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Annali di Stomatologia | 2026; 17(1): 120-147 ISSN 1971-1441 | DOI: 10.59987/ads/2026.1.120-147 Articles |
Cranio-cervical-mandibular disorders and oro-cervical-facial pain: a classification based on anatomical units
Abstract
Objective: To develop an integrated classification of cranio-cervical-mandibular disorders (CCMD) and oro-cervical-facial pain (OCFP), based on anatomical units, to allow for a more precise and useful clinical approach.
Method: A multicenter study was conducted involving 8 clinical specialists from Chilean and Italian universities, as well as 14 students serving as collaborators. The methodology involved organizing the participants into subgroups and holding periodic discussion sessions. Successive drafts were produced until a final classification was agreed upon. Once completed, each included pathology was defined.
Results: The classification is organized into four hierarchical levels: (1) anatomical structure/origin (muscular, osteoarticular, nervous/neurovascular, and associated structures), (2) pathogenetic mechanism (pain/inflammation/degeneration, dysfunction/mobility, growth/development/genetics), (3) pathophysiology, and (4) associated local or systemic pathologies. A list of specific conditions that can affect the suprascapular unit was also included.
Conclusion: The proposal addresses shortcomings in previous organizations by establishing a clear, logical, and hierarchical structure. This first integrative classification favors a more precise, inferential organization of cranio-cervical disorders (CCD) and temporomandibular disorders (TMD), including OCFP. It offers an initial framework that is susceptible to future expansion and adjustments. It also represents a step towards standardizing diagnoses and optimizing treatments in this area.
Keywords: Temporomandibular disorders; Cranio-cervical disorders; Orofacial pain; Cervical pain; Articular pain.
Introduction
The temporomandibular and cranio-cervical units are integrated anatomically and neurophysiologically (1,2). Indeed, pathology in the area above the shoulder belt often affects both units (3). As temporomandibular disorders (TMD) and cranio-cervical disorders (CCD) are related and various pathologies converge, specific diagnoses are required to manage the problem optimally. In relation to diagnosis, the first concept to understand when analyzing or generating a classification is ‘taxonomy’. Taxonomy is the science of classification. It is based on organizing groups into a specific, exclusive hierarchy, meaning that each classified element cannot be integrated into two different hierarchies. Thus, taxonomy is a systematic organization of categories based on common characteristics. Therefore, each element in a group will have similarities with the others (4). Diagnosis is an inferential process based on the analysis of signs and symptoms (neither a sign nor a symptom should be considered a diagnosis). It relies on the clinical presentation of a disease. It determines the disease, which must be defined within a biological, psychosocial, and environmental context (5,6).
The International Classification of Diseases (ICD) is the classification that encompasses nearly all existing pathologies. It has several versions (7 and 8). The ICD provides an index of all pathologies and is divided into 22 chapters (9). Chapter 12 classifies diseases of the skin and subcutaneous tissues, while Chapter 13 classifies diseases of the musculoskeletal system and connective tissue. Diseases of the skin and subcutaneous tissues include diseases of the oral cavity and salivary glands, as well as cheilitis, abscesses, cellulitis, and lesions associated with autoimmune diseases. Diseases of the musculoskeletal system and connective tissue include arthropathies, dentofacial abnormalities, systemic connective tissue disorders, dorsopathies, soft tissue disorders (including muscles and synovium), osteopathies and chondropathies, other musculoskeletal and connective tissue disorders, intraoperative complications and disorders, periprosthetic fractures, and biomechanical injuries that are not classified under this heading. Among the classifications that include temporomandibular disorders (TMD), there are two groups: a) temporomandibular disorders and orofacial pain (TMD/OFP) classifications and b) TMD classifications (Table 1).
The International Classification of Orofacial Pain (ICOP) includes seven domains, two of which are directly associated with temporomandibular disorderrelated pain (10). The first domain, ‘Orofacial Pain’, refers to dentoalveolar, mucosal, salivary gland, and mandibular bone pain. The fourth domain addresses diagnoses related to pain attributed to lesions of the trigeminal and glossopharyngeal nerves. The fifth domain refers to primary headaches, including orofacial migraine, tension-type headache, trigeminal autonomic orofacial pain (including cluster headaches and hemifacial paroxysmal headaches), and neurovascular orofacial pain. The sixth domain addresses pathologies involving idiopathic orofacial pain, such as burning mouth syndrome, persistent idiopathic facial pain, and persistent unilateral facial pain with additional attacks. In terms of specific temporomandibular pathology, this classification system recognizes two distinct categories: one focusing on orofacial myofascial pain, and the other addressing TMJ pain. Both of these are subdivided into primary and secondary pain. Primary pain is considered a disease in its own right, with multifactorial causes. Idiopathic pain, on the other hand, is a symptom for which no definitive cause can be identified. Secondary pain is defined as pain resulting from or caused by another condition. In the case of muscle pathology, secondary pain arises from myofascial structures and tendons. It is indicated that myofascial pain may be attributed to tendinitis, myositis, or spasms. These data allow the determination of whether the etiology is inflammatory due to overload, infectious, or a central response to a noxious agent, such as spasm. Regarding joint pain, the pathology is characterized by inflammation from various causes, tissue sensitization, and structural changes. This domain includes pain associated with arthritis (i.e., joint inflammation), whether systemic or non-systemic. Nonsystemic pain does not reveal possible non-systemic causes; therefore, the diagnosis is non-specific. The following section presents the pathology associated with disc displacement, degenerative disease, and subluxation. The ICD-11 is the most recent version of the International Classification of Diseases (ICD), and it is highly accurate for coding primary and secondary chronic pain. This version includes diagnostic codes for chronic pain conditions, but, according to Treede et al., it is not systematically categorized (10). The relevant clinical disorders are classified into seven groups: primary chronic pain; chronic cancer-associated pain; chronic post-traumatic and post-operative pain; chronic neuropathic pain; chronic headaches and orofacial pain; chronic visceral pain; and chronic musculoskeletal pain. In relation to the TMD/OFP specialist area, the conditions involved are chronic neuropathic pain, chronic headaches, orofacial pain, and chronic musculoskeletal pain. However, TMD/ODP are most prevalent in the chronic headache and orofacial pain group. This group includes chronic headaches and orofacial pain caused by vascular and non-vascular cranial or cervical disorders, substances such as medications, and disorders of the skull, neck, eyes, ears, nose, sinuses, teeth, mouth, and other facial or cervical structures. Referred chronic pain to the teeth is also described, as are chronic neuropathic orofacial pain and chronic pain secondary to temporomandibular disorders. Bell’s pain classification considers two inputs: one somatosensory and the other psychosocial. These inputs generate a condition based on two levels, or axes: one representing the factors responsible for the nociceptive stimulus (axis I), and the other representing the psychological factors that influence the pain experience (axis II) (11). Axis I identifies: 1. Cutaneous and mucogingival pain. 2. Pharyngeal, nasal, and paranasal mucosal pain. 3. Dental pain. 4. Pain in the musculoskeletal structures of the mouth and face. 5. Pain in the visceral structures of the mouth and face. 6. Pain in the neural structures of the mouth and face. Axis II identifies: 1. Anxiety disorders. 2. Mood disorders. 3. Somatoform disorders. 4. Other conditions, such as psychological factors that affect medical conditions. The American Academy of Orofacial Pain (AAOP) classification of orofacial pain (12,13) includes a subclassification of musculoskeletal disorders of the temporomandibular joint (TMD). The full classification considers: 1. Vascular and nonvascular intracranial pain disorders. 2. Primary headaches. 3. Neuropathic pain. 4. Intraoral pain disorders. 5. Temporomandibular disorders. 6. Cervical pain disorders. 7. Orofacial pain of extracranial and systemic causes. As we can see, item 5 covers temporomandibular disorders and uses the classifications provided by the DC/TMD and the expanded TMD taxonomy published by Peck C. (14). This subclassification is no longer exclusively related to pain, providing an approach to integrating painful and non-painful temporomandibular disorders into a single structure. Additionally, the AAOP classification incorporates diagnoses involving TMD/OFP specialists, such as headaches, neuropathic pain, and neck pain disorders. Peck’s expansive taxonomy comprises four domains that lack a specific hierarchy (15). These include temporomandibular joint disorders, masticatory muscle disorders, TMD-associated headaches, and associated structures. J. Okeson’s classification, adapted from his work “Orofacial Pain: Guidelines for Assessment, Diagnosis and Management (third edition, 1996)”, is used to diagnose TMD and includes pathologies not addressed in other classifications (15). It presents four domains: masticatory muscle disorders; temporomandibular joint disorders; chronic mandibular hypomobility; and growth disorders. The International Classification of Diseases (ICD) also includes pathologies of the cranio-cervical unit in chapter 13. This chapter covers diseases of the musculoskeletal system and connective tissue, including arthropathies, systemic connective tissue disorders, dorsopathies, soft tissue disorders, osteopathies, chondropathies, and other unclassified biomechanical disorders, as well as complications, fractures, and injuries. In parallel, there are some more specific classifications. These include the 2021 World Health Organization (WHO) classification, the International Statistical Classification of Diseases and Related Health Problems (ICD), and the International Classification of Functioning, Disability and Health (ICF). The WHO proposes a first-level classification based on anatomical structures, including joints, bones, muscles, the spine, and various body systems or regions. The ICD proposes five pathologies: 1. Cervical pain. 2. Thoracic spine pain. 3. Headaches. 4. Spondylosis with radiculopathy. 5. Cervical disc disorders with radiculopathy. The ICF proposes a simple classification for the cervical region that includes four pain-related lesions: 1. Neck pain with movement disturbance. 2. Neck pain with headaches. 3. Neck pain with coordination disturbance. 4. Neck pain with a referred pattern. Our study aims to develop an integrated classification of cranio-cervical-mandibular disorders and oro-cervical-facial pain (CCMD/OCFP) based on anatomical units. This will allow for a more precise and useful clinical approach.
| ICOP 2020 | IC -11 | BELL |
|---|---|---|
| Orofacial pain | Secondary musculoskeletal pain | Muscle disorders |
| Myofascial pain | Neuropathic pain | Tmj disorders |
| Tmj pain | Pain secondary to headache | Disorders with hypo-mobility |
| Pain of neurological origin | Growth disorders | |
| Pain due to primary headache | ||
| Idiopathic orofacial pain | ||
| Pain associated with psychosocial factors | ||
| AAOP | PECK | OKESON |
| Temporomandibular disorders | Tmj disorders | Muscle disorders |
| Neuropathic pain | Muscle disorders | Tmj disorders |
| Pain secondary to headache | Secondary headache | Disorders with hypo-mobility |
| Cervicogenic pain in headache | Disorders of accessory structures | Growth disorders |
Methods
A multicenter group study was conducted by seven professionals (five dentists and two physiotherapists) from Universidad Diego Portales (Chile), the University of Modena e Reggio Emilia (Italy), and Universidad de La Serena (Chile). The study aimed to develop a classification of cranio-cervical-mandibular disorders and oro-cervical-facial pain based on anatomical units, following a precise hierarchy. The participants were three temporomandibular disorder specialists, two physiology and occlusion experts, two maxillofacial kinesiology and cranio-cervical-mandibular disorder experts, two public health experts, and 14 students from Diego Portales University in Chile specializing in temporomandibular disorders. The working group met periodically in a hybrid format (in person and via streaming). Before the first meeting to develop this integrated classification, a session was held to define concepts and operational definitions and to address the study objectives. Following this, the participants met in affinity groups and spent a week developing the classification. Each group presented its draft classification for discussion, after which the final draft was written. This draft was distributed to all participants for evaluation and, once the necessary changes had been defined, the final classification was produced. Once completed, each pathology was briefly defined (Annex 1, inserted at the end of the article).
Results
According to the applicable taxonomic guidelines, the classification was organized into four hierarchies: affected anatomical structure; general mechanism involved in pathogenesis (with or without a genetic component); pathophysiology associated with each mechanism; and local pathologies (which were further subdivided as necessary). The following were defined according to the affected anatomical structure: 1) Muscular. 2) Osteoarticular. 2A) Temporomandibular joint. 2B) Vertebral/articular component. 3) Nervous and neurovascular component. 4) Associated structures. Three categories were defined for each anatomical group, based on mechanisms: 1) Pain/inflammation/degenerative diseases. 2) Dysfunction/mobility. 3) Growth/development/metabolism. Pathophysiology focuses on defining the processes involved in each mechanism to enable the diagnosis of specific pathologies. This exercise aimed to determine an appropriate management strategy for each pathology. The classification developed is shown in Table 2. Each pathology is then defined separately and presented in alphabetical order. Systemic pathologies that may manifest in structures above the shoulder girdle are listed in Table 3.
| ANATOMICAL STRUCTURE/ORIGIN | MECHANISM (WITH OR WITHOUT GENETIC COMPONENT) | PHYSIOPATHOLOGY | LOCAL PATHOLOGIES | SPECIFIC PATHOLOGIES |
|---|---|---|---|---|
| 1) MUSCULAR | 1.1 Pain/inflammation/degenerative disesases | 1.1.1 Miositis by overloading | 1.1.1.1 Local myalgia | 1A1.1.1.a Pain induced by extreme exercise |
| 1A1.1.1.b Delayed onset muscle soreness | ||||
| 1A1.1.1.c Pain associated to injuries | ||||
| 1.1.1.2 Myofascial pain | ||||
| 1.1.1.3 Myofasical pain with referral | ||||
| 1.1.2 Miositis by infection | 1.1.2.1 Bacterial myositis | |||
| 1.1.3 Miositis by other external agents | 1.1.3.1 Viral myositis | |||
| 1.1.3.3 Parasitic Myositis | ||||
| 1.2 Dysfunction/mobility | 1.2.1 Stiffnes/rigidity | 1.2.1.1 Myostatic contracture | ||
| 1.2.1.2 Myofribrotic contracture | ||||
| 1.2.1.3 Myospasmodic contracture | ||||
| 1.3 Growing/development | 1.3.1 Under development | 1.3.1.1 Atrophy | ||
| 1.3.1.2 Sarcopenia | ||||
| 1.3.2 Over development | 1.3.2.1 Hypertrophy | |||
| 1.3.2.2 Neoplasia | ||||
| 2) OSTEOARTICULAR | ||||
| 2A) TMJ | 2A.1 Pain/inflammation/degenerative disesases | 2A1.1 Arthritis | 2A.1.1.1 Synovitis | |
| 2A.1.1.2 Capsulitis | ||||
| 2A.1.1.3 Retrodiscitis | ||||
| 2A.1.1.4 Of other intracapsular ligaments | ||||
| 2A.1.2 Degenerative disease (DD) | 2A.1.2.1 ED - osteoarthritis/osteoarthrosis | |||
| 2A.1.2.2 Idiopathic condylolysis | ||||
| 2A.1.2.3 Avascular necrosis | ||||
| 2A.1.2.4 Osteochondritis dissecans | ||||
| 2A.1.2.5 Synovial chondromatosis | ||||
| 2A.2 Dysfunction/mobility | 2A.2.1 By interference | 2A.2.1.1 Disc displacement with reduction | ||
| 2A.2.1.2 Disc displacement without reduction with limited opening | ||||
| 2A.2.1.3 Disc displacement without reduction without limited opening | ||||
| 2A.2.1.4 Disc displacement with intermittent locking reduction | ||||
| 2A.2.1.5 Opening lock | ||||
| 2A.2.2 By fixation | 2A.2.2.1 Disc adhesion | |||
| 2A.2.2.2 Sticky or static disc | ||||
| 2A.2.2.3 Capsular fibrosis | ||||
| 2A.2.2.4 Ankylosis | 2A.2.2.4.a Fibrous | |||
| 2A.2.2.4.b Osseous | ||||
| 2A.2.3 Due to hypermobility | 2A.2.3.1 Hypertranslation | |||
| 2A.2.3.2 Dislocation | 2A.2.3.2.a Subluxation | |||
| 2A.2.3.2.b Luxation | ||||
| 2A.2.4 Due to morphological alteration | 2A.2.4.1 Disc deformation | |||
| 2A.2.4.2 Disc perforation | ||||
| 2A.2.5 Due to postural alteration | 2A.2.5.1 Condylar positional asymmetry | |||
| 2A.3 Growing/development | 2A.3.1Lack of development | 2A.3.1.1 Condylar agenesis | ||
| 2A.3.1.2 Condylar aplasia | ||||
| 2A.3.1.3 Condylar hypoplasia | ||||
| 2A.3.2 Overdevelopment | 2A.3.2.1 Condylar hyperplasia | |||
| 2A.3.2.2 Joint neoplasia | ||||
| 2A.3.3 Fractures | 2A.3.3.1 Mandibular | |||
| 2A.3.3.2 Condylar | ||||
| 2B) VERTEBRAL/ARTICULAR | 2B.1 Pain/inflammation/degenerative disesases | 2B.1.1 Arthritis | 2B.1 1.1Facet synovitis (cervical facet syndrome) | |
| 2B.1.2 Degenerative disease (DD) | 2B.1.2.1 Spondylosis | |||
| 2B.1.2.2 Disc disruption | ||||
| 2B.1.2.3 Herniated disc | ||||
| 2B.2 Dysfunction/mobility | 2B.2.1 Displacements | 2B.2.1.1Atlas rotation | ||
| 2B.2.1.2 Axis rotation | ||||
| 2B.2.1.3 Spondylolisthesis | ||||
| 2B.2.2 Fixings | 2B.2.2.1 Atlas-occipital | |||
| 2B.2.3 Postural alteration | 2B.2.3.1 Of cervical curvature | 2B.2.3.1.a Cervical spine rectification | ||
| 2B.2.3.1.b Inversion of the cervical spine | ||||
| 2B.2.3.1.c Hyperlordosis of the cervical spine | ||||
| 2B.2.3.2 Of the hyoid system | 2B.2.3.2.a Hyoid bone elevation | |||
| 2B3. Growing/development | 2B.3.1 Lack of development | 2B.3.1.1 Vertebral agenesis | ||
| 2B.3.1.2 Vertebral aplasia | ||||
| 2B.3.1.3 Vertebral hypoplasia | ||||
| 2B.3.2 Overdevelopment | 2B.3.2.1 Vertebral hyperplasia | |||
| 2B.3.2.2 Neoplasms of the cervical spine | ||||
| 2B.3.3 Fractures | 2B.3.3.1Fractures of the vertebral bodies | |||
| 2B.3.3.2 Fractures of the vertebral arches | ||||
| 2B.3.3.3 Fractures of the vertebral processes | ||||
| 3) NEURAL AND NEUROVASCULAR COMPONENT | 3.1 Pain/inflammation/degenerative disesases | 3.1.1 Episodic neuropathic pain | 3.1.1.2 Neuralgia | 3.1.1.2.a Trigeminal neuralgia |
| 3.1.1.2.b Glossopharyngeal neuralgia | ||||
| 3.1.2 Continuous neuropathic pain | 3.1.2.1 Peripherally mediated neuropathy | |||
| 3.1.2.2 Deafferentation neuropathy | 3.1.2.2.a Neuropathy of dento-alveolar origin | |||
| 3.1.2.2.b Disestesia oclusal | ||||
| 3.1.2.2.c Burning mouth syndrome | ||||
| 3.1.2.3 Centrally mediated neuropathy | 3.1.2.3.a Complex regional pain syndrome | |||
| 3.1.2.3.b Post-herpetic neuralgia | ||||
| 3.1.2.4 Primary headaches | 3.1.2.4.a Migraine | |||
| 3.1.2.4.b Tension-type headache | ||||
| 3.1.2.4.c Trigeminal-autonomic headaches - cluster headache | ||||
| 3.1.2.4.d Trigeminal autonomic headache - paroxysmal | ||||
| 3.1.2.4.e SUNCT Unilateral neuralgiform headache with watering and redness | ||||
| 3.1.2.4.f SUNA Unilateral neuralgiform headache with autonomic symptoms | ||||
| 3.2 Dysfunction/mobility | 3.2.1 Central defense responses | 3.2.1.1 Myospasm | ||
| 3.2.1.2 Protective co-contraction | ||||
| 3.3 Growing/development | 3.3.1 Structural malformations | 3.3.1.1 Neoplasms | ||
| 4) ASSOCIATED STRUCTURES | 4.1 Pain/inflammation/degenerative disesases | 4.1.1 Inflammation of the temporomandibular ligament | ||
| 4.1.2 Temporal tendonitis | ||||
| 4.1.3 Sialadenitis | ||||
| 4.1.4 Parotitis | ||||
| 4.2 Dysfunction/mobility | 4.2.1Cervical injuries associated with the hyoid | |||
| 4.2.2Elevation of the hyoid | ||||
| 4.3 Growing/development | 4.3.1 Eagle syndrome | |||
| 4.3.2 Ernest Syndrome | ||||
| ANATOMICAL STRUCTURE/ORIGIN | MECHANISM (WITH OR WITHOUT GENETIC COMPONENT) | PHYSIOPATHOLOGY | LOCAL PATHOLOGIES |
|---|---|---|---|
| 1) MUSCULAR | 1.1 Pain/inflammation/degenerative diseases | 1.1.1 Due to myositis caused by systemic factors | 1.1.1.1 Dermatomyositis |
| 1.1.1.2 Polymyalgia rheumatica | |||
| 1.2 Dysfunction/mobility | 1.2.1 Due to weakness caused by systemic factors | 1.2.1.1 Myotonic muscular dystrophy type 1 | |
| 1.2.1.2 Facioscapulohumeral muscular dystrophy | |||
| 1.2.1.3 Oculopharyngeal muscular dystrophy | |||
| 1.2.1.4 Mitochondrial myopathy | |||
| 1.2.1.5 Mitochondrial encephalomyopathy | |||
| 1.2.2 Motor disorders | 1.2.2.1 Oromandibular dystonia | ||
| 1.2.2.2 Orofacial dyskinesia | |||
| 1.3 Growing/development | 1.3.1 Due to endocrine myopathies | 1.3.1.1 Hyperthyroidism | |
| 1.3.1.2 Hypothyroidism | |||
| 1.3.1.3 Hyperparathyroidism | |||
| 1.3.1.4 Hypoparathyroidism | |||
| 1.3.1.5 Cushing’s syndrome | |||
| 1.3.1.6 Addison’s disease | |||
| 2) OSTEOARTICULAR | 2A.1 Pain/inflammation/degenerative diseases | 2A.1.1 For underlying rheumatoid arthritis | |
| 2A) TMJ | 2A.1.2 Due to underlying psoriatic arthritis | ||
| 2A.1.3For underlying Lyme disease | |||
| 2A.1.4 Per gout of base | |||
| 2A.1.5 Due to underlying ankylosing spondylitis | |||
| 2A.2 Dysfunction/mobility | 2A.2.1 Due to underlying systemic hypermobility | ||
| 2A.3 Growing/development | 2A.3.1 For systemic rheumatic diseases | ||
| 2B) VERTEBRAL/ARTICULAR | 2B.1 Pain/inflammation/degenerative diseases | 2B.1.1 For rheumatoid arthritis | |
| 2B.1.2 Due to spondyloarthritis | |||
| 2B.1.3 For systemic lupus erythematosus | |||
| 2B.1.4 Due to Sjoegren’s syndrome | |||
| 2B.1.5 Due to scleroderma | |||
| 2B.1.6 For Behcet’s disease - vasculitis | |||
| 2B.1.7 For relapsing polychondritis | |||
| 2B.2 Dysfunction/mobility | 2B.2.1 Due to underlying systemic hypermobility | ||
| 2B3. Growing/development | 2B.3.1 For ankylosing spondylitis | ||
| 2B.3.2 Due to Scheuermann’s disease | |||
| 2B.3.3 For Jarcho-Levin Syndrome | |||
| 2B.3.4 In association with VACTERL | |||
| 2B.3.5 Due to Paget’s disease | |||
| 2B.3.6 For metabolic diseases | |||
| 2B.3.7 Due to systemic sclerosis | |||
| 3) NEURAL AND NEUROVASCULAR COMPONENT | 3.1 Pain/inflammation/degenerative diseases | 3.1.1 Fibromyalgia | |
| 3.1.2 Myofascial pain syndrome | |||
| 3.2 Dysfunction/mobility | 3.2.1 Congenital torticollis | ||
| 3.3 Growing/development | 3.3.1 Due to congenital anomalies | 3.3.1.1 Hydrocephalus | |
| 3.3.2 For genetic disorders | 3.3.2.1 Down syndrome | ||
| 3.3.2.2 Rett syndrome | |||
| 3.3.2.3 Fragile X chromosome syndrome | |||
| 3.3.3 For metabolic disorders | 3.3.3.1 Enzyme deficiencies | ||
| 3.3.4 Due to infections | 3.3.4.1 Meningitis during pregnancy or childhood | ||
| 3.3.4.2 Encephalitis during pregnancy or childhood | |||
| 3.3.5 For neoplasias | |||
| 4) ASSOCIATED STRUCTURES | 4.1 Pain/inflammation/degenerative diseases | 4.1.1 For rheumatoid arthritis | |
| 4.1.2 For lupus erythematosus | |||
| 4.1.3 Due to scleroderma | |||
| 4.1.4 For connective tissue diseases | |||
| 4.2 Dysfunction/mobility | 4.2.1 For Duchenne muscular dystrophy | ||
| 4.2.2Due to Pierre Robin syndrome | |||
| 4.2.3 Due to obstructive apnea | |||
| 4.3 Growing/development | 4.3.1 For ankylosing spondylitis | ||
| 4.3.2 Due to Forestier’s disease |
Discussion
This classification is derived from the rules of taxonomy, which essentially organize groups into a hierarchical structure (4,5,6). Diagnosis is an inferential process based on clinical symptoms, aimed at defining a disease. These signs and symptoms must be specific and defined in the context of the environment. Based on this definition, it is impossible to include signs or symptoms as a diagnosis. Examples of this include bruxism, secondary pain (e.g., headaches resulting from muscle disorders), painful conditions that are not properly considered diseases (e.g., migraines and cluster headaches), arthralgia, and myalgia. A clear diagnosis should inform the clinician’s choice of treatment or management, so diagnostics must consider the disease’s etiology. For example, in the case of arthralgia derived from an inflammatory process (e.g., arthritis), if information about the arthralgia is lacking, a clear diagnosis will not be possible, and an effective treatment will not be defined. Conversely, if the diagnosis is capsulitis rather than arthralgia or arthritis, the clinician has more resources to infer causality: capsule pain on stretching. Therefore, the clinician should identify the cause of the stretching, which may be microtrauma within the stomatognathic system or external trauma. Once the cause is found, the treatment can be correctly applied. Classifications based on pain include some painful temporomandibular disorders, but do not classify these diseases themselves (10, 11). TMD may or may not be associated with pain. If they are associated, they are generally part of nociceptive or nociplastic pain (17). Therefore, TMD and CCD should be classified together as local diseases because they share many signs and symptoms, including muscle pain. In this respect, a new classification has been created that includes TMD, CCD, and pain.
Regarding the two major and useful classifications of TMD in the literature, several issues need to be addressed. Peck’s taxonomy includes four domains that do not follow an explicit hierarchy (15). The articular, muscular, and other structures form an anatomical division, but secondary headache is neither an anatomical structure nor a pathology. Additionally, there are inconsistencies in the definition of a diagnosis, as arthralgia and myalgia are symptoms. Consequently, it is impossible to make a differential diagnosis or propose a treatment. What is the result? Treatments are advocated for the symptomatic management of pain rather than addressing the cause. This problem is solved by the Okeson classification (12), which includes capsulitis, synovitis, and retrodiscitis as inflammatory diseases that cause articular pain (arthralgia), rather than arthralgia or arthritis. Although the expanded TMD taxonomy is derived from reliable diagnostic criteria with proven criterion-related validity, many diseases have not been included, even though they exist. Also, some general diseases or pathophysiological conditions that may affect the temporomandibular structures are included; they cannot be placed within a hierarchy.
On the other hand, the Okeson classification, adapted from Orofacial Pain: Guidelines for Assessment, Diagnosis and Management (3rd ed., 1996) (12), integrates many pathologies into a hierarchy based on a common characteristic. However, it suffers from the same problem: two anatomical domains, one concerning hypomobility disorders and the other including growth and developmental disorders. This classification’s greatest contribution is that it includes some prevalent disorders that are unclassified in other classification systems, such as protective co-contraction, synovitis, capsulitis, and retrodiscitis, as well as disorders classified under hypomobility. As a first approach, integrating and applying both classification systems, alongside those based on pain, in a hierarchical, criterion-based manner can enable a structured classification that includes all pathologies. This study aimed to achieve this, as well as to integrate CCD to generate a universal classification of the suprascapular unit. Information about classifications of cranio-cervical units is scarce and limited, but fortunately, they share all characteristics of TMD. Muscles and joints are common structures with common disorders. There may be some anatomical differences, but the structures, mechanisms, and physiopathology are similar. For this reason, the authors decided to create a common classification of cranio-cervical-mandibular disorders and oro-cervical-facial pain.
Conclusion
This classification of cranio-cervical-mandibular disorders and orocervical-facial pain (CCMD/OCFP) categorizes various local disorders affecting defined anatomical units, including a sub-classification of systemic disorders that impact them. As this is the first integrative classification, it can be modified according to other criteria while maintaining the structure that a diagnostic classification must have, a hierarchical development.
Acknowledgments
The authors want to appreciate our students of the Specialty Program on Temporomandibular Disorders and Orofacial Pain for their excellent contribution. Daniela Aravena DDS, Raúl Acosta. DDS, Daniela Coronado DDS, María Fernanda Durán. DDS, Paulina Espinoza. DDS, Mónica Farías. DDS, Ljubica Malinarich DDS, Viviana Moya DDS, Miguel Perez DDS, Diego Salas DDS, Francisca Urrizola DDS, Nicolás Varela DDS, Ignacio Vásquez DDS, Laura Wistuba DDS.
Funding
This research received no external funding.
Conflicts of Interest
The authors declare no conflicts of interest.
Annex 1.
| Pathology | Definition |
|---|---|
| Ankylosis (fribrous and osseous) | Limited condylar movement, which can result in impaired mouth opening, may be caused by fibrous or bony ankylosis of the temporomandibular joint. This injury can result from trauma, infection or autoimmune diseases (19). However, condylar trauma is widely regarded as one of the primary causes of ankylosis (20). Regarding bony ankylosis, osteogenesis has been observed to occur at the junction between the ankylosed cartilage tissue and the bone segment, primarily through endochondral ossification (21). |
| Atlas rotation | The atlas, the first cervical vertebra, allows flexion and extension of the skull. Through its articulation with the axis, it also enables cranial rotation. The kinematics of the cervical spine and vertebral morphology are closely related (22,23). Cranial flexion and extension occur because the superior articular facets of the atlas are concave in both directions, accommodating the occipital condyles. The atlantoaxial joint, located between the odontoid process of the axis and the anterior arch of the atlas, enables 50–60% of cervical rotation. This joint has three axes of movement with three degrees of freedom, and its wide range of rotational movement is notable. There are no intervertebral discs between the occipital bone and the atlas or between the atlas and the axis. When the odontoid process is normal, the movement of the second cervical vertebra (C2) anteriorly is restricted by the anterior arch of the first cervical vertebra (C1). Posterior movement is limited by the cruciate ligament, primarily the transverse ligament. This unit can accommodate alterations in the position of the atlas, which manifests as a rotation that is quite benign compared to a rare subluxation of the atlas (24). Loss of stability between the atlas and the axis can result from macrotrauma, such as whiplash, or microtrauma associated with poor posture and asymmetric muscle activity. This misalignment can lead to upper cervical pain and altered cranial rotation. If the atlas rotates and misaligns to one side, the alar ligaments will tighten on the side opposite the rotation, thereby impeding proper ipsilateral rotation of the skull. Furthermore, propulsion of the atlas can lead to relative distalisation of the axis, causing the odontoid process to press on the spinal cord and result in pain and/or headaches. However, the consequences of a subluxation can be more complex as it involves the vertebral artery. |
| Atlas-occipital fixing | This injury does not necessarily correspond to ankylosis, a condition involving the fusion of joints. Rather, it represents an instability characterized by a significant reduction in the range of motion between the two vertebrae. This can be caused by trauma, degenerative disease or congenital anomalies, resulting in pain and impaired mobility in the craniocervical region. A rare condition called traumatic atlantoaxial rotatory fixation can also present as atraumatic and may be present alongside congenital torticollis (26,27). |
| Avascular necrosis | Firstly, we believe it is important to clarify the concept of bone marrow edema, given its association with avascular necrosis. This term is used to describe changes in imaging signal intensity that could be attributed to various underlying pathologies. Bone marrow edema is associated with pain, dysfunction and progressive cartilage damage. Detecting it is essential as its presence is associated with pain, decreased function, cartilage damage, structural deterioration, accelerated osteoarthritis and rapid progression to total joint arthroplasty (28). The most common causes of bone marrow edema are reactive bone marrow edema in response to processes such as infections, osteomyelitis, inflammatory arthritis or tumors; ischemic bone marrow edema, such as osteonecrosis and osteochondritis dissecans; and mechanical bone marrow oedema, including joint misalignment, meniscal or ligament injury, contusions or fractures (29). Osteoarthritis is often associated with bone marrow edema, increased fluid levels and pain (30). Avascular necrosis is a condylar lesion resulting from impaired blood flow to the condyle due to factors such as trauma, sickle cell anemia or systemic lupus erythematosus. On a CT scan, the mandibular condyle appears deformed with subchondral sclerosis. On an MRI scan, the bone marrow appears dark on T1-weighted images and shows a mixed signal on T2-weighted images (31). |
| Axis rotation | The axis may also undergo positional changes and become unstable, resulting in neck pain, headaches and vestibular symptoms. Rotation of the axis can result in the complete rotation of the atlas-axis complex, which restricts ipsilateral cranial rotation. |
| Bacterial myositis | It is an inflammatory pathology of infectious origin that occurs following events such as injury, surgery or ischemia. As it can spread from neighboring sites of infection or via the bloodstream, it is categorized as a systemic muscle pathology. |
| Burning mouth syndrome | Burning mouth syndrome is defined as a recurring, daily burning or dysesthetic sensation in the mouth, lasting more than two hours per day for at least three months, with no clinically evident underlying cause (32). Various mechanisms have been proposed to explain the condition, including those involving neural pathways, immunological factors, stress, hormones and neuropsychiatric factors, among others (33). Notably, it has a dual etiology involving both peripheral nerve dysfunction and central sensitization. Although it involves the principles of nociplastic pain, this term should be applied with caution to avoid oversimplification (34). |
| Capsular fibrosis | Capsular fibrosis of a joint is characterized by the excessive differentiation and proliferation of myofibroblasts, and the abnormal secretion and accumulation of the extracellular matrix. Following trauma, the joint capsule contracts (35). |
| Capsulitis | The term ‘capsulitis’ is usually used alongside ‘synovitis’, perhaps because the inner layer of the joint capsule is the synovial membrane. However, unlike synovitis, capsulitis responds to capsule elongation, suggesting that their etiology is somewhat different. Indeed, capsulitis is more frequently associated with occlusal contacts that result in excessive stretching of the capsule, whereas synovitis is associated with compressive overload of the synovial tissue caused by the articular condyle (36). |
| Cervical injuries associated with the hyoid | Cervical injuries associated with the hyoid bone refer to traumatic damage involving both the anterior mid-neck skeleton (notably the hyoid bone) and the cervical spine and its adjacent soft tissue structures. Such injuries frequently result from high-force mechanisms (e.g. blunt anterior neck impact, hyperextension of the neck, strangulation or hanging), which transmit force through the hyoid or cervical segments. As the hyoid bone is located at approximately the level of the C3 vertebra and is positioned between the mandible at the front and the cervical spine at the back, injury to one of these structures can spread to the other. Clinically, suspicion of hyoid injury should prompt evaluation of cervical spine injury (and vice versa), since hyoid fracture or displacement may indicate high-risk cervical trauma. Furthermore, cervical instability may coincide with airway and soft-tissue compromise in the hyoid/laryngeal region (37,38). |
| Cervical lordosis loss | Poor craniocervical posture is a common cause of pain and movement disorders in this area (39). In growing individuals, it can also affect the normal development of bone structures. Loss of cervical stability is associated with altered cervical lordosis, altered muscle function and impaired movement. A high prevalence of disc degeneration has been observed in cases of loss of cervical lordosis, along with pronounced weakness in both the cervical flexors and extensors and an imbalance in the relative cross-sectional areas of the flexors and extensors, which has been attributed to extensor weakness (40). Furthermore, comorbidity between temporomandibular disorders and cervical spine abnormalities has been observed, and a similar connection has been suggested between the temporomandibular joint and the cervical spine (41–43). This may not be a pathological cause-and-effect relationship, but rather a morphofunctional-postural one. However, both rectification and inversion of the cervical spine occur independently of temporomandibular disorders (44). Nevertheless, due to neuroanatomical conditions (e.g. fascia, innervation and biomechanics), it is impossible to ignore the postural relationship between the two regions. |
| Complex regional pain syndrome | This syndrome is a chronic, painful condition that can develop in response to a variety of traumas. It can be classified as type I or type II according to whether or not it has a known cause. The condition involves both peripheral and central (autonomic nervous system) mechanisms. Reduced cortical representation of the affected organ appears to be related to hyperreactive responses or spontaneous sensorimotor activity, suggesting cortical disinhibition (45–48). |
| Condylar agenesis, aplasia, hyperplasia, hipoplasia and neoplasm | Condylar agenesis refers to the complete absence of an organ or tissue, which is associated with an absence of embryonic structure. Aplasia refers to the absence of a structure that shows a rudimentary embryonic outline. Hypoplasia describes incomplete development resulting in smaller-than-normal size, while hyperplasia corresponds to an increase in the number of normal cells. In contrast, neoplasia refers to abnormal cell growth, whether benign or malignant. Congenital deformities of the temporomandibular joint (TMJ) complex typically present as a diverse range of growth disorders affecting the mandibular condyle, articular eminence and temporal bone. Among these, condylar agenesis is extremely rare (49). Condylar hypoplasia can be congenital or acquired, and is sometimes associated with head and neck syndromes (50). Acquired condylar hypoplasia is due to alterations in the condylar growth centre during development. Other morphological alterations of growth and development include bifid and trifid condyles (51). |
| Condylar fractures | Fractures of the mandibular condyle are relatively common among all mandibular fractures, accounting for 19–52% of cases, and can be caused by direct or indirect trauma (52). Various factors can cause the detached bone portion to be displaced, including the direction, magnitude and point of application of the force, the condition of the dentition and the occlusal position (539. A condylar process fracture is defined as a fracture located above the mandibular foramen, extending from the angle of the mandible to the sigmoid notch or condylar head. The condylar process extends upwards as a continuation of the posterior border of the ascending ramus, carrying the condylar head at its upper end and the lower portion of the temporomandibular joint. Three subregions are identified for the classification of fractures: the condylar head, the condylar neck, and the base of the condylar process (54). These subregions are further subclassified according to location (medial or lateral to the head), fragmentation (of the head, neck, or base), vertical apposition (of the head), lateral displacement (of the neck or base), angulation (of the neck or base), displacement of the fragment/fossa towards the cephalic or caudal end (of the entire process), distortion of the condylar head (of the entire process), and general loss of branch height (of the entire process). |
| Condylar positional asymmetry | Mandibular asymmetry is a morphological variation indicating disproportionate size, shape or position between the right and left sides of the jaw. These asymmetries can occur in the vertical, transverse and sagittal planes (55). |
| Degenerative disesase - osteoarthritis/osteoarthrosis | Degenerative TMJ disease is a general term that encompasses degenerative processes in the structure and function of the TMJ (56). These processes range from destructive lesions without active inflammation or pain, but with inflammatory precursors, to active inflammatory lesions characterized by pain and impaired function. The most common clinical sign is crepitus, provided there is no soft tissue between the bony surfaces due to disc perforations, displacement, or rupture of the upper posterior disc tissues. TMJ-DJD is a major public health problem affecting approximately 5% to 12% of the general population, and is the leading cause of chronic non-dental pain in the oral and facial regions. Advanced age is a risk factor for the development of degenerative TMJ disease. Its incidence progressively increases in middle-aged and older groups (20). Regarding occlusion, the literature is inconsistent, but loss of support in the occlusal relationship can lead to degenerative changes in TMJ components, including changes in the morphology and bone density of the condyle, articular fossa and articular eminence (57). In addition to these risk factors, sex and genetic makeup are also important, with genetic polymorphisms being associated with the inflammatory response, sex hormones, oxidative stress and bone metabolism. Lifestyle factors and chewing habits, such as unilateral chewing, have also been studied. |
| Delayed onset muscle soreness | Delayed-onset muscle soreness (DOMS) arises from unusual or repeated muscle contractions involving an eccentric component. These contractions generate high levels of tension and cause structural damage to muscle fibres. DOMS is associated with the release of algesic substances, muscle spasms and inflammation. This involves a combination of mechanical, thermal and chemical nociceptive stimuli that produce micro-injuries which attempt to heal as exercise continues. In this context, DOMS would be associated with bruxism, particularly during waking hours when a greater number of isometric muscle contractions occur (58). However, bruxism-related pain would be short-lived and self-limiting, similar to the pain experienced when people exercise without prior preparation. Therefore, we could say that, when associated with waking bruxism, DOMS corresponds to specific situations rather than periodic overload. In this case, the painful response would be more akin to myofascial pain associated with bruxism. Although data on this topic are limited, the pathophysiological relationship is clear. When recovery is impaired, neuroplastic changes can begin to occur, leading to chronic pain that would correspond to nociplastic pain affecting the myofascial system according to the mechanism. |
| Dental-alveolar pain by deafferentation | Persistent tooth pain, also known as phantom dentoalveolar pain, can occur following damage to the associated nerve component following trauma caused by the removal of the neurovascular bundle, either through tooth extraction or endodontics, or even by damage to the nerve root, whether traumatic or surgical. Dentoalveolar deafferentation is defined as the reduction or loss of peripheral afferent neuronal input related to the dental and masticatory apparatus. This situation involves cortical sensory reorganization and altered functional brain stimulation between sensory centers. These changes, which are related to phantom dentoalveolar pain, also produce alterations in auditory, gustatory and olfactory perception. Memory and cognitive impairment may also occur, as well as impairment of stomatognathic system functions, such as mastication. While a young person may adapt to deafferentation, brain plasticity decreases with age, causing these alterations (59). |
| Descent of the hyoid bone | The descent of the hyoid bone is defined as an abnormally low position relative to the mandible and cervical vertebrae. This condition may be associated with obstructive sleep apnoea, swallowing disorders or dysfunction of the suprahyoid and infrahyoid muscles (60). |
| Disc adhesion | Adherence and adhesion both involve the immobilisation or stagnation of the articular disc, typically beneath the glenoid cavity or the temporal eminence. There are some differences between the two. Adherence refers to the resistive force that prevents one surface from displacing another, i.e. the force that prevents the disc from moving freely beneath the glenoid cavity and eminence. It is suggested that the disc can move normally thanks to phospholipids and hyaluronic acid, which lubricate the joint. However, overload can cause the degradation of hyaluronic acid, exposing the phospholipids and resulting in the smooth articular surfaces becoming highly adherent upon close physical contact. This leaves only a minimal film of fluid between them and creates an adhesion similar to that produced between two glasses with a film of water between them (61). Conversely, adhesion refers to the physical union of two structures. In this regard, closed temporomandibular joint block resulting from disc displacement without reduction, and the tethered disc phenomenon, are among the possible intracapsular aetiologies described in the literature for restricted mouth opening (62,63). It is believed that the tethered disc phenomenon may be erroneously included in blocked closure or disc displacement with restricted opening conditions. This concept arose from the perception that, among patients with unreduced disc displacement, there are individuals with sudden, severe and persistent limited mouth opening. This is too severe to be caused by a deformed and irreducible disc, but rather by total inhibition of disc sliding due to an adhesive phenomenon that can be easily reversed through routine irrigation of the upper joint space (29). Fibrous adhesions are not considered a sustainable assumption for the tethered disc phenomenon because, in general, adhesions are resistant to simple lavage, and strong adhesions cannot explain its sudden onset (27). Thus, while the concept of adhesion associated with static disc syndrome may be true, its classification within the scope of TMJ disorders as a distinct and independent entity from the condition of blockage attributed to unreduced disc displacement with limited opening has not yet been agreed upon (64). In this regard, it has been observed that the presence of adhesions is significantly greater in joints with disc displacement without reduction than in joints with well-positioned discs or discs with displacement with reduction. This leads to the hypothesis that disc hypomobility is an important factor in the development of adhered or adhesive discs (65). |
| Disc deformation | A classification system has been developed to define the morphology of articular discs, particularly displaced discs. In this context, a biconcave shape is considered normal. Biconvex, biplanar and inverted biconcave shapes are defined as disc deformation, which positively correlates with the type of clicking and even the prognosis of injury (66). The temporomandibular joint disc is primarily composed of collagen, and its arrangement facilitates efficient stress distribution. This explains why a non-displaced disc can vary in morphology according to areas of overload. Pathological conditions have been observed to cause a concentration of stress near the injury site due to interfibrillar collagen trafficking patterns, resulting in the early manifestation of damage (67). Therefore, if a disc is located over the condyle and has not yet been displaced, it may exhibit morphological changes that could generate a clicking noise depending on its relationship with the articular condyle during movement. |
| Disc displacement with reduction | For various reasons, including trauma, the articular disc loses its shape. The morphology of the mandibular and temporal bones, along with the activity of the muscles and ligaments, is then unable to hold the disc in position. The disc then shifts from its ‘comfort zone’ and settles in a more anterior position, either laterally, medially or ventrally. Each time the mandibular condyle moves during opening and/or movement in the horizontal plane, the injury is reduced, producing an audible clicking noise. When the mandibular condyle returns, the disc dislocates or shifts from its current location and moves forward, producing a second clicking noise. Regarding the position of the mandibular condyle, the anterior joint space increases in cases of mild to moderate anterior disc displacement but not in more advanced cases. In very rare cases where the articular disc is displaced posteriorly, the posterior joint space increases (68). |
| Disc displacement without reduction with/without limited opening | As in the previous case, the disc shifts from its ‘comfort’ position, but this situation is not resolved by any mandibular movement. This can lead to altered mouth opening and presents as two conditions: disc displacement without reduction with limited mandibular opening and disc displacement without reduction with no limited mandibular opening. When opening is limited, the condyle involved in the injury will be unable to continue moving due to the blockage caused by the displaced disc. Therefore, mandibular opening will show an uncorrected deviation towards the side of the injury. This condition, where the disc blocks the condyle from moving so that a functional opening can occur, is also known as closure blockage. If the condition persists for various reasons and the system begins to adapt, the mandibular condyle will push the displaced disc forward and the range of mandibular opening will progressively increase, potentially reaching normal levels (i.e. disc displacement without reduction or restriction of opening). In this situation, joint blockage no longer occurs during opening. As expected, there are no joint sounds associated with the mechanics of movement in either situation. Literature on this topic has shown that condylar degeneration is often associated with this lesion, which is also linked to severe chronic pain and deformation of the articular disc (69). However, it is important to note that disc displacement without reduction or restriction of opening can also be identified through imaging. |
| Disc displacement with reduction with intermittent locking | This situation corresponds to an overlap of the previous two situations, typically occurring between a displaced disc with reduction and a displaced disc without reduction, resulting in restricted opening. In other words, there are times when the patient experiences no discomfort and only reports a clicking noise, and other times when they report a sensation of blockage when closing their mouth. This blockage may also be observed during clinical examination or imaging. |
| Disc disruption | Disc disruption refers to damage to the intervertebral discs, which can manifest as fissures or tears in the annulus fibrosus. At this stage, the disc does not appear to be herniated, but the patient may experience pain due to the release of inflammatory substances affecting the free ends of the area. Due to its morphological characteristics, this pathology is classified as a degenerative disease of the vertebral disc. The intervertebral disc is primarily composed of extracellular matrix components, such as collagen and proteoglycans. For various reasons, not all of which are understood, the disc undergoes structural and biochemical alterations resulting in functional impairment, degeneration and pain. Oxidative stress, immune system abnormalities, imbalances in mechanical loading, and metabolic alterations are currently believed to play a role in the initiation and progression of disc disruption. Oxidative stress occurs when there is an overproduction of reactive oxygen species and an inability to eliminate them, which alters redox homeostasis within the intervertebral disc. This imbalance in the redox system causes the degradation of the extracellular matrix, inducing cell apoptosis (70). |
| Disc perforation | A displaced articular disc is associated with altered joint biomechanics. This leads to increased compression and shear forces, predisposing specific regions of the disc, particularly the posterior region, to thinning and, ultimately, perforation (71,72). Once perforation has occurred, the disc loses its ability to effectively separate the articular surfaces. This leads to joint inflammation and bone degeneration, resulting in degenerative changes accompanied by symptoms such as crepitus. |
| Dislocation (luxation and subluxation) | Hypermobility disorders include dislocation, which can be divided into two types. The first type involves anterior and superior displacement of the condyle beyond the eminence, preventing the joint from returning to the closed position without a specific manoeuvre by the patient (subluxation). The second type requires professional assistance to return the joint to its normal state (luxation) (14). |
| Eagle syndrome | This corresponds to the mineralization of the stylohyoid ligament or the elongation of the styloid process, but with a variety of concurrent signs and symptoms due to different factors, such as irritation of the carotid artery, pain when rotating the head, dizziness, dysphagia, otalgia, headaches and vague pain (73,74). |
| Elevation of the hyoid | The hyoid bone reflects the tension in the muscles, ligaments and fascia to which it is attached. In a normal cervical lordosis, the hyoid bone is positioned below a control line drawn between the retrognathism and the anteroinferior border of C3. When the cervical spine is straightened, the hyoid bone tends to elevate until it reaches this line. When the spine is inverted, generating a cervical kyphosis, the hyoid bone elevates above the control line (75). During swallowing, elevation of the hyolaryngeal complex is essential to enable the tongue and associated structures to perform the necessary movements to transfer a bolus from the oral cavity through the hypopharynx to the esophagus. During this process, the suprahyoid and longitudinal pharyngeal muscles elevate the hyolaryngeal complex (76). However, when the hyoid bone and the tongue, which is supported by the hyoid bone, are both elevated, swallowing becomes difficult. |
| Ernest Syndrome | This corresponds to the mineralization of the stylohyoid ligament or the elongation of the stylomandibular process, but with a variety of concurrent signs and symptoms due to different factors. For the diagnosis of this syndrome, we can only refer to the clinical presentation: painful digital palpation, persistent pain, pain in the preauricular region and at the angle of the mandible, and limited range of motion are symptoms and signs frequently found in literature reviews (75,77). |
| Facet synovitis (cervical facet syndrome) | As with TMJ, synovitis is defined as an inflammatory process involving the synovial tissue of the intervertebral joints, characterised by arthralgia. Facet synovitis of the cervical vertebral joints can be caused by overload, wear and tear, or various injuries that alter joint function and craniocervical movement. Hyperaemia is observed, as well as an increase in fibroblast- and macrophage-type synoviocytes, and changes in cytokines. Therefore, synovitis progression could lead to osteocartilaginous damage. |
| Herniated disc | A herniated disc occurs when part of the nucleus pulposus of an intervertebral disc moves into the spinal canal, putting pressure on the spinal cord and nerve roots. Herniated discs are uncommon in the cervical spine, and patients may experience intense local radicular pain, as well as neurological changes in the affected areas of the skin (78). |
| Hyperlordosis/Kyphosis of the cervical spine | Poor craniocervical posture is one of the causes of pain and movement disorders in this area. In growing individuals, it can affect the normal development of bone structures (39). Loss of cervical stability is associated with altered cervical lordosis, altered muscle function and impaired movement. A high prevalence of disc degeneration has been observed in cases of loss of cervical lordosis, along with pronounced weakness in both the cervical flexors and extensors and an imbalance in the relative cross-sectional areas of the flexors and extensors, which has been attributed to extensor weakness (40). Furthermore, comorbidity between temporomandibular disorders and cervical spine abnormalities has been observed, and a similar connection has been suggested between the temporomandibular joint and the cervical spine (41–42) perhaps not as a pathological cause-and-effect relationship, but rather as a morphofunctional-postural one. However, both rectification and inversion of the cervical spine can occur independently of temporomandibular disorders (44), although due to neuroanatomical conditions (e.g. fascia, innervation and biomechanics), it is impossible to ignore the postural relationship between the two. |
| Hypertranslation | Joint hypermobility refers to excessive movement of a joint beyond its normal range. TMJ hypermobility, also known as TMJ hypertranslation, is characterised by joint movement beyond the normal range during condylar translation. Joint hypertranslation is one of the conditions classified under hypermobility. TMJ hypertranslation occurs when the disc and condyle protrude beyond the articular eminence, which can lead to sudden, irregular movement accompanied by a clicking sound. The condyles appear to protrude laterally. Additionally, at both the end of maximum opening and the beginning of mouth closure, one condyle may move before the other, causing a sudden lateral oscillation of the mandible before translation occurs (79,80). |
| Idiopathic condylolysis | Condylar resorption is a multifactorial condition that affects the mandibular condyle. It is characterized by changes in shape and a decrease in condylar mass. These changes can lead to malocclusion, temporomandibular joint (TMJ) dysfunction and pain (81). Progressive idiopathic condylar resorption, which has no obvious cause, has been identified as a clinical joint problem that is sometimes associated with orthognathic surgery (82). This aggressive form of the disease is most frequently observed in adolescents and young women, and is attributed to an exaggerated response to mild traumatic injuries induced by an excess of estrogen receptors. Although little is known about this condition, isolated cases have been reported and two forms of condylar resorption have been theorized: (1) in adults, the mandible regresses once growth is complete, and (2) in young people, the potential rate of mandibular growth decreases (83). |
| Inflammation of the temporomandibular ligament | Inflammation of the temporomandibular ligament is an inflammatory process affecting the connective tissue that stabilizes the temporomandibular joint (TMJ), leading to pain and restricted movement. This is often caused by trauma or overuse (84). |
| Inflammation of lateral colateral ligament | The lateral collateral ligament is one of the intracapsular ligaments that can be examined clinically. As with all ligaments, it can become inflamed if overstretched. This occurs in cases of disc displacement, particularly with a lateral component, as the displaced disc elongates the ligament, which is firmly attached to the lateral pole of the condyle. |
| Intervertebral fusion | It refers to a congenital condition that particularly affects the cervical region and is known as Klippel-Feil syndrome. During pregnancy, two or more vertebrae develop incompletely and fuse together, resulting in this condition. Symptoms include a short neck, impaired neck mobility and a low hairline (85). |
| Inversion of the cervical spine | Inversion of the cervical spine is a pathological change in the sagittal alignment of the cervical vertebral column, whereby the normal lordotic curve is reversed or substantially flattened, resulting in a kyphotic (forward-bending) or straightened configuration of the cervical spine. This abnormality in alignment can lead to altered biomechanical loading, potential compression of the spinal cord or nerve roots, pain, a reduced range of motion, and impaired horizontal gaze (86). |
| Joint neoplasia | A temporomandibular joint neoplasia refers to a benign or malignant tumor arising from the bone, cartilage, synovium or soft tissues within or around the joint. This can lead to pain, swelling and impaired function (87). |
| Mandibular fractures | The severity of mandibular fractures varies depending on the number of sites involved, displacement and comminution (88). Examples include condylar, coronoid, body (involving the ramus and angle of the mandible), alveolar process, symphysis, and parasymphysis fractures (89). |
| Mandibular instability | Mandibular function involves several passive structures, such as bones, and active structures, such as muscles. The masticatory process is complex and depends on multiple reflex arcs. Occlusion plays an important role in this process, maintaining harmonious and precise movement, or stable dynamics. Therefore, mandibular biomechanics is the study of biological forms from a functional perspective. As humans are biological units that function according to physiological laws, such as occlusion, and physical laws, such as levers, inclined planes and force transmission, we will also refer to biophysics. This concept encompasses two ideas: stability and equilibrium (90). Stability signifies security in space, both physically and biologically, but it is a static concept in that it refers to a specific time, place or position. Equilibrium, on the other hand, is the state of a system in which the acting forces neutralize each other in such a way that the conditions of rest or movement that characterize the system remain unchanged (91). Therefore, stability is the resistance a body offers to being overturned, whereas balance is a more dynamic concept relating to changes in movement. Combining the concepts of stability and balance provides a dynamic view of mandibular stability. Mandibular stability is defined as the ability of the mandible to maintain balance at all times — whether at rest or in motion — as a result of the interaction between the components of the stomatognathic system, provided there are no symptoms present. At rest, the mandible is in stable balance thanks to the myotatic or stretch reflex. When displaced or in eccentric positions, however, the balance is indifferent since, thanks to the neuromuscular mechanism and awareness, the mandible can remain in a new location for a time. According to the authors of this text, mandibular instability is defined as a state in which the mandible has lost its spatial centricity. This manifests as a discrepancy between its actual centricity and maximum intercuspation, caused by interfering occlusal contacts during mandibular closure. An opening with a slight tendency to deviate towards the lost midline is observed alongside a double closing arc. Additionally, neuromuscular system functionality is imbalanced, resulting in unstable positions and possible fatigue of the associated musculature. |
| Migraine | Migraine is a primary headache disorder and a highly prevalent neurological condition, particularly among women in their twenties and thirties. The main symptom is a moderate to severe headache, which occurs alongside other symptoms such as photophobia, phonophobia, allodynia, nausea, vertigo and dizziness (92,93). Overall, the symptomatology observed is quite heterogeneous and includes attack frequency, the presence of auras, comorbidities and treatment responses. This heterogeneity may have a genetic and molecular basis. Variants that primarily manifest in neurovascular activity and the activity of neuromodulators and neurotransmitters, such as serotonin, calcitonin gene-related peptide, amylin, pituitary adenylate cyclase-activating polypeptide and nitrous oxide, have been identified (94). |
| Muscle Atrophy | The loss of muscle mass is called muscle atrophy. It can be congenital or genetic, or it can be caused by an identifiable factor. Hence its categorization as primary or secondary. The mechanism involves an imbalance between protein synthesis and degradation, resulting in myofiber contraction, changes in fiber types or myosin isoforms, and net losses of cytoplasm, organelles and total protein. As a significant reduction in muscle mass, muscle atrophy can reduce patients’ quality of life and increase morbidity and mortality. It involves an imbalance in protein synthesis and degradation induced by various factors such as ageing, oxidative stress and inflammation. Signal transduction mechanisms include pathways that control protein degradation, such as the ubiquitin protein degradation system, autophagy, caspases and calpains, as well as pathways that control protein synthesis, such as the mammalian target of rapamycin (mTOR) pathway (96). Atrophy is similar to sarcopenia, but it can occur at any age for reasons other than ageing. At the oral level, sarcopenia indicates a decrease in masticatory muscle activity. Masticatory muscle atrophy can be caused by occlusal conditions, TMD, trauma, systemic diseases such as myasthenia gravis, rheumatoid arthritis and polymyositis, masticatory habits and trigeminal motor neuropathy (97,98). |
| Muscle hypertrophy | Masseter and temporalis hypertrophy is a benign condition with various potential causes, including bruxism, temporomandibular disorders and malocclusion. However, the cause is unclear in most cases, which is why it is often classified as idiopathic (99). Theories have been described in the literature, as well as progressive hypertrophy caused by anxiety in romantic relationships. It can be associated with facial pain and asymmetry. Unilateral or bilateral masticatory muscle hypertrophy is a benign condition that most commonly affects the masseter muscles and is rare in the temporalis muscles. Bruxism, temporomandibular disorders and malocclusion have been described as potential causes, but the cause is often unclear (100,101). The average masseter muscle depth has been observed to be 10.8 ± 1.6 mm in men and 8.1 ± 1.4 mm in women. Regarding the normal range of masseter muscle depth, it has been observed that it varies depending on sex-specific facial indices. Euryprosopic individuals have masseter muscle depths averaging 11.5 ± 2.08 mm for males and 8.8 ± 1.4 mm for females. Mesoprosopic individuals have depths of 11.4 ± 1.6 mm for males and 7.8 ± 1.6 mm for females. Leptoprosopic individuals have average depths of 10.08 ± 1.2 mm for males and 7.7 ± 1.4 mm for females (102,103). A diagnosis of masseteric hypertrophy could be considered in male individuals with a masseter muscle depth greater than 12.4 mm and in female individuals with a depth greater than 9.5 mm (26). Other studies have suggested that hypertrophy can be considered in muscles with a depth greater than 13.5 mm, regardless of sex or facial type (104). |
| Muscle neoplasia | Many organs in the body are susceptible to cancer. However, primary cancers rarely affect striated muscles, which include skeletal and cardiac muscles (105). Sarcomas can develop in muscle, fat, or connective tissue, accounting for around 1% of all malignant tumours in adults (106). Sarcomas in the masticatory muscles are particularly rare and may present with symptoms such as trismus, swelling and/or pain. |
| Myofascial pain | Myofascial pain is a multifactorial pathology involving the fascia, with comorbidities and a chronic component. It is therefore associated with nociplastic pain involving peripheral and central sensitization (107). Myofascial pain undoubtedly originates from continuous overload, which generates changes that induce responses in the nervous system. These changes cause the nervous system to ‘learn pain’ and produce sensitization. Therefore, patients with myofascial pain present with muscle pain. Due to the mechanisms underlying neuronal functional changes, the pain becomes more continuous and is expressed over a larger area than the site of the injury. This is why myofascial pain is evident when the patient performs functional and parafunctional movements, or when the physician stimulates sensitive areas. The resulting pain is usually radiated and may be due to palpation of a specific point, known as a trigger point. However, trigger points have primarily been associated with myofascial pain presenting with a referred pattern. |
| Myofasical pain with referral | The only difference between this situation and the previous one is that a trigger point has been clearly identified. When this trigger point is stimulated for 5 seconds with a load of 1 kg/cm2, it generates clear and often specific referred pain in another region. In the case of the masticatory muscles, referred pain is not uncommon. It can originate from the muscles in the teeth or cephalic regions, as well as from the cervical muscles in the head, face and/or fundus. Although common, referred pain derives from activity occurring in different spinal and brainstem structures (108). Most theories accept the phenomenon of convergence, whereby nociceptive afferents converge with other afferents in a second-order neuron. It is also thought that referred pain may be a form of central sensitization of the neurons in question. This involves both a synaptic relationship and a change in the environment of the segmental area. A classic example of this is the convergence of spinal nerves C1–C3, which generate impulses in the trigeminal nerves and produce secondary headaches. Another theory proposes the existence of afferent fibers that branch and distribute to regions of primary dysfunction and other referred areas. Primary lesions stimulate afferent fibers in deep regions, which then trigger the activation of a reflex arc towards the muscle via somatic efferent fibers. |
| Myofribrotic contracture | There is little clear information on this topic. Fibrotic contracture of skeletal muscle is defined as excessive shortening that causes stiffness and deformity. It has been linked to ischemic damage resulting from compartment syndrome. The pathogenesis of this syndrome includes necrosis, fibroblastic proliferation and the formation of a shrinking scar and myotendinous adhesion following prolonged ischemia. Other causes of fibrotic contracture, such as trauma or infection, have also been documented (79,110,111). |
| Myositis | Myositis is defined as painful inflammation of a muscle or muscle tissue resulting from a specific localized cause. It is typically linked to infection or trauma, and is characterized by swelling, restricted movement, redness, increased muscle temperature, and persistent, widespread pain in a specific area that worsens with movement. Ossification can occur as a result of inflammation, leading to myositis ossificans. Based on the definition of myositis as ‘inflammation of a muscle’, we cannot ignore painful muscle pathology caused by inflammation due to overload (microtrauma), even though it is not as extensive as the aforementioned situation. Before continuing with the analysis of each pathology, it should be noted that the term ‘local myalgia’ indicates local muscle pain, i.e. a symptom, and therefore should not be included as a diagnosis. According to the literature, myalgia has been defined as a disorder caused by an inflammatory process rather than a symptom synonymous with myositis. In this context, it has been proposed that to be diagnosed as ‘myalgia’, muscle pain must be affected by movement or function and must be recognized by the patient and confirmed by the physician (in the case of TMD, it must also be associated with mandibular dysfunction) (69). Muscle pain, or myalgia, is generally caused by an inflammatory process associated with overload. As this persists, the pathogenesis changes. Therefore, three pathologies indicating a cause-related diagnosis are classified under this mechanism: pain induced by extreme exercise, delayed-onset muscle soreness and pain associated with injuries. |
| Myospasm | Myospasm is a response of the central nervous system to injury. In the oral area, it results in motor disturbance of the trigeminal nerve, which is defined as trismus. Trismus is not a pathology, but rather limited jaw mobility due to various causes such as trauma, oral inflammation and infections, temporomandibular disorders, coronoid hyperplasia, neoplasia, surgery and autoimmune connective tissue disorders such as lupus erythematosus. It corresponds to electromyographic activity that is not under voluntary control. Trismus is defined as the inability to open the mouth widely. It can be caused by a central motor disturbance or other factors, including joint ankylosis, infection, trauma, toothache, TMD, tumors and drugs (114–118). In other words, trismus is a symptom, not a pathology, and for this reason it is not included among TMDs. |
| Myospasmodic stiffness or contracture | When analyzing this topic, it is important to clearly understand the difference between stiffness and contracture. As we have seen previously, the term ‘contracture’ refers to changes in muscle fibers, both dimensional and structural. However, ‘stiffness’ implies greater electrical activity in the muscles and, consequently, greater muscle contraction due to central activity. |
| Myostatic contracture | This contracture, such as myostatic contracture, can be caused by muscle disuse. It occurs in the rectus femoris muscles due to shortening caused by cranial extension. This situation is quite similar to an analgesic contracture, which is a compensatory phenomenon involving multiple reflexes. Disuse contractures of this type are not as severe as those seen in cerebral palsy. Cerebral palsy is an encephalopathy that causes myopathic contractures due to a lack of descending information, resulting in complete muscle inactivity. |
| Neoplasms in neural tissues | Neural tissue neoplasms are abnormal proliferations of cells originating from neurons or glial components of the peripheral or central nervous system. These neoplasms can be either benign, such as schwannomas, or malignant, such as neuroblastomas (119). |
| Neoplasms of the cervical spine | These are tumors that originate in the vertebrae, cartilage or soft tissues of the cervical spine. They can be benign or malignant and can potentially cause pain, neurological deficits and spinal instability (120). |
| Neuralgia (trigeminal and glossopharyngeal) | Trigeminal neuralgia is a painful condition characterized by chronic neuropathic pain, which causes sudden, recurrent and intense pain, usually on one side of the face. It affects one or more branches of the trigeminal nerve and patients often describe the sensation as similar to an electric shock (10,121). Glossopharyngeal neuralgia is a similar condition, but the pain is distributed along the auricular and pharyngeal branches of the glossopharyngeal and vagus nerves (122). |
| Neuropathy of dento-alveolar origin by deafferentation | This is a nerve condition that develops following the loss of sensory input from teeth or oral tissues. It is usually the result of tooth extractions, apicoectomies, pulp removal, periodontal surgery or injury to the inferior alveolar nerve. It presents as persistent pain or paresthesia in the affected area, and has similarities with other deafferentation pain syndromes (123). |
| Occlusal dysesthesia by deafferentation | Occlusal dysesthesia (OD), or phantom bite syndrome (124), refers to the persistent sensation of an uncomfortable bite without any obvious occlusal discrepancy. This rare condition is usually associated with emotional distress and is often triggered by dental treatment (125). OD can occur after any dental procedure, even in the absence of treatment. Therefore, rather than being an occlusal problem, it is considered to be a psychosomatic condition involving an alteration or maladjustment in signal processing (126). |
| Opening lock | Before analyzing this topic, we must remember that there is a condition called ‘blocking in closure’. This condition involves the articular disc, which prevents the articular condyle from moving and thus impairs mandibular opening. If a blockage is subclassified as ‘closing’, then by nomenclature there must be a pathological situation involving the opposite movement. The authors of this classification therefore propose the condition known as ‘blocking in opening’, which indicates a type of dislocation caused not by bone interference, but by disk interference. In other words, the mandible would be unable to close due to interference from an adherent disc. It is important to clarify this, since the diagnosis should guide the clinician towards treatment. In this case, despite being similar to blocking in opening, a dislocation requires diametrically opposite treatment. Oro-facial dyskinesia Unlike orofacial dystonia, dyskinesia involves the involuntary, repetitive and excessive movement of the jaw, tongue and lips. Rather than irregular tone, it reveals kinetic disturbances. It can be spontaneous or associated with certain medications, such as L-dopa and anticholinergics (127,128). |
| Oro-mandibular dystonia | Dystonia is a movement disorder involving muscle tone with no apparent cause. It is characterised by involuntary muscle contractions that cause abnormal movements and/or postures. It primarily affects individuals between 45 and 70 years of age and women more frequently than men. Oromandibular dystonia manifests in the jaw, face and tongue. Patients with oromandibular dystonia may present with symptoms associated with temporomandibular disorder (TMD)/functional disorder (FOD), such as pain in the masticatory or facial muscles, bruxism, and so on. It may also be associated with TMD, such as dislocations. The involuntary twisting of the lips and tongue has a constant movement pattern in the same direction and is generally exacerbated by voluntary movements (129). |
| Osteochondritis dissecans | This joint pathology is a type of injury in which a section of bone, along with its associated cartilage, separates from the joint surface. It primarily affects children and adolescents and is caused by a lack of blood supply. While imaging findings can vary widely, the most common include the presence of loose intra-articular calcified bodies (single or multiple), signs of degenerative bone changes, disc displacement, widening of the joint space, and alterations in condylar morphology (130). |
| Other intracapsular ligaments pain | The intracapsular ligaments of the TMJ, such as the collateral ligaments, stabilise the articular disc within the joint capsule. Pathology or inflammation of these ligaments may lead to internal derangement and pain (131). |
| Pain associated to lesions | Pain associated with lesions is either nociceptive or neuropathic, and originates from structural or inflammatory damage caused by factors such as trauma, infection, or neoplastic processes. This involves the activation of peripheral and central pathways that transmit pain signals from the injured tissue (132). |
| Pain induced by extreme exercise | It corresponds to short, intense activity that causes immediate fatigue and pain. The acute, transient and non-threatening local muscle pain caused by short, extreme, high-intensity activity differs significantly from other types of local muscle pain, such as delayed-onset muscle soreness, injury-related pain or chronic pain (133). This type of exercise-induced pain has the same mechanism as experimentally induced pain, for example when a patient is asked to clench their teeth at maximum force or to remain in a specific position that overloads a defined muscle group. This type of exercise-induced pain is caused by harmful chemical nociceptive stimuli. These are metabolites resulting from anaerobic energy, such as potassium and hydrogen ions, substance P, histamines, prostaglandins, serotonin, bradykinin and adenosine. These metabolites accumulate in the intramuscular space and stimulate the free nerve endings that supply unmyelinated type C afferent nerve fibers. The pain increases linearly with effort, remaining at an extreme intensity and requiring predominantly anaerobic metabolic input. Clinically, the pain originates in the active muscles involved in the exercise. It is acute, tonic and transient, occurring during exercise and being harmless. It is also a potential indicator of the metabolic and/or cardiorespiratory demands generated by exercise. When this activity is repeated, the experience of induced pain becomes associated with a change in motor behavior aimed at minimizing further tissue damage or injury as the body attempts to alleviate the load on sore tissue and reduce the perception of pain. This involves changes in behavioral coping strategies (e.g. exercise intensity) or other psychophysiological strategies. If exercise is continued without prior preparation and accompanied by a change in strategy, another type of situation begins to arise: exercise-induced injuries associated with delayed-onset muscle soreness. |
| Parasitic Myositis | This is a type of infectious myositis in which muscle inflammation is typically caused by trichinosis, cysticercosis or toxoplasmosis, although other parasites may also be involved (134). |
| Parotitis | Parotitis is defined as the acute or chronic inflammation of the parotid gland. Triggering factors include microbial agents (bacterial or viral), allergies, and autoimmune diseases such as Sjögren’s syndrome. Genetic/hereditary factors may also play a role (135,136). |
| Peripherally mediated neuropathy | Peripheral neuropathies are diseases of the peripheral nervous system. They can be categorised as mononeuropathies, multifocal neuropathies or polyneuropathies. Symptoms often include numbness and paresthesia (137). Chronic polyneuropathy has an estimated worldwide prevalence of 1%, which increases with age. Mononeuropathy affects a specific area; carpal tunnel syndrome is an example of this. There are also immune neuropathies, such as Guillain-Barré syndrome, which are less common (139–141). |
| Post-herpetic neuralgia | Postherpetic neuralgia is the most common and severe chronic complication of the herpes zoster virus. It is characterized by a burning, electric-like pain or a sensation of tearing that persists for more than three months after the lesion has healed (141). There is an association between age and immune dysfunction (IL-10), which increases the risk of developing the disease. This suggests that an imbalance in the immune system plays a key role in its development. T-cell dysfunction and inflammatory imbalance, in particular, can lead to delayed viral clearance and persistent nerve damage (142,143). |
| Protective co-contraction | Protective co-contraction involves the co-activation of muscles to prevent potential muscle damage, rather than producing or regulating coordinated movements as co-contraction does. Protective co-contraction demonstrates a limitation of mandibular kinematics in the frontal plane (145). Conversely, an occlusal condition that generates instability, or acute changes to the occlusal condition, can affect muscle function via a central stimulus-dependent mechanism. These situations can generate a neuromuscular response called protective co-contraction, which causes muscle pain and is frequently associated with the development of new muscle engrams. The patient adapts to these engrams with little effect; one consequence is difficulty moving the mandible during manipulation (146). It should be noted that skeletal muscle contractures represent the permanent shortening of a muscle-tendon unit, which occurs when the soft tissue loses elasticity and is unable to stretch either passively or under the influence of antagonist muscles. Contractures are probably the most clinically significant consequence of altered passive mechanical properties of muscle. Contractures can be caused by an upper motor neuron injury, such as a stroke, head injury or cerebral palsy, or by a muscle disease such as spinal muscular atrophy or muscular dystrophy, as well as by other neuromuscular disorders and analgesic reflex responses (147,148). Furthermore, active cellular contractility can increase the stiffness of fascial tissues, thereby contributing to musculoskeletal dynamics. Various studies indicate that the presence of myofibroblasts within fascia may enable these tissues to alter their stiffness. This contractile tissue behaviour has been observed not only in various pathological fibrotic contractures, but also in normal fascia. In our field, we have observed muscle shortening or contractures associated with muscle disuse, infection or central responses. |
| Retrodiscitis | Retrodiscitis is an inflammatory joint condition that occurs in the posterior region of the disc. It includes the area from the posterior edge of the disc and extends to encompass the entire posterior synovium. It can therefore be caused by macro-trauma producing acute overload in the posterior synovial area (149), such as the trauma generated by the condyle on the posterior edge of the disc when displaced (150). As this area is so extensive, the authors of this text prefer to use the term ‘posterior synovitis’ when an overload of the posterior synovium is generated by a macro- or microtraumatic event, and ‘retrodiscitis’ when inflammation of the specific area of the retrodisc is caused by micro-trauma generated by the condyle on the posterior edge of the articular disc when it is displaced. |
| Sarcopenia | Sarcopenia is a disease characterised by muscle weakness and loss of muscle mass that accumulates throughout life. It is common among older adults, but can also occur at a younger age (151). With regard to the masticatory muscles, there is some suggestion that tooth loss is associated with an increased risk, but the data concerning oral muscles and indices of oral hypofunction are inconclusive (152). Furthermore, low muscle mass has been shown to increase the risk of sarcopenia, perhaps also being associated with the loss of molar support, especially in men. Body mass index and age may also influence the mass of skeletal muscles distant from the axial skeleton. Notably, insulin-like growth factor 1 (IGF-1) levels are positively associated with masseter muscle volume, and the alpha-actinin-3 (ACTN3) genotype has been associated with its reduction only in men (153). Similar trends are indicated for oral function and skeletal muscle in cases of sarcopenia, which may show low oral function (154). |
| Sialadenitis | Sialadenitis is the term used to describe inflammation or infection of the salivary glands. This condition can be caused by various processes, including infectious, obstructive and autoimmune ones (155). |
| Spondylolisthesis | This injury involves one vertebra being displaced ventrally over another, which can result in pain and impaired mobility. At the cervical level, it can result in neck pain and stiffness, as well as heterotopic pain in areas corresponding to the affected dermatomes. Maintaining an upright posture and balance requires proper spinal alignment, which refers to the arrangement of the vertebrae and the curvature of the spine (156). When cervical spondylolisthesis occurs, it is generally associated with mild degenerative changes due to the interaction of anatomical structures, biomechanical effects and neurosensory factors, particularly when treating elderly patients who require balance and stable posture (157). |
| Spondylosis | Spondylosis is a degenerative condition affecting the bones and intervertebral discs of the spine. When it occurs at the suprascapular level, it is known as cervical spondylosis. There are different pathophysiological mechanisms. As well as stress and overload, which are associated with ageing, there are a number of related factors. These include an imbalance in the nervous, immune and endocrine systems, which generate various biological signals that act on different receptors in the cervical region (158). Biomechanical alterations affect the vertebral artery and the surrounding muscles and connective tissues, generating inflammatory cascades associated with cervical spondylosis. These cascades promote the release of various hormones that affect the central nervous system through the neuroendocrine-immune system, inducing or exacerbating negative emotional feedback and establishing a vicious ‘central-local-central’ cycle. One of the most common symptoms of cervical spondylosis is cervical pain, which originates in the facet joints, intervertebral discs and cervical muscles. It is also one of the most important factors affecting patients’ quality of life. Magnetic resonance imaging offers good resolution of the spinal cord, intervertebral discs, muscles and other soft tissues for diagnostic imaging. Computed tomography, on the other hand, provides excellent contrast for evaluating bony structures such as the vertebrae. In both cases, sagittal views clearly demonstrate the intervertebral discs and cervical sagittal balance, while axial views provide an accurate assessment of nerve root compression and muscle fatty infiltration (159). |
| Sticky or static disc | The ‘sticky or static disc’ phenomenon refers to the limited mobility of the articular disc in the TMJ due to adhesions or loss of lubrication. This can result in disc anchorage, clicking, locking, or restricted movement (61). |
| SUNA Unilateral neuralgiform headache with autonomic symptoms | SUNA syndrome (unilateral neuralgiform headache of short duration with cranial autonomic symptoms) is on the same spectrum as SUNCT. It is characterised by brief, repeated attacks of unilateral pain accompanied by one or more cranial autonomic symptoms, but not conjunctival redness and tearing (160). |
| SUNCT Unilateral neuralgiform headache with watering and redness | SUNCT syndrome (short-term unilateral neuralgiform headache with autonomic symptoms) is a rare type of autonomic trigeminal headache. It is characterised by brief, recurrent and intense attacks of unilateral pain in the orbital or temporal region. These attacks are necessarily accompanied by ipsilateral conjunctival injection and tearing (160). |
| Synovial chondromatosis | It is also known as synovial osteochondromatosis or synovial chondrometaplasia. It is a joint disorder in which nodules of cartilage form and detach from the synovial membrane of the joints. These nodules then remain floating within the capsular space. This can lead to oedema, pain and disorders affecting joint movement. This benign, locally aggressive tumour rarely affects the TMJ (161). Differential diagnoses for this condition include pigmented villonodular synovitis, tenosynovial giant cell tumour and chondrosarcoma. Synovial chondromatosis frequently occurs in large joints, such as the knee, hip and temporomandibular joint. It is most commonly diagnosed in the fifth decade of life. However, the disorder can also occur in children (162). |
| Synovitis | Synovitis is defined as an inflammatory process or arthritis involving the synovial tissue and characterized by arthralgia. Synovitis is an initial process that alters joint function and mandibular movement. Hyperemia, an increase in fibroblast- and macrophage-type synoviocytes, and changes in cytokines are observed. Therefore, the progression of synovitis could lead to osteocartilaginous damage. It is also known that persistent inflammation in the TMJ causes neoangiogenesis, which could affect the soft tissues of the capsule, including the retrodiscal tissue and the articular disc, as well as the glenoid fossa and the mandibular condyle (163). |
| Temporal tendinitis | Temporal tendinitis is an inflammatory and degenerative disorder affecting the fibrous insertion of the temporalis muscle tendons into the coronoid process of the mandible (164). |
| Tension-type headache | Tension-type headache is the most common primary headache disorder, affecting around 2.1 billion people worldwide. It has a multifactorial pathophysiology. Consistent findings from neuroimaging and neurophysiological studies point to alterations in brain regions involved in pain modulation, particularly the anterior cingulate cortex and insula. Peripheral factors, such as myofascial pain and muscle tenderness, are believed to play a role in the onset and persistence of symptoms. Central sensitisation and impaired descending pain inhibition are also believed to play a central role. In turn, sensitisation may be confined to the brainstem rather than involving cortical structures. Calcitonin gene-related peptide and vascular mechanisms appear to be involved to a limited extent, except in subgroups of mixed headaches (165). |
| Trigeminal autonomic headaches | This type of headache belongs to a group of primary headaches characterised by short-term, intense, unilateral pain in the dermatomes associated with the trigeminal nerve. These headaches are accompanied by parasympathetic autonomic symptoms, including conjunctival injection and/or tearing, nasal congestion and/or rhinorrhoea, oedema of the eyelids, sweating of the forehead and face, miosis and/or ptosis, and restlessness or agitation. Examples include cluster headaches, paroxysmal hemicrania, short-term unilateral neuralgiform headache attacks, hemicrania continua and probable trigeminal autonomic headaches (118,119). |
| Vertebral agenesis | It is a congenital condition in which one or more vertebrae fail to form properly. It is rare in the cervical spine, but more commonly observed in the sacral region. It may be associated with syndromes involving cardiorespiratory problems and premature death, but little information is available on this subject (166). |
| Vertebral aplasia and hypoplasia | Underdevelopment of the vertebral column manifests as hypoplasia or aplasia of the vertebral centrum specifically, without any corresponding alterations to the dorsal vertebral arch, as this occurs in the final stage of gestation. Images reveal a partial or complete absence of the vertebral centrum, with intact pedicles and a posterior body extending up to the neurocentral synchondrosis. This spectrum also includes dorsal hemivertebrae with an isolated absence or wedging of the ventral portion of the centrum (167). |
| Vertebral fractures | Vertebral fractures are caused by axial loads, either with or without a rotational or dislocation component. These loads may be abnormal, such as those generated by trauma, or normal loads acting on weakened bone (for example, due to osteoporosis or neoplasia) (168). According to the AO Foundation classification (169), trauma is subdivided into four regions. One region is the upper cervical spine, which extends from the occipital condyle to the axis. The other corresponds to the subaxial cervical spine between C3 and C7. Each region has a subclassification. Fractures of the upper cervical spine can involve the occipital condyle, the atlas ring or the axis. The severity of each fracture varies, ranging from an isolated injury without displacement or ligament injury without displacement to instability and/or translation of the fractured body. At the subaxial level, fractures can be compression fractures of the processes or body ranging from minor to burst fractures, or involve injuries to the tendon band that are unilateral or bilateral, vertebral body displacement, or facet injuries that are either without displacement or lead to pathological subluxation. |
| Vertebral hyperplasia | Vertebral hyperplasia primarily affects adults and older adults. It is increasingly associated with prolonged sitting, which can lead to inactivity and poor posture (170–172). There have also been reports of cases of partial congenital hyperplasia of some vertebral bone structures (173,174). |
| Vertebral neoplasm | Osteosarcoma is a rare malignant tumour that can affect the vertebrae, including those in the neck. Vertebrae can be affected by neoplastic tumours that, when confined to the spongy nucleus, do not cause spinal instability. However, if they extend to the cortex, pathological compression fractures can occur (175). |
| Viral myositis | Viral myositis is a rare and acute disease of the skeletal muscles. It is characterised by inflammation, pain and muscle weakness that occur during or after a viral infection. It is most commonly caused by influenza A and B viruses (176). |
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