Etiology of Class II malocclusions.

In reviewing the literature relative to the development of Class II malocclusions, it can be learned that "not every Class II is a Class II." We must remember that behind the soft tissue drape of the patient’s face is a totally dynamic process that can be influenced by our heritage and altered by our environment. We realize when performing an occlusal evaluation of our young patients, findings like distal step molar relation or an unusually large overjet may be presenting a false impression of what appears to be a true skeletal Class II malocclusion. In addition to distal step molar relation, or an unusually large overjet, tooth size discrepancy with or without malrelated mandible and maxilla may also give the first impression of a true skeletal Class II malocclusion. Skeletal Class II malocclusions can be found to have variants in one or more of the following regions: (1) maxillo-mandibular relationship (mandibular retrognathism, midface protrusion or both); (2) the cranial base (increased length of the anterior cranial base will contribute to the midface protrusion, while lengthening of the posterior cranial base will tend to position the temporomandibular articulation more retrusively); (3) vertical dysplasia (anterior upper face height often greater than normal); (4) steep occlusal plane (a reflection of vertical skeletal dysplasia). What role does genetics play in the etiology of Class II malocclusions? According to the study by Lundstrom (1984), investigations published prior to that article have suggested that about 40% of common anomalies in tooth position and in the relationship between maxillary and mandibular dental arches are due to genetic differences between individuals. Corruccini and Potter (1980), in studies of different dental and occlusal variables, found the heritability of dental overjet was reduced to zero. Several syndromes have Class II malocclusions as a major finding. Of these syndromes, Treacher Collins, hemifacial microsomia, achondroplasia, and mobius syndrome are a few of the more widely known. Inter-arch problems such as Class II and Class III malocclusions are genetic in nature, while intra-arch problems also have an environmental component as well. Looking at the importance of environmental vs. inherited factors in the etiology of malocclusions, it was suggested that urbanization (and evolution) influence malocclusions, making them more severe. The evolutionary factors involved are: a decrease in the size of the jaws, size and number of the teeth. We have no control over these evolutionary factors (as well as the hereditary factors), whereas the environmental factors can often be eliminated through preventive or interceptive treatment at the appropriate time. Mandibular growth deficit following condylar fractures or major trauma to the joint complex is highly likely. Proffit (1980) found between 5 and 10% of all severe mandibular deficiency or asymmetry problems were related to previous fracture of the mandibular condylar process. In this article, Proffit cites Walker and also Gilhuus-Moe as noting that the younger the patient at the time of the injury, the greater the potential for complete regeneration of the condyle, and healing without residual deficit. Proffit (1978) states that Lund found essentially complete recovery in 75% of the children with early condylar fractures. The treatment goals for patients with condylar fractures include the restoration of joint function, occlusion, and facial symmetry. The current theory on early treatment of condylar fracture in the growing child calls for firm fixation for only I week, with physical therapy and mouth opening exercises beginning immediately after release of the rigid fixation. Condylar fractures often go unnoticed and result in Class II malocclusions with asymmetry or severe mandibular deficiency. Progressive deformity is associated with mechanical limitations on growth and the resulting condition is referred to as "functional