Philippe Orcel
Research Subjects
Philippe Orcel has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Johann Beaudreuil
Services de rhumatologie, médecine physique et de réadaptation, groupe hospitalier Lariboisière-Fernand-Widal, université Paris 7, AP–HP, 2, rue Ambroise-Paré, 75010 Paris, France
3 shared publications Alain Yelnik
2 shared publicationsAntoine Ferenczi
1 shared publication- Christian Roux
Rheumatology Department, Paris Descartes University, Cochin Hospital, Paris, France
1 shared publication Mickaël Rousière
1 shared publicationSophie Roux
INSERM U349, Lariboisière Hospital, Paris, France
1 shared publication
Latest Publications
- 1 September 2017
- Published by Elsevier in Annals of Physical and Rehabilitation Medicine
- Vol. 60, e29
Reliability study of sub-acromial impingement tests including a new clinical manoeuver
- 1 September 2017
- Published by Elsevier in Annals of Physical and Rehabilitation Medicine
- Vol. 60, e29
Reliability study of sub-acromial impingement tests including a new clinical manoeuver
- 30 April 2005
- Published by Elsevier in La Presse Médicale
- Vol. 34 (8) , 612-616
Maladie de Paget, prise en charge thérapeutique
- 30 April 2005
- Published by Elsevier in La Presse Médicale
- Vol. 34 (8) , 612-616
Maladie de Paget, prise en charge thérapeutique
- 15 March 2002
- Vol. 52 (6) , 621-6
[Bone diseases of the hip].
Hip pain is likely to be due to a local or regional bone disease when the hip joint is painless and of normal mobility by physical examination. Targeting the right diagnosis is easy in a patient affected by bone disease (osteoporosis, Paget's disease) or when the background of the patient is suggestive (malignancy, pregnancy). However it could be more tricky in most cases: transient osteoporosis of the hip, bone fissures, Paget's coxopathy, and tumoral cell osteolysis of bones surrounding the hip are the main causes, in addition to femoral head osteonecrosis, which is detailed in another chapter.
- 15 March 2002
- Vol. 52 (6) , 621-6
[Bone diseases of the hip].
Hip pain is likely to be due to a local or regional bone disease when the hip joint is painless and of normal mobility by physical examination. Targeting the right diagnosis is easy in a patient affected by bone disease (osteoporosis, Paget's disease) or when the background of the patient is suggestive (malignancy, pregnancy). However it could be more tricky in most cases: transient osteoporosis of the hip, bone fissures, Paget's coxopathy, and tumoral cell osteolysis of bones surrounding the hip are the main causes, in addition to femoral head osteonecrosis, which is detailed in another chapter.
- 1 January 2002
- Published by Elsevier in Joint Bone Spine
- Vol. 69 (1) , 19-27
Bisphosphonates in bone diseases other than osteoporosis
- 1 January 2002
- Published by Elsevier in Joint Bone Spine
- Vol. 69 (1) , 19-27
Bisphosphonates in bone diseases other than osteoporosis
- 30 September 2001
- Published by Elsevier in Revue du Rhumatisme
- Vol. 68 (8) , 678-684
Ostéoporose cortisonique
- 30 September 2001
- Published by Elsevier in Revue du Rhumatisme
- Vol. 68 (8) , 678-684
Ostéoporose cortisonique
- Open Access
- 6 September 2000
- Published by Springer Nature in Arthritis Research & Therapy
- Vol. 2 (6) , 451-456
Bone loss: Factors that regulate osteoclast differentiation - an update
Osteoclast activation is a critical cellular process for pathological bone resorption, such as erosions in rheumatoid arthritis (RA) or generalized bone loss. Among many factors triggering excessive osteoclast activity, cytokines such as IL-1 or tumour necrosis factor (TNF)-α play a central role. New members of the TNF receptor ligand family (namely receptor activator of nuclear factor-κB [RANK] and RANK ligand [RANKL]) have been discovered whose cross-interaction is mandatory for the differentiation of osteoclasts from hemopoietic precursors, in both physiological and pathological situations. Osteoprotegerin, a decoy receptor which blocks this interaction, decreases osteoclast activity and could have a fascinating therapeutic potential in conditions associated with upregulated bone resorption.
- 6 September 2000
- Published by Springer Nature in Arthritis Research & Therapy
- Vol. 2 (6) , 451-456
Open AccessBone loss: Factors that regulate osteoclast differentiation - an update
Osteoclast activation is a critical cellular process for pathological bone resorption, such as erosions in rheumatoid arthritis (RA) or generalized bone loss. Among many factors triggering excessive osteoclast activity, cytokines such as IL-1 or tumour necrosis factor (TNF)-α play a central role. New members of the TNF receptor ligand family (namely receptor activator of nuclear factor-κB [RANK] and RANK ligand [RANKL]) have been discovered whose cross-interaction is mandatory for the differentiation of osteoclasts from hemopoietic precursors, in both physiological and pathological situations. Osteoprotegerin, a decoy receptor which blocks this interaction, decreases osteoclast activity and could have a fascinating therapeutic potential in conditions associated with upregulated bone resorption.