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Current facts on para-osteo-arthropathy (POA)

Spinal Cord volume 11, pages 36–78 (1973)Cite this article

Abstract

1. Twelve cases of chronic POA and five cases of acute POA from clinical and radiologic onset were studied in the light of the following parameters: X-rays; lower limb angiographies with venous and arterial blood gas analysis; serial determinations of urine hydroxyproline; urine calcium, serum calcium and phosphorus; creatinephosphokinase; alkaline phosphatase; bone scans; skin temperatures; bone biopsies in evolving POA; light and electron microscopic studies; analysis of amorphous and crystalline components and fluorescent study of ectopic bone marked with tetracycline.

2. The most common localisation of heterotopic ossifications is periarticular; however, it may also be observed at some distance from the skeleton (cases 1 and 16).

3. Onset of POA is accompanied by angiographic modifications showing regression as the POA ages. However, one may not conclude from the persistance of angiographic modifications that the POA is not yet mature. Nor does normalisation of an initially pathological angiogram signify that the maturation of the ectopic bone formation is complete and the POA stabilised.

The angiographic modifications associated with POA are secondary to the POA and not the cause.

4. Arteriovenous blood gas determinations correspond in general to the angiographic modifications and are of no value in judging the degree of maturity of the ectopic bone.

5. The development of POA may be associated with elevated urine Hyp. Normalisation of Hyp levels does not mean that the POA has stabilised; persistance of elevated values does not mean that the POA has not stabilised. Urine Hyp determinations do not permit any conclusion as to the degree of maturity of the POA lesion.

6. Elevation of serum alkaline phosphatase is a sign of the presence of pathologic growing bone, a contra-indication to POA surgery. Normalisation of this enzyme value does not constitute adequate proof of the stabilisation of the osteogenic process.

7. Infrequent isolated determinations of the alkaline phosphatase and of urine Hyp are of practically no value in following the evolution of POA. As for angiographies and bone scans, the dynamic picture produced by serial determinations gives a better idea of the status of the lesion.

8. Elevation of serum CPK suggests a participation of striated muscular tissue in the developing POA mass.

9. Determinations of serum calcium and phosphorus have been of no value in the diagnosis of POA, nor in the evaluation of the maturity of the ectopic mass.

10. In serial bone scans, a decrease in radionuclide uptake over a period of time seems to suggest a slowing of the disease process: an increase signifies active disease, a contraindication to surgery.

11. Multiple foci of osteogenesis of simultaneous onset do not necessarily evolve identically (case 2).

12. Serial bone scans seem to be the most reliable parameter for deciding when a POA is mature and may be operated. Although not constituting absolute proof of stabilisation of the osteogenic process, serial determinations of serum alkaline phosphatase are next in order of reliability.

13. POA may develop without any connection with muscular tissue but, most often, the POA develops in the muscular periphery, deriving from the interfascicular connective tissue, giving rise to a picture seen in some types of myositis ossificans, particularly the post-traumatic type. Histologic studies have shown that atrophic muscular fibres may occasionally be incorporated within the bony mass.

14. Light and electron microscopic examinations of 12 long standing POA (nine hips, two elbows, one knee) and of five recent POA (four hips, one knee) have shown that POA are the result of metaplasic osteogenesis, associated with some chondrogenesis, forming lamellar cortico-spongiosal bone. Therefore, the term ‘calcification’ does not apply to POA and may be abandoned.

15. The study of the ultrastructure and distribution of mineral salts in POA tissue, from early deposition to maturity, has shown that the sequence of transformation involves a progressive increase in the degree of mineralisation with a relative decrease of the amorphous phase and an enlargement in crystal size. After 30 months, the pattern in POA tissue approaches that of normal young adult bone.

16. Injury may certainly be a causative factor in the onset of POA, as shown by cases 2, 4, and 16, but other factors must be considered as well. The role of physiotherapy must be mentioned as a possible aetiologic factor, especially in association with marked spasticity (Hossack & King, 1967). Microscopic interstitial haemorrhages may result from too brisk a mobilisation.

17. If POA do occur more frequently in spastic patients, they may also take place in the absence of any spasticity, as shown by cases 1, 6, and 10.

18. Contrary to the views of Silver (1969), Stryker frames or turning beds, anticoagulant therapy and pressure sores do not appear to play an important role in the onset of POA. Cases 10 and 12 were not associated with any of these factors at any time during their treatment.

19. Eleven POA were resected in seven patients (nine hips, two elbows). There were recurrences in two patients attributed to lack of experience at the time these patients were operated. With the exception of one elbow with a recurrence, all other operated joints enjoyed a significant improvement in articular freedom.

20. This study has produced valuable parameters for the determination of POA maturation allowing for the correct timing of operation with minimal risk of recurrence.

The question of the pathogenesis of POA has been answered only in part, and further study is needed, possibly with the help of bio- and histochemical techniques.

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Author information

Affiliations

  1. Spinal Cord Injury Centre, Institute for Physical Medicine and Rehabilitation, University Hospital, Geneva, Switzerland

    A B Rossier

  2. Radiological Institute, Chief of the Angiography Unit, University Hospital, Geneva, Switzerland

    Ph Bussat

  3. Laboratory of the Surgical Clinic, University Hospital, Geneva, Switzerland

    F Infante

  4. Laboratory of La Chaux-de-Fonds Hospital, University Hospital, Geneva, Switzerland

    R Zender

  5. Department of Internal Medicine, Medical Therapeutic Clinic, University Hospital, Geneva, Switzerland

    B Courvoisier

  6. Division of Orthopaedics, Department of Surgery, University Hospital, Geneva, Switzerland

    G Muheim

  7. Division of Nuclear Medicine, Department of Internal Medicine, University Hospital, Geneva, Switzerland

    A Donath

  8. Division of Orthopaedics, Department of Surgery, University Hospital, Geneva, Switzerland

    H Vasey

  9. Division of Orthopaedics, Department of Surgery, University Hospital, Geneva, Switzerland

    W Taillard

  10. Department of Pathology, University Hospital, Geneva, Switzerland

    R Lagier

  11. Department of Pathology, University Hospital, Geneva, Switzerland

    G Gabbiani

  12. Department of Morphology, University Medical School, University Hospital, Geneva, Switzerland

    C A Baud

  13. Department of Morphology, University Medical School, University Hospital, Geneva, Switzerland

    J A Pouezat

  14. Department of Morphology, University Medical School, University Hospital, Geneva, Switzerland

    J M Very

  15. Spinal Cord Injury Centre, Institute for Physical Medicine and Rehabilitation, University Hospital, Geneva, Switzerland

    H J Hachen

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Rossier, A., Bussat, P., Infante, F. et al. Current facts on para-osteo-arthropathy (POA). Spinal Cord 11, 36–78 (1973). https://doi.org/10.1038/sc.1973.5

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