SciELO - Scientific Electronic Library Online

vol.28 issue2Synovial chondromatosis of the temporomandibular jointTreatment of rhinophyma with CO2 laser: A case report author indexsubject indexarticles search
Home Pagealphabetic serial listing  


Services on Demand




Related links

  • On index processCited by Google
  • Have no similar articlesSimilars in SciELO
  • On index processSimilars in Google


Revista Española de Cirugía Oral y Maxilofacial

On-line version ISSN 2173-9161Print version ISSN 1130-0558

Rev Esp Cirug Oral y Maxilofac vol.28 n.2 Barcelona Mar./Apr. 2006




Synovial chondromatosis of the temporomandibular joint

Condromatosis sinovial de la articulación temporomandibular



Rafael Martín-Granizo López

Servicio de Cirugía Oral y Maxilofacial
Hospital Clínico San Carlos, Madrid, España



In this article the authors give a detailed description of an interesting case report of synovial chondromatosis (SC) of the temporomandibular joint (TMJ) with extra-articular extension. A detailed radiological and histological analysis is carried out, and an adequate explanation of its physiopathology is provided. This pathology of the joints was described as early as 1558 by Ambroise Paré, although it was not until the 20th century, in the year 1933, that Georg Axhausen described a case in the TMJ.1

The authors use the term "joint meniscus" to describe the structure that is interposed between the surfaces of the TMJ: the condyle and temporal bone. This terminology has been widely debated in the literature and most authors call it "joint disc". It is a very complex structure, as it is composed of a central portion of hard, aneural, avascular fibrocartilage with a slightly concave shape and the size of a euro coin (I personally prefer to call this part "meniscus"). This central part is in turn inserted into the ends of the joint by means of a tissue that is the opposite of the first one; it is a connective lax tissue, which is highly vascular and innervated, and it allows the displacement of the central portion. It accompanies the condyle when it moves (I call both structures "discs"). The use of this terminology would be of great help when trying to define the physiopathology of the joint appropriately.

The joint disc divides the TMJ into two asymmetric compartments: the upper and lower compartment, and all these tissues are covered by a fine, smooth layer of synovial tissue. This is where SC is produced, a benign metaplasia of the synovium. 2 This pathology could therefore arise in both compartments, although it is not known why, in the majority of cases, SC appears in the upper joint space. This is one of the first mystery regarding this entity.

The second mystery is why it appears only in one joint. Of the more than 80 cases published in the literature,3 only 2 refer to bilateral involvement.4,5 In some cases, when an arthroscopy of both joints has been carried out, the opposite joint to the one with SC has been completely normal.2

The third mystery surrounds its etiopathogeny. Only two cases of those described entail trauma to the jaw.3 However, the physiopathology is in the process of being understood, and very recently British investigators (results as yet unpublished) have proposed a somatic mutation of a gene that provokes a deregularization in the differentiation of mesenchymal progenitor cells (stem cells), after carrying out cell cultures in a case of SC of the knee and comparing these cultures with synovial cells in knees with osteoarthrosis.6 These progenitor cells would be capable of self-differentiation into different cell lines such as bone, cartilage, adipocytes or ligaments. Other authors have detected in the synovial liquid of joints with SC, a substance which was FGFR-3 (fibroblast growth factor receptor), a marker of cartilaginous progenitor cells and stem cells, which would support this theory.7 SC is known to be an active process that can be divided into various developmental phases. Ever since Milgram8 an orthopedic surgeon described these, in 1977, and after these were later updated by Balnkenstijn and cols.,9 they have been linked by some authors with a variety of intra-articular substance increases in the active phases, such as TGF-beta and tenascin.10

The histopathologic phases have been perfectly described in this article and we will try to correlate these with our personal arthroscopic finding. SC can therefore be divided into a primary or active type (a pathological entity as such, Fig. 1), or a secondary-passive type (presence of cartilaginous loose bodies for a different reason, such as arthrosis, trauma, etc., Fig. 2). Primary or true SC has three phases: the first or early phase entails metaplastic activity of the synovial membrane with a proliferation of undifferentiated stem cells, but with no loose bodies (Fig. 3). The second, or transitional phase, is characterized by progressive metaplasia that slowly leads to the formation of loose bodies with active chondrocytes inside (Fig. 4). Finally, in the third or advanced stage there is no metaplasia, although there is calcification within the mature loose bodies that are covered by normal synovial membrane (Fig. 1).

Finally, and as is indicated by the authors, surgical treatment is the treatment of choice. We recommend an arthroscopy in primary SC cases in the third phase, when the metaplastic phenomena in the synovium no longer exist, and when the loose bodies measure less than 2mm, as otherwise the complete removal by means of the arthroscopic cannulas is difficult. Some authors recommend treatment that is more conservative in this phase that does not include a synovectomy.11 In spite of this, the patient must always be aware that opening the joint for extraction may be necessary. In the primary and secondary phase we recommend an arthrotomy in order to carry out a complete synovectomy adequately, which is very difficult to perform by arthroscopy, so that possible relapses are avoided.



1. Axhausen G. Pathologie und Therapie des Kiefergenlenks. Fortschr Zahnheilk 1933;9:171.

2. Martin-Granizo R, Sanchez JJ, Jorquera M, Ortega L. Synovial chondromatosis of the temporomandibular joint: A clinical, radiological and histological study. Med Oral Patol Oral Cir Bucal 2005;10:272.

3. Ardekian L, Faquin W, Troulis MJ, Kaban LB, August M. Synovial chondromatosis of the temporomandibular joint: Report and analysis of eleven cases. J Oral Maxillofac Surg 2005;63:941.

4. Wong WC, Cheng PW, Chan FL. MRI appearance of synovial chondromatosis in the temporomandibular joint. Clin Radiol 2001;56:773.

5. Keogh CF, Torreggiani WC, Munk PL. Bilateral synovial chondromatosis of the temporomandibular joint [carta]. Clin Radiol 2002;57:862.

6. Crawford A, Frazer A, Lippitt JM, Buttle DJ, Smith T. A case of chondromatosis indicates a synovial stem cell involvement (en prensa). Rheumatol 2005.

7. Robinson D, Hasharoni A, Evron Z, Segal M, Nevo Z. Synovial chondromatosis: the possible role of FGF9 and FGF receptor 3 in its pathology. Int J Exp Path 2000;81:183.

8. Milgram JW. The classification of loose bodies in human joints. Clin Orthop 1977; 124:282.

9. Balnkenstijn J, Panders AK, Vermey A, Scherpbier AJ. Synovial chondromatosis of the temporo-mandibular joint: Report of three cases and a review of the literature. Cancer 1985;55:479.

10. Fujita S, Yoshida H, Tojyo I, Wada T, Murakami K, Iizuka T. Synovial chondromatosis of the temporomandibular joint: Clinical and immunohistopathological considerations. Br J Oral Maxillofac Surg 2004;42:259.

11. Holmlund AB, Eriksson L, Reinholt EP. Synovial chondromatosis of the temporomandibular joint. Clinical, surgical and histologic aspects. Int J Oral Maxillofac Surg 2003;32:143.

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License