Generalized osteoarthritis associated with increased insulin‐like growth factor types i and ii and transforming growth factor β in cortical bone from the iliac crest. possible mechanism of increased bone density and protection against osteoporosis

Dequeker, Jan; Mohan, Subburaman; Finkelman, Richard D.; Aerssens, Jeroen; Baylink, David J.

doi:10.1002/art.1780361209

Cited by 191 publications

(139 citation statements)

References 48 publications

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“…Other studies showed a higher presence of bone growth factors in patients with DISH, and suggested a possible relevant role for those substances in the pathogenesis of the disease [30]. The finding may be confirmed by the presence of hyperostosis in some disorders with a high production of growth factors [7]. In fact, DISH is a diffuse systemic condition in which it is likely that both mechanical and local factors act on the propensity to deposit new bone.…”

Section: Discussionmentioning

confidence: 84%

“…More recently it has been suggested that systemic metabolic factors may be involved in the new bone growth that characterises the disease. On the other hand, the presence of such systemic factors has been hypothesised also in primary osteoarthritis (OA); in fact, increased skeletal concentrations of insulin-like growth factor I, insulin-like growth factor II and transforming growth factor b have been considered as possible mechanisms that increase bone density in OA [7]. Although DISH is often considered to be a variant of OA, diarthrodial joints are not involved, intervertebral joints spaces are preserved and apophyseal joints appear to be normal.…”

Section: Introductionmentioning

confidence: 99%

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Study of Peripheral Bone Mineral Density in Patients with Diffuse Idiopathic Skeletal Hyperostosis

Franco

Mauceri

Scavalli

et al. 2000

Clinical Rheumatology

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Diffuse idiopathic skeletal hyperostosis (DISH) is an ossifying systemic enthesopathy which involves not only the spine but which may also appear in other sites. Degenerative, inflammatory and metabolic factors have been reported for a possible pathogenic role in the new bone growth that characterises DISH. In the present study peripheral bone mineral density (BMD) has been measured in patients affected by DISH and the results compared to those of a control group. Forty-two patients (33 females and 9 males) affected by DISH and 84 controls (66 females and 18 males) were examined. All subjects underwent radiological study of the lumbar and dorsal spine and the pelvis. BMD was evaluated using dual-energy X-ray absorptiometry and the examination was performed in the distal radius. In DISH patients the mean value of BMD was significantly higher than in controls (P50.002), even when it was referred to sex subgroups. Statistical analysis showed significant differences between both the two male groups (P50.002) and the two female groups (P50.01). In the two female subgroups (DISH patients and controls) BMD was significantly inversely related to age and to the duration of the postmenopausal period. The present study showed higher BMD in DISH patients than in the control group.

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Section: Discussionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Study of Peripheral Bone Mineral Density in Patients with Diffuse Idiopathic Skeletal Hyperostosis

Franco

Mauceri

Scavalli

et al. 2000

Clinical Rheumatology

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“…Gevers and Dequeker also showed elevated serum osteocalcin levels in women with hand OA, and elevated osteocalcin in cortical bone explants [24]. Moreover, levels of growth factors such as insulin-like growth factor (IGF)-1 and -2 and transforming growth factor (TGF)-β1 are also higher in samples of iliac crest bone of patients with OA [25]. Considering that this bone is a non-weight-bearing site and at some distance from joints, this would suggest a generalised dysfunction in bone metabolism.…”

Section: Correlation Between In Vivo Findings In Animals and Human Oamentioning

confidence: 91%

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

Tat

Lajeunesse

Pelletier

et al. 2010

Best Practice & Research Clinical Rheumatology

153

121

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Over the past few decades, significant progress has been made with respect to new concepts about the pathogenesis of osteoarthritis (OA). This article summarises some of the knowledge we have today on the involvement of the subchondral bone in OA. It provides substantial evidence that changes in the metabolism of the subchondral bone are an integral part of the OA disease process and that these alterations are not merely secondary manifestations, but are part of a more active component of the disease. Thus, a strong rationale exists for therapeutic approaches that target subchondral bone resorption and/or formation, and data evaluating the drugs targeting bone remodelling raise the hope that new treatment options for OA may become available.

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“…A role of bone has also been speculated, in that obesity increases subchondral bone stiffness, making bone less adept at coping with impact loads (7,8). The increased stiffness of bone may subsequently redistribute a greater force across the underlying articular cartilage, increasing its vulnerability to degenerative changes (9).…”

mentioning

confidence: 99%

Obesity and osteoarthritis: Is leptin the link?

Sandell¹

2009

Arthritis & Rheumatism

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There is significant interest in the correlation between adipose regulators of metabolism, inflammation, and the occurrence of osteoarthritis (OA). In this issue of Arthritis & Rheumatism, Griffin and colleagues report the results of their investigation of the role of leptin (1). The investigators hypothesized that obesity in mice resulting from deletion of the leptin gene (ob/ob) or deletion of the leptin receptor gene (db/db) would result in an increased incidence of knee OA, systemic inflammation, and altered subchondral bone morphology. In both of these mouse strains, adiposity was increased by ϳ10-fold compared with controls. Surprisingly, the incidence of OA was not higher in ob/ob and db/db mice than in the control background strain, C57BL/6J mice.These results suggest that obesity alone does not cause OA. However, other changes occurred in these mice due to the loss of leptin function. Leptin-deficient mice had reduced subchondral bone thickness and increased relative trabecular bone volume in the tibial epiphysis, as previously reported (for review, see ref.2). An extensive analysis of inflammatory molecules was carried out by Luminex bead assay, which revealed an increased level of only interleukin-8 (IL-8) and thus not an overall inflammatory effect of leptin deficiency. These results imply that leptin may be involved in the development of OA. Without leptin, adiposity is insufficient to induce systemic inflammation and knee OA, suggesting a potential role of leptin itself in regulating skeletal and immune functions.

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Generalized osteoarthritis associated with increased insulin‐like growth factor types i and ii and transforming growth factor β in cortical bone from the iliac crest. possible mechanism of increased bone density and protection against osteoporosis

Cited by 191 publications

References 48 publications

Study of Peripheral Bone Mineral Density in Patients with Diffuse Idiopathic Skeletal Hyperostosis

Study of Peripheral Bone Mineral Density in Patients with Diffuse Idiopathic Skeletal Hyperostosis

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

Obesity and osteoarthritis: Is leptin the link?

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