Research article

Nodular osteochondrogenic activity in soft tissue surrounding osteoma in neurogenic para osteo-arthropathy: morphological and immunohistochemical study

T Youssefian¹ , R Sapena¹ , R Carlier² , C Bos¹ , A Denormandie³ , P Denys⁴ , A Cormier¹ and M Bandelier¹

¹SYMPATHOS Laboratory, 67 boulevard du Général Martial Valin, 75015, Paris, France

²Medical Imaging department, Raymond Poincaré teaching hospital, APHP 104 Boulevard Raymond Poincaré, 92380, Garches, France

³Orthopedic deparment, Raymond Poincaré teaching hospital, APHP 104 Boulevard Raymond Poincaré, 92380, Garches, France

⁴Rehabilitation department, Raymond Poincaré teaching hospital, APHP 104 Boulevard Raymond Poincaré, 92380, Garches, France

author email corresponding author email

BMC Musculoskeletal Disorders 2004, 5:46doi:10.1186/1471-2474-5-46

Published:	25 November 2004

Abstract

Background

Neurogenic Para-Osteo-Arthropathy (NPOA) occurs as a consequence of central nervous system injuries or some systemic conditions. They are characterized by bone formation around the main joints.

Methods

In order to define some biological features of NPOAs, histological and immunohistological studies of the soft tissue surrounding osteoma and Ultrasound examination (US) of NPOA before the appearance of abnormal ossification on plain radiographs were performed.

Results

We have observed a great number of ossifying areas scattered in soft tissues. US examination have also shown scattered ossifying areas at the early stage of ossification. A high osteogenic activity was detected in these tissues and all the stages of the endochondral process were observed. Mesenchymal cells undergo chondrocytic differentiation to further terminal maturation with hypertrophy, which sustains mineralization followed by endochondral ossification process.

Conclusion

We suggest that periosteoma soft tissue reflect early stage of osteoma formation and could be a model to study the mechanism of osteoma formation and we propose a mechanism of the NPOA formation in which sympathetic dystony and altered mechanical loading induce changes which could be responsible for the cascade of cellular events leading to cartilage and bone formation.