Bone remodelling.

Hill, Peter A.

doi:10.1093/ortho/25.2.101

Cited by 213 publications

(157 citation statements)

References 31 publications

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“…The equilibrium between the activities of these two cells preserves the mineral component of calcium and phosphorous molecules. Bone remodelling includes several distinct phases, namely the activation, resorption, reversal and formation processes [1][2][3]. In this cycle, several components, including the specific cells, the osteoblasts, osteocytes and osteoclasts; inorganic non-collagenic substances, such as proteoglycans; and a collagenic component of which collagen type I is the major constituent, are all closely modulated.…”

Section: Introductionmentioning

confidence: 99%

“…Osteoclasts are derived from the haematopoietic progenitors of the monocyte-macrophage lineage and can be distinguished by their multinucleated giant cell appearance together with specific features such as polarised morphology and an apical differentiation adjoining the calcified matrix in resorption (ruffled border) [1][2][3]. They are responsible for the acidification of the extracellular matrix followed by the release of proteolytic enzymes, which leads to the breakdown of the bone matrix.…”

Section: Introductionmentioning

confidence: 99%

“…They are responsible for the acidification of the extracellular matrix followed by the release of proteolytic enzymes, which leads to the breakdown of the bone matrix. The osteoblasts are derived from bone marrow cells and are responsible for the production of new matrix [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

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

Tat

Lajeunesse

Pelletier

et al. 2010

Best Practice & Research Clinical Rheumatology

151

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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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Tat

Lajeunesse

Pelletier

et al. 2010

Best Practice & Research Clinical Rheumatology

151

121

View full text Add to dashboard Cite

show abstract

“…As is well known, the process of bone remodeling is the coupling of osteoclastic bone resorption followed by osteoblastic bone formation, under tight regulation by systemic hormones and by local factors released by osteoclasts and osteoblasts with reciprocal regulatory effects on their activity [35]. In humans, bone remodeling takes place in bone metabolic units (BMU); however, rodents lack traditional BMUs, so it is debatable whether the coupled processes of formation and resorption that occur in rats represent true remodeling [24].…”

Section: Experiments Imentioning

confidence: 99%

Changes in bone Pb accumulation: Cause and effect of altered bone turnover

Brito

Costa

Silva

et al. 2014

Bone

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This paper assesses the magnitude of Pb uptake in cortical and trabecular bones in healthy animals and animals with altered balance in bone turnover, and the impact of exposure to Pb on serum markers of bone formation and resorption. The results reported herein provide physiological evidence that Pb distributes differently in central compartments in Pb metabolism, such as cortical and trabecular bone, in healthy animals and animals with altered balance in bone turnover, and that exposure to Pb does have an impact on bone resorption resulting in OC-dependent osteopenia. These findings show that Pb may play a role in the etiology of osteoporosis and that its concentration in bones varies as a result of altered bone turnover characteristic of this disease, a long standing question in the field. In addition, data collected in this study are consistent with previous observations of increased half-life of Pb in bone at higher exposures. This evidence is relevant for the necessary revision of current physiologically based kinetic models for Pb in humans. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Abstract This paper assesses the magnitude of Pb uptake in cortical and trabecular bones in healthy animals and animals with altered balance in bone turnover, and the impact of exposure to Pb on serum markers of bone formation and resorption. The results reported herein provide physiological evidence that Pb distributes differently in central compartments in Pb metabolism, such as cortical and trabecular bone, in healthy animals and animals with altered balance in bone turnover, and that exposure to Pb does have an impact on bone resorption resulting in OC-dependent osteopenia. These findings show that Pb may play a role in the etiology of osteoporosis and that its concentration in bones varies as a result of altered bone turnover characteristic of this disease, a long standing question in the field. In addition, data collected in this study are consistent with previous observations of increased half-life of Pb in bone at higher exposures. This evidence is relevant for the necessary revision of current physiologically based kinetic models for Pb in humans. Keywords Pb exposureBone turnover Osteoporosis Kinetic models 1

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“…This dynamic process enables the bone to adapt to the functional demands of each skeletal area and to actively participate in the maintenance of the mineral homeostasis to control serum calcium and phosphorus concentrations. 2,3,6,15 The skeleton renews completely at variable time intervals according to the patient's age. 22 Teeth, particularly root structures, do not have bone turnover, 1,8,12,17 a consequence of the activity of osteoblasts, osteocytes, macrophages and osteoclasts.…”

mentioning

confidence: 99%