## 1 Introduction  
The temporomandibular joint (TMJ) is a highly specialized ginglymoarthrodial joint that facilitates both rotational and translational movements essential for mastication, speech, and other jaw functions [1]. The TMJ consists of the mandibular condyle and the glenoid fossa of the temporal bone, separated by a fibroxtilaginous articular disc [2, 3]. This disc divides the joint into superior and inferior compartments, allowing complex movements such as opening, closing, and lateral excursions [2, 3]. The joint is stabilized by the joint capsule and reinforced by ligaments, including the temporomandibular ligament, which limits excessive posterior and inferior displacement [2, 3]. The TMJ functions in close coordination with the masticatory muscles, including the masseter, temporalis, and medial and lateral pterygoids, which collectively generate the forces required for mandibular movements essential in mastication and articulation [2; 3]. These muscles, innervated by the mandibular division of the trigeminal nerve, play a pivotal role in jaw stabilization and movement [2; 3]. The vascularization of the TMJ is derived predominantly from branches of the external carotid artery [3]. The superficial temporal artery and maxillary artery supply the joint capsule, surrounding tissues, and synovial membrane, ensuring adequate perfusion for joint function and repair [3]. Sensory innervation to the TMJ is primarily provided by the auriculotemporal nerve, a branch of the mandibular nerve, which conveys proprioceptive and nociceptive inputs. Additional contributions may arise from the masstereric and deep temporal nerves, ensuring comprehensive motor and sensory control of the joint [3]. Temporomandibular disorders (TMDs) encompass a spectrum of conditions affecting the TMJ, masticatory muscles, or associated structures, often characterized by symptoms such as pain, joint noises, and restricted mandibular movement [4; 5]. The etiology of TMDs is multifactorial, involving biological, mechanical, psychological, and environmental factors [6; 7]. Key contributors include trauma, bruxism, malocclusion, and stress-induced muscle tension, alongside systemic conditions such as arthritis and genetic predispositions [8; 9]. These diverse factors underscore the complexity of TMDs, which range from muscle-related pain to joint pathologies such as disc displacement, degenerative changes, and inflammatory conditions [3; 10]. Adolescents are particularly vulnerable to TMDs due to craniofacial growth, hormonal fluctuations, and musculoskeletal adaptations during critical developmental stages [5; 11; 12]. Common symptoms include joint pain, restricted mandibular movement, and muscle tenderness, often accompanied by headaches and neck discomfort, significantly impacting daily functioning [11; 13; 14]. The prevalence of TMDs among adolescents ranges from 20% to 74%, influenced by diagnostic criteria and population demographics [13; 14; 15]. [PERSON] et al. (2001) noted that untreated symptoms often persist into adulthood, highlighting the need for early diagnosis and intervention [15]. Severe cases, such as TMDs associated with juvenile idiopathic arthritis (JIA), can result in joint damage, requiring targeted management strategies [16]. Minimally invasive procedures, such as arthocentesis and intra-articular injections, have proven effective in symptom relief and functional improvement in pediatric populations [17]. Females exhibit a higher prevalence of TMDs, linked to hormonal factors such as estrogen, which increases pain sensitivity and tissue inflammation [5; 11; 12]. Additionally, psychological factors, including stress and anxiety, and parafunctional habits like bruxism exacerbate TMDs symptoms [5; 13; 14]. Structural differences, such as smaller joint structures and reduced muscle mass, further increase susceptibility to mechanical overload [5].