Osteoarthritis (OA), one of the most common forms of arthritis occurring in the temporomandibular joint (TMJ), is the most prevalent leading cause of pain and disability in the aging population. TMJ OA is a low-level inflammatory and slowly progressive degenerative disorder characterized by damage to the articular cartilage and changes in the subchondral bone [1]. Excessive mechanical loading associated with occlusal treatment, trauma, unstable occlusion, or reductions in host adaptive capacity with aging can possibly damage the TMJ, leading to TMJ OA [2].

Cone-beam computed tomography (CBCT) provides detailed 3-dimensional images to aid in the diagnosis of degenerative changes in the TMJ. Different signs of TMJ OA represent different stages of the disease. Erosive lesions and joint space narrowing indicate acute or early changes, whereas sclerosis, flattening, subchondral cysts, and osteophytes may indicate late changes in the TMJ [3,4]. At the advanced stage of TMJ OA, the structural deterioration of the subchondral bone leads to thickening of the subchondral bone plate, and an increase in bone density becomes evident. This elevated bone density is called subcortical sclerosis and is strongly associated with the formation of subchondral cysts [1].

Radiolucent lesions in the subchondral bone, which are commonly referred to as ‘subchondral cysts’, are often reported in patients with OA. These subchondral cysts do not contain any evidence of an epithelial lining; therefore, they are often referred to as ‘pseudo-cyst’ or ‘geodes’, indicating the formation of a lesion in response to stress. Subchondral cysts often occur as multiple lesions varying in size, while solitary and large cysts are unusual. Previous studies have revealed that nearly two-thirds of osteoarthritic cysts completely disappear radiographically or shrink without needing any additional treatment. However, subchondral cysts can also progress over time. Recent evidence has suggested that the frequency of subchondral cysts is related to the severity of degenerative changes and pain, along with a higher risk of joint replacement [5-7].

To our knowledge, very few reports on the long-term follow-up of subchondral cysts in patients with TMJ OA exist. This study therefore aimed to (1) report the case of a symptomatic TMJ OA patient with a large subchondral cyst that decreased in size after being treated with conservative therapy with long-term radiographic follow-up, and (2) provide useful information on subchondral cysts with a literature review. This study protocol was approved by the Ethics Committee of Pusan National University Hospital (PNUH; approval no. 2203-004-112) and the written informed consent was waived by the committee.

A 67-year-old male visited the Department of Oral Medicine, Pusan National University Hospital, with the chief complaint of limitation of mouth opening and pain on the left TMJ area. He noticed a progressive limitation of mouth opening with pain on preauricular region during the past 3 years. His medical history revealed that he underwent surgery for bronchiectasis in 1996. However, he had no history of previous trauma or surgery on the left TMJ or the ear. There was noticeable dental etiology is that he has been chewing on the right side since left posterior tooth prosthetic treatment 15 years ago. He has not received any treatment for TMJ disorder other than physical therapy at the pain clinic only when the pain was severe.

On clinical examination, he had a maximum comfortable opening (MCO) of 17 mm with left TMJ crepitus sound and deflection mouth opening path. Tenderness elicited on left TMJ area on opening and closing mouth. Mandibular asymmetry and occlusion change were absent. Panoramic radiograph evaluations showed that there were radiolucent and sclerotic lesion in the left mandibular condyle (Fig. 1). CBCT was taken 2 weeks after first visit. It revealed cortical erosion, severe sclerotic change with large subchondral cyst on left mandibular condyle (Fig. 2A, D).

To improve symptom association with TMJ of patient, medication (NSAIDs, muscle relaxants), supplemental physical and self-exercise therapy were administered. Also, interocclusal stabilization splint was worn to decrease load in TMJ. He recorded numeric analog scale (NAS) for his symptom every visit. At first visit of NAS was 3 in left TMJ pain. After 7 months, CBCT was additionally taken, it was seen more sclerotic change and slightly progression of flattening. The size of subchondral cyst was decreased (Fig. 2B, E). Clinical symptoms also improved, MCO was improved (28 mm) and he complained mild discomfort as 1 in NAS. Injection of hyaluronic acid (HA) was performed once to improve the opening length. On 18 months after first visit of CBCT finding, it was seen subchondral cyst almost disappeared with an apparent sclerosis (Fig. 2C, F). Although there was bony change in left condyle, no right condyle bony changes radiographically during the follow-up period. At the final follow-up (32 months after first visit) our patient was assessed clinically. Occlusal condition was stable, MCO was recovered to 38 mm and pain did not worse (NAS 1).

OA is a chronic, progressive, and debilitating disease characterized by the gradual degeneration of the cartilage and subchondral bone. Although OA has long been considered a primary disorder of the articular cartilage, the contribution of subchondral bone to the physiopathology of OA has aroused interest [1]. Subchondral bone and articular cartilage are dynamic stress-bearing structures that play complementary roles in the load-bearing of joints such as the hip and knee. The subchondral bone supports the overlying articular cartilage and distributes mechanical loads across joint surfaces with a gradual transition in stress and strain. Subchondral bone deterioration is commonly associated with overlying articular cartilage thinning and defects [8]. Early stage OA is characterized by increased bone remodeling and reduced bone density. Repetitive joint loading causes an initial increase in bone remodeling, possibly as an adaptation to repair the damage caused by loading. As the disease progresses, the remodeling rate decreases; however, an imbalance between bone resorption and formation leads to a net increase in bone formation. This process increases the bone volume and density, and can be associated with apparent sclerosis. However, subsequent mineralization is reduced owing to the impaired regulation of osteoblasts. The sclerosis of the subchondral bone may be a biomechanical compensational adaptation to the widespread subchondral cysts in the subchondral bone, which renders the subchondral bone structure more fragile [9,10].

Despite a continuous focus on the occurrence of subchondral cysts in OA over several decades, their etiology is still being debated. Currently, there are two conflicting hypotheses that could explain the origin of subchondral cysts in OA: the synovial fluid invasion theory and the bony contusion theory. The ‘synovial fluid intrusion’ theory proposes that synovial fluid intrudes into subchondral bone, leading to formation of subchondral cysts, due to the breach of the osteochondral junction. The ‘bone contusion’ theory suggests that subchondral cysts originate from the necrotic lesions in subchondral bone, which are induced by abnormal mechanical stress. Subchondral cysts were initially thought to result from degenerative changes in the cartilage, creating a communication between the subchondral bone and synovial space. However, this theory fails to explain the incidence of subchondral cysts that are not in continuity with the joint space. Subsequent evidence supports the bony contusion theory, in which the violent impact between opposing surfaces of the joint results in areas of primary subchondral bone osteolysis, particularly when the overlying cartilage has been eroded, where synovial breach is a secondary event [11-17].

Subchondral cysts can be resolved without therapy, but may progress with time if a pathway to the joint space exists [7,16]. These cysts may expand upwards and damage the subchondral plate and calcified cartilage, facilitating further biochemical catabolic enzyme transportation between the subchondral bone and cartilage. This can cause structural changes across the entire joint. Furthermore, the inhomogeneity of the subchondral bone and calcified cartilage, which is caused by intruding subchondral cysts and microdamage, can lead to high tensile and shear stresses at the bone-cartilage interface. The abnormal stress distribution at the bone-cartilage interface will subsequently degrade the overlying cartilage, and cartilage damage could, in turn, influence subchondral bone deterioration [5,11]. This vicious cycle leads to OA progression. Therefore, the optimal strategy may be to promote the maintenance of subchondral bone integrity.

The treatment strategy for TMJ OA aims to relieve pain, prevent the progression of cartilage and subchondral bone destruction, and restore joint function. Potential therapies for TMJ OA may be divided into conservative, invasive, or surgical modalities. Occlusal splint, medication, physical therapy and injection of HA are common conservative modalities of management. Most patients with TMJ OA can be successfully managed with these procedures; however, their long-term therapeutic effect on the pathologic articular structure is unsatisfactory. To date, no treatment has been able to successfully repair and restore the mandibular condylar cartilage degradation in TMJ OA because of its limited regeneration capacity [10,18]. Thus, treatments that prevent the progression of cartilage degradation and subchondral bone damage should be further explored. Regeneration of the TMJ may provide an ideal long-term solution.

In summary, we reported the longitudinal osseous changes of a large subchondral cyst in the mandibular condyle of an elderly patient with TMJ OA and conservative treatment modalities that assist long-term TMJ OA improvement. We believe that this study provides insight into the mechanisms leading to subchondral cyst formation in OA and provides useful information for the management of advanced-stage TMJ OA in clinical practice. It remains unclear whether subchondral cyst is initiated by the loss of cartilage integrity, or as a result of subchondral bone resorption. Moreover, this debate is common in OA research, and future studies should strive to characterize the response of both tissues to pathological stress conditions.

No potential conflict of interest relevant to this article was reported