PDF: Condylar hyperactivity: diagnosis and treatment - case reports

Skeletal asymmetries of the mandible caused by condylar hyperactivity can pose serious functional, esthetic and psychosocial problems for patients.

Although their etiology is still unknown, some authors believe they can be caused by trauma, inflammation, hypervascularity, genetic factors and hormonal disorder.

Several classifications are available. Some are etiology-related while others divide these anomalies according to the growth factors involved in its development. 

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Asymmetries can therefore be acquired or developmental, and since each situation presents with different features a differential diagnosis can be more easily established. Acquired asymmetries involve pain, symptom changes, alterations in facial appearance and function with time. The volume of facial muscles remains unchanged.

Other features include TMJ crepitation (crackling/popping sounds), limited mandibular movements (rotation, protrusion and mouth opening), severe crossbite and irregular condyle anatomy.

Developmental changes do not involve pain, symptoms usually remain unchanged over time, changes may occur in the size or function of the facial muscles, no functional changes take place in the TMJ, there may be limited protrusion without limiting mandibular rotation movements, a pronounced dental compensation in the asymmetric mandible may be present and the condyle remains pronounced and smooth, even in the presence of volumetric changes.

According to Obwegeser and Makek, hyperactivity can be classified into three different types: hemimandibular hyperplasia (HH), hemimandibular elongation (HE) and a hybrid form. Many authors use the term condylar hyperplasia to refer to these three forms, but this is not appropriate, since it is only in HH and hybrid cases that a true condylar hyperplasia is found.