone density much faster than normal. This means they’re at greater risk of a fracture.

Osteoporosis can affect men and women. It’s more common in older people, but it can also affect younger people.

Osteoporosis in women

Women are more at risk of developing osteoporosis than men because the hormone changes that occur in the menopause directly affect bone density.

The female hormone oestrogen is essential for healthy bones. After the menopause (when monthly periods stop), oestrogen levels fall. This can lead to a rapid decrease in bone density.

Women are at even greater risk of developing osteoporosis if they have:

• an early menopause (before the age of 45)
• a hysterectomy (removal of the womb) before the age of 45, particularly when the ovaries are also removed
• absent periods for more than six months as a result of overexercising or too much dieting

Osteoporosis in men

In most cases, the cause of osteoporosis in men is unknown. However, there’s a link to the male hormone testosterone, which helps keep the bones healthy.

Men continue producing testosterone into old age, but the risk of osteoporosis is increased in men with low levels of testosterone.

In around half of men, the exact cause of low testosterone levels is unknown, but known causes include:

• the use of certain medications, such as oral corticosteroids
• alcohol misuse
• hypogonadism (a condition that causes abnormally low testosterone levels)

Risk factors for Osteoporosis

Many hormones in the body can affect the process of bone turnover. If you have a condition of the hormone-producing glands, you may have a higher risk of developing osteoporosis.

Hormone-related conditions that can trigger osteoporosis include:

• hyperthyroidism (overactive thyroid gland)
• disorders of the adrenal glands, such as Cushing’s syndrome
• reduced amounts of sex hormones (oestrogen and testosterone)
• disorders of the pituitary gland
• hyperparathyroidism (overactivity of the parathyroid glands)

Other risk factors

Other factors thought to increase the risk of osteoporosis and broken bones include:

• a family history of osteoporosis
• a parental history of hip fracture
• a body mass index (BMI) of 19 or less
• long-term use of high-dose oral corticosteroids (widely used for conditions such as arthritis and asthma), which can affect bone strength
• having an eating disorder, such as anorexia or bulimia
• heavy drinking and smoking
• rheumatoid arthritis
• malabsorption problems, as experienced in Celiac disease and Crohn’s disease
• some medications used to treat breast cancer and prostate cancer which affect hormone levels
• long periods of inactivity, such as long-term bed rest

Osteoporosis treatment

Treating osteoporosis involves treating and preventing fractures, and using medication to strengthen bones.

A number of different medications are used to treat osteoporosis. Your doctor will discuss the treatments available and make sure the medicines are right for you.

A number of factors are taken into consideration before deciding which medication to use. These include your:

• age
• bone mineral density (measured by your T score)
• risk factors for fracture

Bisphosphonates

Bisphosphonates slow the rate that bone is broken down in your body. This maintains bone density and reduces the risk of fracture.

There are a number of different bisphosphonates, including:

• alendronate
• ibandronate
• risedronate
• zoledronic acid

They’re given as a tablet or injection.

You should always take bisphosphonates on an empty stomach with a full glass of water. Stand or sit upright for 30 minutes after taking them. You’ll also need to wait between 30 minutes and 2 hours before eating food or drinking any other fluids.

Bisphosphonates usually take 6 to 12 months to work, and you may need to take them for 5 years or longer. You may also be prescribed calcium and vitamin D supplements to take at a different time to the bisphosphonate.

The main side effects associated with bisphosphonates include:

• irritation to the oesophagus (the tube that food passes through from the mouth to the stomach)
• swallowing problems (dysphagia)
• stomach pain

Not everyone will experience these side effects.

Osteonecrosis of the jaw is a rare side effect linked with the use of bisphosphonates, although most frequently with high-dose intravenous bisphosphonate treatment for cancer and not for osteoporosis.

In osteonecrosis, the cells in the jaw bone die, which can lead to problems with healing. If you have a history of dental problems, you may need a check-up before you start treatment with bisphosphonates. Speak to your doctor if you have any concerns.

Selective estrogen receptor modulators (SERMs)

SERMs are medications that have a similar effect on bone as the hormone estrogen. They help to maintain bone density and reduce the risk of fracture, particularly of the spine.

Raloxifene is the only type of SERM available for treating osteoporosis. It’s taken as a daily tablet.

Side effects associated with raloxifene include:

• hot flushes
• leg cramps
• a potential increased risk of blood clots

Parathyroid hormone (teriparatide)

Parathyroid hormone is produced naturally in the body. It regulates the amount of calcium in bone.

Parathyroid hormone treatments (human recombinant parathyroid hormone or teriparatide) are used to stimulate cells that create new bone (osteoblasts). They’re given by injection.

While other medication can only slow down the rate of bone thinning, parathyroid hormone can increase bone density. However, it’s only used in a small number of people whose bone density is very low and when other treatments aren’t working.

Nausea and vomiting are common side effects of the treatment. Parathyroid hormone treatments should only be prescribed by a specialist.

Calcium and vitamin D supplements

Calcium is the major mineral found in bone, and having enough calcium as part of a healthy, balanced diet is important for maintaining healthy bones.

For most healthy adults, the recommended amount of calcium is 700 milligrams (mg) of calcium a day, which most people should be able to get from a varied diet that contains good sources of calcium.

However, if you have osteoporosis, you may need more calcium, which will usually be in the form of supplements. Ask your GP for advice about taking calcium supplements.

Vitamin D is needed to help the body absorb calcium. All adults should consume 10 micrograms (mcg) of vitamin D a day from October to March.

Because vitamin D is found in only a small number of foods, it might be difficult to get enough from your diet alone – so all adults should consider taking a daily supplement containing 10mcg of vitamin D.

Hormone replacement therapy (HRT)

HRT is sometimes recommended for women who are experiencing the menopause, as it can help control symptoms.

HRT has also been shown to maintain bone density and reduce the risk of fracture during treatment.

However, HRT isn’t specifically recommended for treating osteoporosis and isn’t often used for this purpose.

This is because HRT slightly increases the risk of developing certain conditions – such as breast cancer, endometrial cancer, ovarian cancer, stroke and venous thromboembolism – more than it lowers the risk of osteoporosis.

Discuss the benefits and risks of HRT with your doctor.

Testosterone treatment

In men, testosterone treatment can be useful when osteoporosis is caused by insufficient production of male sex hormones (hypogonadism).

Osteomalacia causes

Osteomalacia results from a defect in the bone-maturing process. Your body uses the minerals calcium and phosphate to help build strong bones. You might develop osteomalacia if you don’t get enough of these minerals in your diet or if your body doesn’t absorb them properly. These problems can be caused by:

• Vitamin D deficiency. Sunlight produces vitamin D in your skin. People who live in areas where sunlight hours are short or eat a diet low in vitamin D can develop osteomalacia. Vitamin D deficiency is the most common cause of osteomalacia worldwide.
  • Lack of vitamin D produced by the skin may occur in people who:
    • Live in climates with little exposure to sunlight
    • Must stay indoors
    • Work indoors during the daylight hours
    • Wear clothes that cover most of their skin
    • Have dark skin pigmentation
    • Use very strong sunscreen
• Certain surgeries. Normally, the stomach breaks down food to release vitamin D and other minerals that are absorbed in the intestine. This process is disrupted if you have surgery to remove part or all of your stomach, and can result in vitamin D and calcium deficiency. Surgery to remove or bypass your small intestine also can lead to vitamin D and calcium deficiency.
• Celiac disease. In this autoimmune disorder, consuming foods containing gluten, a protein found in wheat, barley and rye, can damage the lining of your small intestine. A damaged intestinal lining doesn’t absorb nutrients well, and can lead to vitamin D and calcium deficiency.
• Kidney or liver disorders. These organs are involved in activating vitamin D in your body. Problems with your kidneys or liver can interfere with your body’s ability to make active vitamin D.
• Drugs. Some drugs used to treat seizures, including phenytoin (Dilantin, Phenytek) and phenobarbital, can cause severe vitamin D deficiency and osteomalacia.
• You may not get enough vitamin D from your diet if you:
  • Are lactose intolerant (have trouble digesting milk products)
  • Do not eat or drink milk products (more common in older adults)
  • Follow a vegetarian diet

Risk Factors for Osteomalacia

Risk of osteomalacia is increased by:

• Inadequate dietary intake of vitamin D, for instance due to lactose intolerance
• Inadequate exposure to sunlight (ultraviolet radiation), which produces vitamin D in the body (increased risk in elderly people who are housebound)
• Malabsorption of vitamin D by the intestines
• Inherited or acquired disorders of vitamin D metabolism
• Advanced renal disease
• Liver disease, and therefore cannot convert vitamin D to its active form
• Cancer
• Phosphate depletion associated with low dietary intake of phosphates
• Certain medications such as those used to treat epilepsy

Osteomalacia prevention

Osteomalacia caused by inadequate sun exposure or a diet low in vitamin D often can be prevented by getting enough vitamin D.

• Eat foods high in vitamin D. Foods naturally rich in vitamin D include oily fish (salmon, mackerel, sardines) and egg yolks. Also look for foods fortified with vitamin D, such as cereal, bread, milk and yogurt.
• Take supplements, if needed. If you don’t get enough vitamins and minerals in your diet or if you have a medical condition affecting the ability of your digestive system to absorb nutrients properly, ask your doctor about taking vitamin D and calcium supplements.

Unprotected sun exposure can increase your risk of skin cancer. There’s no consensus among experts about what amount of sun exposure is safe and enough to prevent or treat osteomalacia.

How long should you spend in the sun?

Most people can make enough vitamin D from being out in the sun daily for short periods with their forearms, hands or lower legs uncovered and without sunscreen from late March or early April to the end of September, especially from 11am to 3pm.

It’s not known exactly how much time is needed in the sun to make enough vitamin D to meet your body’s requirements. This is because there are a number of factors that can affect how vitamin D is made, such as your skin color or how much skin you have exposed. But you should be careful not to burn in the sun, so take care to cover up, or protect your skin with sunscreen, before your skin starts to turn red or burn.

Your risk of sunburn depends on 2 things. How sun-sensitive your skin is, and how strong the UV rays are you’re exposed to. Different people will have a different risk of sunburn on the same day, so it’s a good idea to know when your risk is high, so you can protect your skin.

In general people who have one or more of the following are at more risk:

• skin that burns easily
• light or fair colored skin, hair, or eyes
• lots of moles or freckles
• a history of sunburn
• a personal or family history of skin cancer

People with dark skin, such as those of African, African-Caribbean or south Asian origin, will need to spend longer in the sun to produce the same amount of vitamin D as someone with lighter skin.

• Children aged under six months should be kept out of direct strong sunlight. To ensure they get enough vitamin D, babies and children aged under five years should be given vitamin D supplements even if they do get out in the sun.
  

How long it takes for your skin to go red or burn varies from person to person. You’re the best person to know how your skin reacts in the sun. The more easily you get sunburnt, the more careful you need to be. Remember, you don’t need to peel – if your skin’s gone red or pink in the sun, that’s sunburn, and it’s dangerous. For people with darker skin it may feel irritated, tender or itchy. The longer you stay in the sun, especially for prolonged periods without sun protection, the greater your risk of skin cancer. Using sunbeds is not a recommended way of making vitamin D.

Other things that affect the strength of UV rays are the:

• Time of year – the highest risk months in the US are April to September. Near the equator, there are strong UV rays all year round.
• Altitude – UV rays are stronger the higher you go. So skiers and mountaineers can easily get caught out.
• Cloud cover – over 90% of UV can pass through light cloud.
• Reflection – up to 80% of UV rays are reflected back from snow, 15% from sand, 10% from concrete and up to 30% from water (depending on how choppy it is).

Osteomalacia symptoms

The most common symptoms of osteomalacia are pain in the bones and hips, bone fractures that happen without a real injury, and muscle weakness. Patients can also have difficulty walking.

Symptoms may also occur due to low calcium level. These include:

• Numbness around the mouth
• Numbness of the arms and legs
• Spasms of the hands or feet.

Osteomalacia diagnosis

Osteomalacia can be difficult to diagnose. To pinpoint the cause and to rule out other bone disorders, such as osteoporosis, you might undergo one or more of the following tests:

• Blood and urine tests. These help detect low levels of vitamin D and calcium and phosphate, electrolytes, creatinine, alkaline phosphatase, and parathyroid hormone levels.
• Bone x-rays and a bone density test. Slight cracks in your bones that are visible on X-rays are characteristic of osteomalacia.
• Bone biopsy. Using general anesthesia, a surgeon inserts a slender needle through your skin and into your pelvic bone above the hip to withdraw a small sample of bone. Although a bone biopsy is accurate in detecting osteomalacia, it’s rarely needed to make the diagnosis.

The most important indicator of osteomalacia is low levels of vitamin D, but low levels of calcium or a significant drop in phosphate levels may also indicate osteomalacia. X-rays may be taken to see if there is any evidence of osteomalacia. Also, a bone mineral density scan may be helpful in evaluating the amount of calcium and other minerals present in a patient’s bone segment. These scans are not required to make the diagnosis of osteomalacia. However, they may give important information about a patient’s bone health.

Rarely, the doctor may perform a bone biopsy, in which a sample of bone tissue is taken and examined.

Osteomalacia treatment

Fortunately, getting enough vitamin D through oral supplements for several weeks to months can cure osteomalacia. Maintaining normal blood levels of vitamin D usually requires continuing to take the supplements.

Your health care provider might also recommend that you increase your calcium or phosphorus intake, either through supplements or diet. Treating conditions that affect vitamin D metabolism, such as kidney and liver disease or low phosphate levels, often helps improve the signs and symptoms of osteomalacia.

Dosing of vitamin D depends upon the nature and severity of the deficiency. In patients with normal absorptive capacity, for every 100 units of added vitamin D3 (cholecalciferol), serum calcidiol [25(OH)D] concentrations increase by approximately 1.0 ng/mL. Multiple dosing regimens have been shown to treat vitamin D deficiency effectively. In a 2-month trial of oral vitamin D3 (cholecalciferol) repletion in elderly women with hip fracture, the same cumulative dose given daily (1500 units), weekly (10,500 units), or monthly (45,000 units) resulted in similar increments in serum calcidiol [25(OH)D] levels. Although large annual doses of vitamin D3 (cholecalciferol) increase serum calcidiol [25(OH)D] levels, they are not recommended as undesirable effects of increasing falls and fractures in older adults are seen.

Various regimes which can be used are as follows ³¹⁾:

• High-risk individuals with serum calcidiol [25(OH)D] concentrations <20 ng/mL should be treated with 50,000 IU of vitamin D2 (ergocalciferol) or D3 (cholecalciferol) orally once per week for 6–8 weeks, followed by 800 units of vitamin D daily thereafter.
• For high-risk individuals with serum calcidiol [25(OH)D] levels of 20–30 ng/mL, initial supplementation with 600–800 units of vitamin D3 (cholecalciferol) daily may be sufficient to maintain levels in the target range.
• In pregnant women, weekly doses of 50,000 units for 6–8 weeks are not recommended and 600–800 units of vitamin D3 (cholecalciferol) daily are thought to be safer. Urinary calcium excretion increases in pregnancy, and it should be monitored when treating vitamin D deficiency, especially in women with a history of renal stones.
• In malabsorption or patients with gastrectomy, generally high doses of vitamin D of 10,000–50,000 units daily are needed to correct the deficiency. Hydroxylated vitamin D metabolites are good options because they are more readily absorbed.

The above recommendations are in agreement with Endocrine Society practice guidelines on the treatment of vitamin D deficiency. In adults with vitamin D deficiency, however, the Endocrine Society guidelines suggest a maintenance dose of vitamin D2 or D3 (1500–2000 IU daily) to maintain a serum 25(OH)D concentration above 30 ng/mL ³²⁾.

All patients should consume total calcium of at least 1000 mg (for ages 19–70 years) to 1200 mg (for women of ages 51 through 70 years and for all adults 71 years and older) per day. The upper level (UL) of intake for calcium in most adults is 2000–2500 mg daily. However, a higher calcium dose (up to 4 g/day) may be necessary in patients with malabsorption. Parenteral calcium as calcium gluconate (10–20 mg of elemental calcium per kg intravenously slowly over 5–10 minutes, usually given as 1–2 mL/kg of 10% calcium gluconate) becomes necessary in case of manifest tetany or convulsions. Repeat boluses may also be necessary. In addition, calcitriol may be necessary in doses of 20–100ng/ kg/day in two to three divided doses until calcium levels normalize. High doses of calcium are necessary early in the course of therapy, after which doses are reduced by half for the next 1–2 weeks. Once vitamin D supplementation has been reduced to 400 IU/day with normal PTH and calcidiol [25(OH)D] levels, calcium supplementation is usually not necessary.