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Bone Loss, Osteopenia and Multiple Sclerosis Explored in New Scholarly Review

In a recent review published in the journal Seminars in Arthritis and Rheumatism, German researchers explored the complexity of interwoven pathways of osteopenia, and how it relates to diseases such as MS.

Osteopenia is a bone condition characterized by a decreased density of bone, which leads to bone weakening and an increased risk of breaking a bone (fracture). Osteopenia and osteoporosis are related conditions. The difference between osteopenia and osteoporosis is that in osteopenia the bone loss is not as severe as in osteoporosis. This means that someone with osteopenia is more likely to fracture a bone than someone with a normal bone density but is less likely to fracture a bone than someone with osteoporosis.

The condition is common in patients with syndromes such as ankylosing spondylitis, rheumatoid arthritis, psoriasis, pemphigus vulgarism, systemic lupus erythematosus, multiple sclerosis, and inflammatory bowel diseases.

Multiple sclerosis (MS) is a chronic inflammatory disease affecting the brain and spinal cord, leading to muscle weakness, coordination and balance problems, as well as sensation disorders, visual and cognitive deficits, and gradual limitation of functioning. Subjects with MS have multiple risk factors for osteopenia.

In the pathological lesion of the brain and spinal cord that characterizes MS, there are differences in the disease according to the evolution of the lesion (i.e., progressive MS vs relapsing remitting), including residual mobility and functionality, the ability to walk and stand, and drug treatment (i.e., corticosteroid therapy, interferon therapy). In addition, there are differences in the degree of spasticity experienced by MS subjects, a complication caused by alterations in the nerve impulses to the muscles resulting in spasms and stiffness. Disturbed coordination and balance in these subjects cause frequent falls.

There are several studies of bone mass loss in women with MS. Women with serious disabilities have low bone density related to the lack of activity (reduced mobility, reduced loading on bone) and worsening of the disability. Bone loss is associated with an activation of the immune system or inflamm-aging in the form of chronic active and acute, or chronic smoldering inflammation, bone loss is typically discussed to be an “accident of inflammation.”

In their study titled “Evolutionary medicine and bone loss in chronic inflammatory diseases-A theory of inflammation-related osteopenia,” Rainer Straub from the Laboratory of Experimental Rheumatology and Neuroendocrine Immunology, University Hospital Regensburg in Germany and colleagues examined articles published in PubMed regarding the topic of osteopenia and diseases such as MS.

The researchers determined that evolutionary medicine (which include energy regulation and neuroendocrine regulation of homeostasis and immune function) reveals that adaptive programs for acute inflammation are wrongly used in chronic inflammation. One of these adaptive programs in acute inflammation is provision of calcium and phosphorus from bone to the non-skeleton tissues.  However, when acute inflammation enters a chronic state due to the inability to terminate inflammation (e.g., in autoimmunity or in continuous immunity against microbes), the acute program of bone loss is a misguided adaptive program.

According to the researchers, while these considerations might explain the deeper meaning of bone resorption in inflammation, the final answers to these questions remain dependent on finding the major molecular pathways to better treat these disease sequelae. As the researchers concluded, their review aims at exploring the idea that sometimes the critical pathways leading to osteopenia can be outside usual mainstream thinking. It also demonstrates that osteopenia must be a multifactorial affair — all insights that could shape the development of next-generation treatment approaches for MS patients suffering from bones loss.

Story Source: The above story is based on materials provided by MULTIPLESCLEROSISNEWSTODAY
Note: Materials may be edited for content and length

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