Effects of Neurological Disorders on Bone Health - Kelly et al 2020

Sly Saint · Dec 1, 2020

Neurological diseases, particularly in the context of aging, have serious impacts on quality of life and can negatively affect bone health. The brain-bone axis is critically important for skeletal metabolism, sensory innervation, and endocrine cross-talk between these organs. This review discusses current evidence for the cellular and molecular mechanisms by which various neurological disease categories, including autoimmune, developmental, dementia-related, movement, neuromuscular, stroke, trauma, and psychological, impart changes in bone homeostasis and mass, as well as fracture risk.

Likewise, how bone may affect neurological function is discussed. Gaining a better understanding of brain-bone interactions, particularly in patients with underlying neurological disorders, may lead to development of novel therapies and discovery of shared risk factors, as well as highlight the need for broad, whole-health clinical approaches toward treatment.
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Chronic Fatigue
Chronic fatigue syndrome (CFS) is a complex neurological disorder associated with persistent, overwhelming fatigue that affects > 3% of the population in Western countries and is more prevalent in women (Griffith and Zarrouf, 2008).

Diagnostic criteria include severe, persistent fatigue for at least 6 months, exclusion of other medical disorders, and observation of at least four minor symptoms, including impaired memory, nausea, extreme post-exertion fatigue, headaches, muscle pain, sore throat, and poor sleep (Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome et al., 2015).
There remains a lack of treatment and diagnostics tools for CFS, although glucocorticoids have been used (McKenzie et al., 2000).

Bone loss and increased fracture risk have been reported in individuals with CFS, independent of glucocorticoid use. Hoskin et al. found that hip BMD was approximately 7% lower in women with CFS (Hoskin et al., 2006). A prospective study reported a 1.16-fold increased risk of fracture in the CFS cohort without osteoporosis compared to the non-CFS cohort (Chen C.-S. et al., 2014).

However, no mechanistic insights were provided in these studies. Other studies have reported that IGF-1 levels are altered in CFS patients (Buchwald et al., 1996; Berwaerts et al., 1998; Cleare et al., 2000; Nijs et al., 2003). IGF-1 is essential for osteoblast proliferation, thus impaired secretion could lead to bone loss.

Studies are needed to further characterize those CFS patients with low serum IGF-1 to determine if these subgroups have increased fracture risk compared to CFS patients with normal or high levels of IGF-1. High prevalence of mycoplasma infections has also been reported in CFS patients (Choppa et al., 1998; Nasralla et al., 1999), which can stimulate macrophage activation and release of pro-inflammatory cytokines that enhance osteoclast activity. M. fermentans has been shown to produce 2-kDa macrophage-activating lipopeptide (MALP-2), which stimulates macrophages and bone resorption in a dose-dependent manner and is increased with CFS (Piec et al., 1999). Thus, chronic fatigue may induce bone loss or increase fracture risk through increased inflammation and/or dysregulation of growth factors.
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https://www.frontiersin.org/articles/10.3389/fpsyg.2020.612366/full

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Effects of Neurological Disorders on Bone Health - Kelly et al 2020

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