Osteoporosis is a major cause of hip fractures, broken wrists and spinal problems in those aged 50 and over. Early screening of people at risk is important for the prevention of osteoporosis.
There are many risk factors for osteoporosis including endocrine, metabolic and nutritional disorders, as well as some prescription medication. The list below outlines factors associated with increased risk:
There have been a number of reports showing evidence of reduced bone mineral density, osteopenia or osteoporosis in 20-50% of patients newly diagnosed with coeliac disease (1).
Some risk factors, specifically related to coeliac disease, may increase the risk of osteoporosis. These include:
These factors need careful assessment. Many of the above problems may result in chronic malabsorption of foods with calcium. The presence of malabsorption leads to greater bone loss.
Studies have shown that more than 75% of adults with untreated coeliac disease suffer from osteopenia or osteoporosis. Even in people with few symptoms of coeliac disease, bone mineral density can be significantly lower than the general population (2).
People with coeliac disease who are on a glutenA protein that is found in the cereals wheat, barley and rye. -free diet show a lower level of bone loss than those not following a gluten-free diet. Therefore, the gluten-free diet may improve bone mineral density (BMDThe strength of your bones. The lower your bone mineral density, the greater your risk of breaking bones. Bone mineral density is measured by having a bone density scan known as a Dual Energy X-ray Absorptiometry (DEXA) scan.). However, research shows BMD may not return to that seen in a matched population (3,4,5).
The prevalence of reduced bone density after one year of following a gluten-free diet is similar to that after three years. This suggests that the extent of bone mass gain in the first year of dietary treatment is indicative of overall BMD improvement (6).
Reduced BMD is also seen in dermatitis herpetiformisUsually shortened to DH, this is a form of coeliac disease where the skin is affected with small blisters. (DH), although to a lesser extent than in coeliac disease, except where the body mass index (BMI) is less than 20kg/m (3,6).
The cause of changes in bone health in coeliac disease is multifactorial - both systemic and local mechanisms may play a role.
Intestinal damage seen in untreated coeliac disease can lead to chronic malabsorption of nutrients including calcium. Calcium malabsorption and subnormal levels of serum calcium result in damage to bone health. Intestinal malabsorption can also result in a reduced BMI.
Hypocalcaemia (low serum calcium) can lead to secondary hyperparathyroidism. Hypothyroidism leads to high levels of parathyroid hormone which results in calcium being absorbed from the bones into the blood.
Several other mechanisms may effect calcium levels and bone health.
Some people with coeliac disease can have lactose intolerance. Many foods which contain lactose are higher in calcium. People following a low lactose diet can have a reduced intake of calcium which can impact on bone health. Calcium levels can also be affected by increased intestinal secretion or decreased re-absorption.
Osteoblasts play a role in the formation of bone. Osteoclasts are cells which are responsible for the removal of bone. The balance of osteoblasts and osteoclasts is important for bone repair.
Pro-inflammatory cytokines are responsible for osteoclast activation. Cytokines can have an impact on both normal and abnormal bone formation.
In coeliac disease increased resorption (where old bone is removed from the skeleton) is not balanced out by increased bone formation. These changes in bone are similar to those seen in Crohn's disease.
In women with coeliac disease, the role of associated gynaecological disorders should be considered. Amenorrhoea is a more common finding in coeliac disease than the general population and sex hormone imbalance represents an important risk factor for the development of osteoporosis.
There is evidence that early diagnosis and treatment of coeliac disease in childhood prevents bone loss. Early diagnosis also allows preventative action to be taken. Most children can then reach normal peak bone mass. (8)
Diagnosis of osteoporosis in people with coeliac disease is determined by a Dual energy X-ray absorptiometry (DEXA) scan which measures bone density.
The World Health Organisation (WHO) has criteria for measuring bone mass. WHO recommend using measurements from a T-score.
The T-score is an index representing the number of standard deviations by which the patient value differs from the average peak bone mass of a young adult reference population.
A diagnosis of osteopenia is made when the T-score is between -1 and -2.5. A diagnosis of osteoporosis is made when the T-score is less than -2.5.
There are no clear guidelines on whether people diagnosed with coeliac disease should receive a DEXA scan. There are also no recommendations for repeat measurements to be carried out (9,10).
There is, however, suggested guidance on the diagnosis and treatment of osteoporosis in coeliac disease (6).
Due to the benefit of early diagnosis of coeliac disease on bone health, there is no need to measure bone density in children who are fully compliant with the diet.
For people with coeliac disease who are diagnosed in adulthood, an approach based on clinical presentation should be followed.
People with coeliac disease and malabsorption are potentially at a higher risk of osteoporosis and bone fractures than people with coeliac disease that are asymptomatic. It has been suggested that people with symptoms should have their BMD measured at diagnosis and after two years on a strict gluten-free diet. Only people whose baseline BMD is below normal will require any further follow-up scan.
Asymptomatic patients may not require bone measurement at diagnosis, but instead BMD should be measured after the first year of strict adherence to a gluten-free diet.
In women, if the diagnosis is made earlier the BMD should be measured at the menopause. A single measurement at menopause may not be enough. This is because there is variation in the rate and duration of bone loss before and after menopause. Therefore, it is suggested to repeat the BMD after two years (10).
Further information on the management of osteoporosis and coeliac disease is on our website.
1 Bianchi ML & Bardella MT (2002) Bone and Celiac Disease. Calcif Tissue Int 71: 465-471
2 Corazza GR, Di Sario A, Cecchetti L et al (1996) Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease. Bone 18: 525-530.
3 Corazza GR, Di Sario A, Cecchetti L, et al (1995) Bone mass and metabolism in patients with celiac disease. Gastroenterology. 109(1): 122-8.
4 McFarlane XA, Bhalla AK, Reeves DE et al (1995) Osteoporosis in treated adult coeliac disease. Gut. 36(5): 710-4.
5 Pazianas M, Butcher GPGeneral Practitioner, or local doctor, Subhani JM, et al (2005) Calcium absorption and bone mineral density in celiacs after long term treatment with gluten-free diet and adequate calcium intake. Osteoporosis International. 16(1): 56-63.
6 Corazza GR, Di Stefano M, Maurino E, et al (2005) Bones in coeliac disease: diagnosis and treatment. 19(3): 453-65
7 Sugai E, Chernavsky A, Pedreira S, et al (2002) Bone specific antibodiesExist in the blood and are used by the immune system to attack viruses or bacteria. in sera from patients with coeliac disease: characterisation and implications in osteoporosis. Journal of Clinical Immunology. 22(6): 353-62
8 Mora S, Barera G, Ricotti A, et al (1993) Effect of gluten-free diet on bone mineral content in growing patients with coeliac disease. American Journal of Clinical Nutrition. 57(2): 224-8.
9 Lewis NR & Scot BB (2005) Should patients with coeliac disease have their bone mineral density measured? European Journal of Gastroenterology and Hepatology. 17(10):1065-70
10 Scot EM, Gaywood I, Scott BB et al (2000) Guidelines for osteoporosis in coeliac disease and inflammatory bowel disease. British Society of Gastroenterology. Gut. 46(S1): i1-8