Relationship between Cervical Spine and Skeletal Class II in Subjects with and without Temporomandibular Disorders

Aim. To assess changes in the craniocervical structure and in hyoid bone position in skeletal Class II subjects with and without temporomandibular disorders (TMD). Materials and Methods. The cephalometric analysis of 59 subjects with skeletal Class II was evaluated and compared. The measurements considered were ANB as a parameter of Class II and C0-C1 distance, C1-C2 distance, craniocervical angle, and hyoid bone position for the cervical spine analysis. Patients were divided into patients with TMD (group A) and patients without TMD (group B). TMD were evaluated with Diagnostic Criteria for TMD (DC/TMD). Descriptive statistics and Pearson’s and Spearman’s correlation analysis, with p value <0,005, were performed. Results. C0-C1 and C1-C2 distance values and hyoid bone position resulted within the normal range in the majority of patients examined. Craniocervical angle was altered in 33 patients. The reduction of this angle with the increase of the ANB value resulted to be statistically significant in group A, according to Pearson’s correlation index. No other data were statistically significant. Conclusions. The significant relationship between skeletal Class II and cervical spine cannot be highlighted. The alteration of craniocervical angle seems to be mildly present, with backward counterclockwise rotation of the head upon the neck in the sample (groups A and B). The presence of TMD as a key factor of changes in neck posture could explain the different result between the two groups about the relationship between ANB and craniocervical angle. This result should be further analyzed in order to better understand if cervical spine changes could be related to mandibular postural ones in the craniocervical space or to temporomandibular joint retropositioning, more recognizable in Class II with TMD, which could determine functional changes in other structures of this unit; neck posture could be the result of a compensatory/antalgic mechanism in response to TMD.