The Relationship Between Degenerative Changes and Osteoporosis in the Lumbar Spine

Margulies, Joseph Y.; Payzer, A; Nyska, Meir; Neuwirth, Michael G.; Floman, Yizhar; Robin, Gordon C.

doi:10.1097/00003086-199603000-00017

Cited by 71 publications

(50 citation statements)

References 17 publications

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“…Similarly, in a previous study patients with severe osteoporosis of the distal radius were found to have more severe OA of the lumbar disc and facets (38). Furthermore, it has been shown that antiresorptive agents, such as estrogen and some bisphosphonates, may have chondroprotective benefits, although this is not a uniform finding (11,39).…”

Section: Discussionmentioning

confidence: 89%

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

Blair-Levy

Watts

Fiorientino

et al. 2008

Arthritis & Rheumatism

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Objective. This study was undertaken to test the hypothesis that abnormalities of the subchondral bone can result in osteoarthritis (OA).Methods. We used a knockin model of human osteogenesis imperfecta, the Brittle IV (Brtl) mouse, in which defective type I collagen is expressed in bone. OA in individual mice was documented by micro-magnetic resonance imaging (micro-MRI) and micro-computed tomography (micro-CT). Alterations in the knee joints were confirmed by histopathologic and immunohistochemical analysis. In addition, atomic force microscopy (AFM) was used to assess the ultrastructure of the articular cartilage and subchondral bone matrix.Results. Brtl mice had decreased integrity of bone but initially normal articular cartilage. However, by the second month of life, Brtl mice developed alterations of the cartilage that were characteristic of OA, as documented by micro-CT, micro-MRI, and histologic evaluation. In addition, chondrocyte loss and breakdown of the collagen matrix in the residual cartilage were demonstrated using AFM.Conclusion. The Brtl mouse model demonstrates that progressive destruction of articular cartilage characteristic of OA may be secondary to altered architecture of the underlying subchondral bone.

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Section: Discussionmentioning

confidence: 89%

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

Blair-Levy

Watts

Fiorientino

et al. 2008

Arthritis & Rheumatism

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“…The vast majority of the studies on spinal arthropathy and disc degeneration suggest that increased mineral density of spinal and appendicular bones plays a role in etiopathogenesis (13)(14)(15)(16)(17). On the contrary, a few studies demonstrated that low spinal BMD is associated with degenerative changes in the lumbar spine (18,19).…”

Section: Discussionmentioning

confidence: 99%

Vertebral body bone mineral density in patients with lumbar spondylolysis: a quantitative CT

Gezer

Balcı²,

Kalemcı³

et al. 2017

Diagn Interv Radiol

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“…Both degeneration of the intervertebral disc and degeneration of the facet joints have been reported to be observed clinically in concert and independently [245] and there is still controversy over the time course of these events and which tissue degenerates first or follows. Margulies et al [255] found a significant correlation between the presence of lumbar degenerative disc disease and facet arthrosis and proposed a degeneration process by which the disc disease follows facet degeneration in small underweight persons presenting with osteoporosis. In that schema, the proposed pathologic process starts as osteoporosis that creates microfractures in the vertebral bodies which result in the facets' malalignment and then leads to cartilage wear and tear.…”

Section: Intervertebral Disc and Facet Joint Degenerationmentioning

confidence: 99%

“…In that schema, the proposed pathologic process starts as osteoporosis that creates microfractures in the vertebral bodies which result in the facets' malalignment and then leads to cartilage wear and tear. This degeneration of the facet leads to the mechanical instability of the vertebral motion segment that increases the mechanical stresses supported by the disc, damaging its tissues and causing its progressive degeneration [255]. However, several studies have concluded that in most cases, facet joint degeneration is always associated with and preceded by adjacent disc degeneration [92,242,245,256].…”

Section: Intervertebral Disc and Facet Joint Degenerationmentioning

confidence: 99%

Spinal Facet Joint Biomechanics and Mechanotransduction in Normal, Injury and Degenerative Conditions

Jaumard¹,

Welch²,

Winkelstein³

2011

J. Biomech. Eng.

272

225

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The facet joint is a crucial anatomic region of the spine owing to its biomechanical role in facilitating articulation of the vertebrae of the spinal column. It is a diarthrodial joint with opposing articular cartilage surfaces that provide a low friction environment and a ligamentous capsule that encloses the joint space. Together with the disc, the bilateral facet joints transfer loads and guide and constrain motions in the spine due to their geometry and mechanical function. Although a great deal of research has focused on defining the biomechanics of the spine and the form and function of the disc, the facet joint has only recently become the focus of experimental, computational and clinical studies. This mechanical behavior ensures the normal health and function of the spine during physiologic loading but can also lead to its dysfunction when the tissues of the facet joint are altered either by injury, degeneration or as a result of surgical modification of the spine. The anatomical, biomechanical and physiological characteristics of the facet joints in the cervical and lumbar spines have become the focus of increased attention recently with the advent of surgical procedures of the spine, such as disc repair and replacement, which may impact facet responses. Accordingly, this review summarizes the relevant anatomy and biomechanics of the facet joint and the individual tissues that comprise it. In order to better understand the physiological implications of tissue loading in all conditions, a review of mechanotransduction pathways in the cartilage, ligament and bone is also presented ranging from the tissue-level scale to cellular modifications. With this context, experimental studies are summarized as they relate to the most common modifications that alter the biomechanics and health of the spine-injury and degeneration. In addition, many computational and finite element models have been developed that enable more-detailed and specific investigations of the facet joint and its tissues than are provided by experimental approaches and also that expand their utility for the field of biomechanics. These are also reviewed to provide a more complete summary of the current knowledge of facet joint mechanics. Overall, the goal of this review is to present a comprehensive review of the breadth and depth of knowledge regarding the mechanical and adaptive responses of the facet joint and its tissues across a variety of relevant size scales.

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The Relationship Between Degenerative Changes and Osteoporosis in the Lumbar Spine

Cited by 71 publications

References 17 publications

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

Vertebral body bone mineral density in patients with lumbar spondylolysis: a quantitative CT

Spinal Facet Joint Biomechanics and Mechanotransduction in Normal, Injury and Degenerative Conditions

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