Abstract
BackgroundLow bone mass is prevalent in ambulatory multiple sclerosis (MS) patients even shortly after clinical onset. The mechanism is not known, but could involve shared etiological risk factors between MS and low bone mass such as hypovitaminosis D operating before disease onset, or increased bone loss after disease onset. The aim of this study was to explore the mechanism of the low bone mass in early-stage MS patients.Methodology/Principal FindingsWe performed a population-based case-control study comparing bone turnover (cross-linked N-terminal telopeptide of type 1 collagen; NTX, bone alkaline phosphatase; bALP), metabolism (25-hydroxy- and 1, 25-dihydroxyvitamin D, calcium, phosphate, and parathyroid hormone), and relevant lifestyle factors in 99 patients newly diagnosed with clinically isolated syndrome (CIS) or MS, and in 159 age, sex, and ethnicity matched controls. After adjustment for possible confounders, there were no significant differences in NTX (mean 3.3; 95% CI −6.9, 13.5; p = 0.519), bALP (mean 1.6; 95% CI −0.2, 3.5; p = 0.081), or in any of the parameters related to bone metabolism in patients compared to controls. The markers of bone turnover and metabolism were not significantly correlated with bone mass density, or associated with the presence of osteoporosis or osteopenia within or between the patient and control groups. Intake of vitamin D and calcium, reported UV exposure, and physical activity did not differ significantly.Conclusions/SignificanceBone turnover and metabolism did not differ significantly in CIS and MS patients with prevalent low bone mass compared to controls. These findings indicate that the bone deficit in patients newly diagnosed with MS and CIS is not caused by recent acceleration of bone loss, and are compatible with shared etiological factors between MS and low bone mass.
Highlights
Multiple sclerosis (MS) is a demyelinating inflammatory disease of the central nervous system [1]
Conclusions/Significance: Bone turnover and metabolism did not differ significantly in clinically isolated syndrome (CIS) and multiple sclerosis (MS) patients with prevalent low bone mass compared to controls. These findings indicate that the bone deficit in patients newly diagnosed with MS and CIS is not caused by recent acceleration of bone loss, and are compatible with shared etiological factors between MS and low bone mass
The overall aim of this study was to explore the mechanism of the low bone mass previously recorded in patients newly diagnosed with CIS and MS compared to controls [15]
Summary
Multiple sclerosis (MS) is a demyelinating inflammatory disease of the central nervous system [1]. Vitamin D is essential for bone growth, preservation, and mineral homeostasis, and has immunomodulatory effects [10] Environmental factors such as hypovitaminosis D acting from conception to early adult life might be of importance for the risk of MS [11,12,13]. We have earlier found that low bone mass was more prevalent in newly diagnosed patients with MS and clinically isolated syndrome (CIS) suggestive of demyelinating disease than in controls [15]. This finding is compatible with the hypothesis that MS and osteoporosis share etiological factors, and that the bone deficit in the newly diagnosed patients could be explained by low bone mass before disease onset. The aim of this study was to explore the mechanism of the low bone mass in early-stage MS patients
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