Diseases of the Temporomandibular Joint

Abstract

Disorders of the temporomandibular joint are mostly recognized by their impairment of normal jaw mobility, thus causing difficulties in chewing and mouth opening that are the result of pathologic changes in one or more of the tissues that together compose the temporomandibular joint: bone and cartilage, interarticular disc, and the lining synovial membrane. Alterations occurring at this anatomical site are classified as reactive, degenerative, inflammatory and neoplastic.

12.1 Introduction

The temporomandibular joint (TMJ) allows the mobility of the mandible. The joint consist of the mandibular condyle, the fossa in the skull base and the intervening disc that ventrally is connected with the tendon of the lateral pterygoid muscle. Disorders of the mandibular joint are mostly recognized by their impairment of normal jaw mobility, leading to difficulties in chewing and mouth opening.

Pathologic tissue alterations of the joint may involve bone and cartilage, the disc or the lining synovial membrane. A surgical specimen from this area mostly consists of the mandibular condyle – partly of completely removed -, sometimes together with the disc, parts of the synovial membrane and with attached capsular fibrous tissue.

To appreciate the morphological basis of the diseases that may occur in these structures, a concise outline of their histomorphology will be given. The mandibular condyle consists of a core of cancellous bone with an outer cortical layer. The articular surface is different from most of other joints as it lack a covering layer of hyaline cartilage. Instead, the surface is formed by a fibrous layer. Between the superficial fibrous layer and the underlying bone, remnants of cell-rich mesenchyme and calcified cartilage can be observed but with increasing age, these components disappear (Fig. 12.1). Alterations in the TMJ can be classified as reactive, degenerative, inflammatory and neoplastic [1, 2].

Fig. 12.1

Normal histology of the mandibular condyle. The surface is composed of fibrous cartilage. The next layer is the undifferentiated mesenchyme that is the source of cells for the fibrous cartilage above and the hyaline cartilage below. With advancing age, the undifferentiated mesenchyme disappears and the hyaline cartilage may show some calcification

12.2 Reactive Changes

The mandibular condyle is able to adapt itself to changing spatial dimensions by changing its contour through either regressive or progressive remodeling. In case of regressive remodeling, resorption cavities develop at the interface of bone and covering soft tissues, thus creating interruptions in the subchondral bone plate. The overlying soft tissue cap thus suffers from lack of support in that particular area and a concavity in the articular surface at that site is established (Fig. 12.2). In case of progressive remodeling, the superficial soft tissue layer increases and to re-establish its original thickness, a new subchondral bone plate is formed. In combination with the pre-existent subchondral bone plate, a double layered border between bone and covering tissues will develop (Fig. 12.3). When the changes in spatial dimensions are too excessive to be counteracted by remodeling, osteoarthritis develops.

Fig. 12.2

Occurrence of regressive remodeling can be recognized by the presence of resorption cavities at the interface between bone and overlying condylar cartilage. This causes a depression in the condylar surface overlying this area

Fig. 12.3

Occurrence of progressive remodeling can be recognized by a duplication of the osteochondral junction

12.3 Osteoarthritis

Osteoarthritis in the TMJ does not show any changes different from those present in the hip or knee with advancing age. The fibrous tissue covering fragmentates and the exposed bone shows eburnation. Moreover, irregular proliferations of cartilage and bone may occur as a futile attempt to re-establish an intact articular surface. Through cracks in the surface, synovial fluid is squeezed into the marrow cavities and creates cavities lined by granulation tissue, also sometimes surrounded by bone resulting in the radiologically well-known subchondral bone cysts typical for degenerative joint changes (Figs. 12.4, 12.5 and 12.6).

Fig. 12.4

Low power view of a mandibular condyle showing osteoarthritis. The exposed bony surface shows sclerosis and there are also remnants of cartilage. At the left side, an osteophyte covered with a cartilaginous cap is shown

Fig. 12.5

Detail of surface with osteoarthritic changes, sclerosis of subchondral as well as underlying cancellous bone and reactive proliferation of cartilaginous remnants

Fig. 12.6

Synovial fluid enters into the bone marrow through cracks in the articular surface; walling off through subsequent reactive changes including bone remodeling forms intramedullary pseudocysts known as subchondral bone cysts by the radiologist

12.4 Inflammatory Disorders

As any other joint, the TMJ may be afflicted by generalized joint diseases such as rheumatoid arthritis, M. Bechterew, gout and pseudogout. More typical for the TMJ is joint disease due to continuous spread from mandibular osteomyelitis (Fig. 12.7). In case of extensive urate deposits, gout may mimic tumor (Fig. 12.8) but the presence of feathery extracellular material bordered by inflammatory cells on histological examination offers no support for a diagnosis of neoplasia (Figs. 12.9, 12.10 and 12.11). Gout and pseudogout may however evoke hypertrophic cartilaginous proliferations that can be mistaken for chondrosarcoma (Figs. 12.12 and 12.13).

Fig. 12.7

Mandibular condyle changed into a sequestrum due to osteomyelitis. Overlying soft articular layers have disappeared completely

Fig. 12.8

Case of gout in the temporomandibular joint. Radiography shows space occupying lesion due to extensive deposition of urate crystals suggesting neoplasia

Fig. 12.9

As in any other joint, urate crystals may evoke a foreign body reaction with concomitant inflammation

Fig. 12.10

At higher magnification, the feathery nature of the urate deposits is easily appreciated

Fig. 12.11

Metaplastic bone formation may form part of the reactive tissue proliferation shown in gouty arthritis

Fig. 12.12

As part of the gout-induced reactive changes, condylar cartilage may show proliferation with cytonuclear atypia that can be mistaken for condylar chondrosarcoma

Fig. 12.13

High power view from same case as shown in Fig. 12.12 to illustrate the reactive atypia in gout associated chondroid proliferations

12.5 Neoplasms

Tumours of the mandibular body may extend into the mandibular condyle and thus involve the joint. They may be primary tumours but metastasis also occurs (Fig. 12.14). Osteosarcoma and osteochondroma are the primary lesions most often encountered, osteoblastoma only rarely found [3]. Moreover, giant cell granuloma – most often seen in the mandibular body – may involve the TMJ. At that site, it has to be differentiated from chondroblastoma that also may contain abundant giant cells. However, the matrix deposition and peculiar chickenwire calcification that may occur in chondroblastoma is sufficiently distinct to avoid misdiagnosis. For more details on giant cell granuloma and chondroblastoma, see their description in Chaps. 8 and 10.

Fig. 12.14

Mandibular condyle with metastatic breast carcinoma

Pigmented villonodular synovitis is rarely seen in the temporomandibular joint. It does not show any differences from similar lesions elsewhere in the skeleton but at this site, differential diagnosis includes giant cell granuloma of the mandibular bone spreading into the adjacent soft tissues [4].

12.6 Synovial Chondromatosis

Although more generally seen in other joints, synovial chondromatosis may occur in the temporomandibular joint area [5]. Many cartilage nodules may be found within the joint cavity (Fig. 12.15). As the chondroid nodules may show some cytonuclear atypia, they may be confused with chondrosarcoma (Figs. 12.16 and 12.17). However, clinical and gross features are distinct enough to rule out chondrosarcoma in spite of these histological characteristics. Rarely, undisputed chondrosarcoma may develop in synovial chondromatosis (Figs. 12.18, 12.19, 12.20 and 12.21) [6].

Fig. 12.15

Gross appearance of synovial chondromatosis. Many translucent nodules were removed from the temporomandibular joint cavity

Fig. 12.16

Low power view of synovial chondromatosis. Nodules are composed of rather cellular cartilage

Fig. 12.17

At higher magnification, slight atypia of the chondrocytes sometimes occurring in synovial chondromatosis is illustrated. Clinical context however is entirely different from chondrosarcoma

Fig. 12.18

MRI showing soft tissue mass surrounding right mandibular condyle. Condyle itself appears to be uninvolved

Fig. 12.19

Biopsy from the mass shown in Fig. 12.18 showing cartilage. Chondrocytes are mainly arranged in nests but there are also diffuse areas of larger and atypical chondrocytes suspicious for chondrosarcoma developing in synovial chondromatosis

Fig. 12.20

Other area from the same case in which the difference between areas still compatible with chondromatosis (right side) and more atypical areas suggesting chondrosarcoma (left side)

Fig. 12.21

In the cellular areas shown in Fig. 12.20, an occasional mitotic figure is present

12.7 Condylar Hyperplasia

Condylar hyperplasia is an idiopathic disease characterized by a progressive, unilateral overgrowth of the mandible. The condylar head is usually obviously larger than normal. Due to this excessive growth of the mandibular condyle, the mandible shows a shift to the healthy side due to a surplus of mandibular bone at the affected side. The growth of the mandibular condyle causing this symptom may be the result of two different pathological conditions [7].

The first manifests itself in the adolescent or the young adult and represents an exaggerated, normally proceeding growth and maturation process. The histological structure of the condyle in these cases is age-dependent as is shown by a conversion of hyaline growth cartilage into fibrocartilage occurring at about 20 years of age. Histologically, the architecture is likely to be relatively normal; however, there may be some thinning of the articular fibrocartilage and early signs of osteoarthrosis. So in these cases, histological examination only serves to rule out other reasons for condylar enlargement such as neoplasia as these condyles do not show any histologic features different from the normal condyle. Only the gross size is increased but this is not reflected in histological abnormalities (Figs. 12.22, 12.23 and 12.24).

Fig. 12.22

Low power view of condylar hyperplasia due to an increase in normal growth. The surface shows the several layers in a normal arrangement. The cancellous bone shows a striking arrangement perpendicular to the surface which may be due to rapid increase in size

Fig. 12.23

Detail from Fig. 12.18 to show the layered architecture of the cartilaginous cap: superficial fibrous cartilage, layer of undifferentiated mesenchyme, layer of hyaline cartilage and area of endochondral ossification. Remnants of cartilage in the cancellous bone also indicate growth activity, the cartilage not yet being replaced by bone through remodeling. This appearance is normal in the growing child but should not be present in the normal adult condyle

Fig. 12.24

Detail from a enlarged condyle showing a picture almost similar to Fig. 12.1 which is normal for the adult condyle. The combination of an enlarged mandibular condyle with a normal histological appearance of the joint surface indicates increased growth in the past with subsequent normal maturation

The second type of condylar hyperplasia, seen in older people, probably represents reactive growth as a response to an eliciting agent that mostly can be identified. In these cases the histological architecture of the condyle is distorted (Fig. 12.25) or may be covered by large masses of hyaline or fibrous cartilage (Figs. 12.26 and 12.27).

Fig. 12.25

Low power view of a posttraumatic case of condylar hyperplasia showing distorted architecture of condylar surface. Irregular masses of cartilage extend deeply into the underlying cancellous bone

Fig. 12.26

Low power view of condylar hyperplasia due to an increase in thickness of the cartilage that covers parts of the mandibular condyle

Fig. 12.27

Detail from Fig. 12.22 to illustrate the massive increase in thickness of the cartilage which mainly involves the superficial fibrous part of it