Background: Pediatric temporomandibular joint (TMJ) dysfunction, resulting from either soft tissue or skeletal disorders, may be congenital, developmental, or post-traumatic in origin. Congenital TMJ dysfunction is the least common. Here, we review our experience with pediatric TMJ dysfunction and develop a new classification system.

Method: Records of all patients with trismus or restricted mandibular excursion treated at the Institute of Reconstructive Plastic Surgery between 1976 and 2006 were reviewed. Clinical records, cephalograms, computed tomography, magnetic resonance images, and pathologic specimens were reviewed. All cases were stratified according to soft tissue and/or skeletal pathology. Skeletal abnormalities were further characterized as intra-, peri-, or extra-capsular.

Results: Thirty-three patients (ranging in age from 2 days of life to 19 years at diagnosis; mean age 5.4 years) were identified with TMJ dysfunction. Nine cases (27%) were due exclusively to soft tissue pathology, including post-irradiation scarring, fibrosis, infection, and tumor. The remaining 24 cases (73%) were skeletal in origin and were evenly divided between acquired and congenital cases. Acquired skeletal deformities included 11 (91.7%) intracapsular ankyloses and 1 (8.3%) extracapsular ankylosis (coronoid process to zygoma); etiology included infection, trauma/surgery, and degenerative rheumatic disorders. In contrast, congenital skeletal deformities accounted for 2 intracapsular ankyloses (16.7%) and 10 (83.3%) extracapsular ankyloses or mechanically restrictive skeletal disorders (e.g., coronoid hypertrophy without ankylosis).

Conclusion: The data appear, at first, consistent with previously published population studies that principally attribute TMJ dysfunction to acquired pathology, specifically trauma (or surgery) and infection. However, in contradistinction to prior published reports, we observed a significantly higher percentage of congenital cases of TMJ skeletal disorders. Classification based upon joint involvement revealed that most of these cases involved extracapsular pathology, such as coronoid hypertrophy or zygomatic hypoplasia. Only a minority of congenital cases were intracapsular ankyloses characterized by gleno‑condylar fibro-osseous fusion. Because precise diagnosis and classification directs the choice of therapy, we provide a new classification scheme to differentiate between soft tissue and skeletal pathologies and to better characterize the extent of capsular involvement. Protocol-based preoperative CT is recommended to aid in classification and the selection of treatment modalities, which are discussed critically.