Newer Therapies for Osteoporosis

Palaniswamy, Chandrasekar; Selvaraj, Dhana Rekha; Rao, Varuni; Patel, Umesh

doi:10.1097/mjt.0b013e3181a6ee1c

Cited by 5 publications

(3 citation statements)

References 19 publications

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“…Several new therapeutic targets for building bone have profoundly changed our understanding as to why age-related bone loss occurs. Two inhibitory proteins, known as sclerostin (Burgers & Williams, 2013) and Dickkopf-1 (DKK1), have been identified and both proteins interact with the Wnt coreceptors LRP5/6 to inhibit the canonical Wnt/beta-catenin signaling pathway, causing a decrease in bone formation (Moester et al, 2010;Palaniswamy et al, 2010;Paszty et al, 2010;Lewiecki, 2011;Costa & Bilezikian, 2012;Ke et al, 2012;Lim & Clarke, 2012;Ohlsson, 2013). DKK1 appears to have a greater role in developing animals than in adults (Ke et al, 2012).…”

Section: Anabolic Therapies and Skeletal Painmentioning

confidence: 99%

The neurobiology of skeletal pain

Mantyh

2014

Eur J of Neuroscience

154

158

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Disorders of the skeleton are one of the most common causes of chronic pain and long-term physical disability in the world. Chronic skeletal pain is caused by a remarkably diverse group of conditions including trauma-induced fracture, osteoarthritis, osteoporosis, low back pain, orthopedic procedures, celiac disease, sickle cell disease and bone cancer. While these disorders are diverse, what they share in common is that when chronic skeletal pain occurs in these disorders, there are currently few therapies that can fully control the pain without significant unwanted side effects. In this review we focus on recent advances in our knowledge concerning the unique population of primary afferent sensory nerve fibers that innervate the skeleton, the nociceptive and neuropathic mechanisms that are involved in driving skeletal pain, and the neurochemical and structural changes that can occur in sensory and sympathetic nerve fibers and the CNS in chronic skeletal pain. We also discuss therapies targeting nerve growth factor or sclerostin for treating skeletal pain. These therapies have provided unique insight into the factors that drive skeletal pain and the structural decline that occurs in the aging skeleton. We conclude by discussing how these advances have changed our understanding and potentially the therapeutic options for treating and/or preventing chronic pain in the injured, diseased and aged skeleton. GRAPHICAL ABSTRACT: Skeletal pain is common and frequently difficult to fully control. Recent data suggests that the skeleton is innervated by a restricted set of nociceptors and that many skeletal pains have both a nociceptive and a neuropathic component. Significant progress has been made in defining the mechanisms that drive skeletal pain and the factors that control skeletal remodeling. These insights have the potential to fundamentally transform our understanding and ability to prevent and/or treat skeletal pain due to injury, disease, and aging.

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Section: Anabolic Therapies and Skeletal Painmentioning

confidence: 99%

The neurobiology of skeletal pain

Mantyh

2014

Eur J of Neuroscience

154

158

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“…Recently, significant progress has been made in identifying several novel osteo-anabolic therapeutic targets (Palaniswamy et al 2010; Lim and Clarke 2012; Ohlsson 2013). Here, we focus on one of these which is the protein sclerostin, a small (24 kDa) secreted glycoprotein that is expressed in the adult skeleton osteocytes and chondrocytes.…”

Section: Introductionmentioning

confidence: 99%

Sclerostin Immunoreactivity Increases in Cortical Bone Osteocytes and Decreases in Articular Cartilage Chondrocytes in Aging Mice

Thompson

Jiménez-Andrade

Mantyh

2015

J Histochem Cytochem.

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Sclerostin is a 24-kDa secreted glycoprotein that has been identified as a negative modulator of new bone formation and may play a major role in age-related decline in skeletal function. Although serum levels of sclerostin markedly increase with age, relatively little is known about whether cells in the skeleton change their expression of sclerostin with aging. Using immunohistochemistry and confocal microscopy, we explored sclerostin immunoreactivity (sclerostin-IR) in the femurs of 4-, 9-, and 24-month-old adult C3H/HeJ male mice. In the femur, the only two cell types that expressed detectable levels of sclerostin-IR were bone osteocytes and articular cartilage chondrocytes. At three different sites along the diaphysis of the femur, only a subset of osteocytes expressed sclerostin-IR and the percentage of osteocytes that expressed sclerostin-IR increased from approximately 36% to 48% in 4- vs. 24-month-old mice. In marked contrast, in the same femurs, there were ~40% fewer hypertrophic chondrocytes of articular cartilage that expressed sclerostin-IR when comparing 24- vs. 4-month-old mice. Understanding the mechanism(s) that drive these divergent changes in sclerostin-IR may provide insight into understanding and treating the age-related decline of the skeleton.

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“…Typically, in osteoporotic patients high levels of Ros and persistent low grade inflammation are observed (116). clinical data have postulated that tomatoes have a beneficial effect to bone health (117).…”

Section: Consequences Of Chronic Inflammationmentioning

confidence: 99%

Tomatoes as functional food

Hazewindus¹

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Newer Therapies for Osteoporosis

Cited by 5 publications

References 19 publications

The neurobiology of skeletal pain

The neurobiology of skeletal pain

Sclerostin Immunoreactivity Increases in Cortical Bone Osteocytes and Decreases in Articular Cartilage Chondrocytes in Aging Mice

Tomatoes as functional food

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