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 Table of Contents  
Year : 2019  |  Volume : 14  |  Issue : 2  |  Page : 100-101

Low bone mass and its correlation in systemic sclerosis

Department of Endocrinology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication8-Jul-2019

Correspondence Address:
Dr. Subhash Yadav
Professor Endocrinology, ‘C’ Block, Department of Endocrinology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebareli Road, Lucknow - 226 014, UP
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-3698.260823

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How to cite this article:
Gunna SH, Yadav S. Low bone mass and its correlation in systemic sclerosis. Indian J Rheumatol 2019;14:100-1

How to cite this URL:
Gunna SH, Yadav S. Low bone mass and its correlation in systemic sclerosis. Indian J Rheumatol [serial online] 2019 [cited 2021 May 6];14:100-1. Available from:

Osteoporosis, which means porous bone, is characterized by low bone density in microarchitectural distribution of the bone tissue. Osteoporosis is estimated to affect 200 million women worldwide approximately one-tenth of the women aged 60 years, and worldwide, osteoporosis causes more than 8.9 million fractures annually, resulting in an osteoporosis fracture every 30 s. In India, it appears that Indians have poor bone health, and osteoporosis is common. In 2013, sources estimated that 50 million Indians are either osteoporosis or have low bone mass (osteopenia). Studies indicate that osteoporosis and osteopenia may occur at relatively younger age in Indian population.[1]

Bone mass can be assessed at a number of sites including the lumbar spine, the hip, and the forearm. Dual-energy X-ray absorptiometry technology is the gold standard for diagnosing osteoporosis by measuring bone density. The World Health Organization has defined osteoporosis as a bone mineral density (BMD) more than 2.5 standard deviations (SDs) below the young normal mean and osteopenia is defined as BMD between 1 and 2.5 SDs below the young normal mean.[2]

It is evident from various studies that lower the bone density, the greater is the risk for fracture. The risk depends on the bone (hip vs. lumbar spine), ethnicity, body mass index, gender, and health of the person. Conditions such as aging, menopause, metabolic and endocrine diseases, inadequate physical activity, smoking, alcohol intake, Vitamin D deficiency, thyroid dysfunction, and family history of osteoporosis have been proposed as an associated risk factor of low BMD.[3]

Systemic sclerosis (SSc) is an uncommon connective tissue disease characterized by progressive fibrosis of the skin, vasculopathy, and immune activation. Skeletal manifestations of SSc may include fibrosis of the joint capsule, flexion contractures, thickened tendon, or inflammatory erosive and nonerosive arthritis.[4] There have been conflicting data reporting whether SSc increases the risk of osteoporosis. This is mainly because of heterogeneous nature of the SSc which affects various organ systems of the body. Risk factors specific to SSc that may increase the risk of osteopenia or osteoporosis include chronic inflammation, early menopause, immobilization, soft tissue calcification, depleting calcium store, and disturbances of Vitamin D metabolism in the skin, kidney, and gastrointestinal tract. Above all, long-term glucocorticoid widely used in the treatment of SSc increases the risk of osteoporosis and fractures. Glucocorticoids have direct and indirect effects on bone remodeling. Vertebral fractures are the most common fractures associated with glucocorticoids. The risk increases within 3 months and peaks at 12 months of use.[5]

Sharma et al. studied the prevalence of osteoporosis and osteopenia in 100 patients of SSc and correlated with parathyroid hormone (PTH).[6] They found that 28% of the patients had osteoporosis at the lumbar spine and 6% at the femoral neck while 44% had osteopenia at spine and 36% at the femoral neck. High PTH was observed in 21% of patients and it was significantly correlated with low bone mass at the hip but not at the spine. Surprisingly, 41% of the patients had low calcium, not a common finding, which may be related to low calcium diet or poor absorption of calcium from the gut (oral calcium intake not mentioned). Most probable cause for the high prevalence of osteopenia and osteoporosis was of chronic nature of the disease, very high prevalence of Vitamin D deficiency, and prolonged use glucocorticoid used by the patients. However, this study was carried out in SSc patients only and not compared with controls. Another reason for high prevalence of osteoporosis and osteomalacia may be the data of SSc patients were compared to western normative data, not with the Indian data. It is known fact that overall, the BMD at all sites in the Indian populations seems to be 5%–15% lower than that in Caucasians.[7]

Hence, overall significantly decreased BMD was observed in this study by Sharma et al. The goal of the osteopenia/osteoporosis therapy is the prevention of fracture. The first line of management includes lifestyle modification that is cessation of smoking, reduction of alcohol consumption, and increase physical activity. Vitamin D supplementation (600–800 IU/day) and adequate calcium intake (1000–1200 mg/day) are recommended as preventive treatment in patients at the risk of or with osteoporosis. Pharmacological treatment for osteoporosis patient of SSc includes estrogen, bisphosphonates, selective estrogen receptor modulators, recombinant PTH, strontium ranelate, and monoclonal antibody against the receptor activator of nuclear factor KB ligand. The 2017 Guidelines of the American College of Rheumatology recommend pharmacologic treatment to prevent additional fractures in any patient with a previous osteoporotic fracture who is receiving glucocorticoids. The American College of Rheumatology also recommended pharmacologic treatment for adults who are 40 years of age or older and if the 10-year risk of major osteoporotic fracture is at least 20% or if the risk of hip fracture is at least 3% according to the FRAX tool.[8]

  References Top

Mithal A, Bansal B, Kyer CS, Ebeling P. The Asia-Pacific regional audit-epidemiology, costs, and burden of osteoporosis in India 2013: A report of international osteoporosis foundation. Indian J Endocrinol Metab 2014;18:449-54.  Back to cited text no. 1
Consensus development conference: Prophylaxis and treatment of osteoporosis. Osteoporos Int 1991;1:114-7.  Back to cited text no. 2
Wee J, Sng BY, Shen L, Lim CT, Singh G, Das De S. The relationship between body mass index and physical activity levels in relation to bone mineral density in premenopausal and postmenopausal women. Arch Osteoporos 2013;8:162.  Back to cited text no. 3
Rachner TD, Khosla S, Hofbauer LC. Osteoporosis: Now and the future. Lancet 2011;377:1276-87.  Back to cited text no. 4
Loucks J, Pope JE. Osteoporosis in scleroderma. Semin Arthritis Rheum 2005;34:678-82.  Back to cited text no. 5
Sharma S, Dhooria A, Singh T, Dhir V, Chattopadhyay A, Mishra D, et al. Bone mineral density is decreased in patients with systemic sclerosis and correlates with serum intact parathormone levels: A cross-sectional study. Indian J Rheumatol 2019;2. [In press].  Back to cited text no. 6
Tandon N, Marwaha RK, Kalra S, Gupta N, Dudha A, Kochupillai N. Bone mineral parameters in healthy young Indian adults with optimal vitamin D availability. Natl Med J India 2003;16:298-302.  Back to cited text no. 7
Buckley L, Guyatt G, Fink HA, Cannon M, Grossman J, Hansen KE, et al. 2017 American College of Rheumatology guideline for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Rheumatol 2017;69:1521-37.  Back to cited text no. 8


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