## 1 Introduction  
**Temporomandibular joint (TMJ) is a synovial joint comprising the mandibular fossa of the temporal bone and mandibular condyle. The articular disc is located between these structures and it is a hard-dense fibrous connective tissue with compressed collagen fibers lying bilaterally, allowing the functions of the stomatalognathic system. The TMJ is covered with an articular capsule, which is a thick connective tissue membrane, largely divided into an outer fibrous layer and inner synovial membrane. The pathological frameworks that involve TMJ are quite heterogeneous concerning etiology, pathogenesis, and clinic events [1]. **  
**Temporomandibular disorders (TMD) encompass several clinical conditions with multifactorial etiopathogenesis involving the stomatalognathic system, in particular the masticatory muscles, TMJ and the structures associated [1]. **  
**One of the main causes of TMJ pain is temporomandibular synovitis inflammation on the synovial membrane of TMJ. Temporomandibular synovitis is due to the excessive force to TMJ, which causes over-stretching and sprain of the articular capsule, articular ligament, and surrounding tissue of articular disc, or osteoarthritis (OA) of TMJ [1]. **
**Temporomandibular joint osteoarthritis (TMJOA) is classified as a \"low-inflammatory arthritic condition\" and can be unilateral or bilateral, as opposed to rheumatoid arthritis, which is a high-inflammatory condition [2]. The clinical evidence of this pathological condition occurs in 8-16% of the population with a strong preference for women [2; 3]. Subversion of loads at the joint level involves a chronic trauma associated with morphological changes resulting in flattening of the articular heads. Clinical diagnosis is based on the presence of several signs and symptoms: pain (most commonly described as a deep ache) in the pre-auricular area with or without associated earache, coarse crepitus in the joint with or without clicking [4], pain in one or both joints during palpation and usually complemented with radiological evidence of arthrosis [3]. Recently, cone-beam computed tomography (CBCT) has provided a more detailed change of TMJ bone than conventional radiographic methods (tomography, Schuller's projection, spiral computed tomography, etc. ), demonstrating a special advantage in TMJOA diagnosis [1]. According to the American Academy of Orofacial Pain, TMJOA is categorized into primary and secondary: (1) primary TMJOA is characterized by the absence of any distinct local or systemic factor; (2) secondary TMJOA is associated with a previous traumatic event or disease [2]. Some of the circumstances involved in TMJOA are functional overload and parafunction (like tooth grinding during sleeping), unstable occlusion (for example due to a too high restored tooth that does not interact properly with the others), or trauma (microtrauma and macrotrauma) [3; 5]. TMJOA could also be a consequence of a dysfunctional articular remodeling due to a decreased adaptive capacity of the articulating structures of the joint [3]. Excessive mechanical loading on normal articular cartilage or normal mechanical loading on impaired articular cartilage is generally speculated to initiate the disruption of cartilage matrix homeostasis [1; 6]. The degeneration of the structure and function of articular cartilage is accompanied by the corresponding bone changes, characterized by a defective adhesion of chondrocytes to proteins of the extracellular matrix, including fibronectin, resulting in a deficit of the tissue mechanical integrity and cartilage repair process [7; 8; 9]. Therefore, the last stage in the development and progression of TMD is represented by cartilage degradation, characterized by secondary inflammation resulting in the degenerative condition of OA [1; 8]. In general, the natural course of TMJOA is favorable and can be divided into three slow progressive phases, with periods of remission and cartilage regeneration [2].