Electronic Letters to:

Endocrine Care: Allan D. Padbury, Jr., Tolga F. Tözüm, Mario Taba, Jr., Erin L. Ealba, Brady T. West, Richard E. Burney, Paul G. Gauger, William V. Giannobile, and Laurie K. McCauley The Impact of Primary Hyperparathyroidism on the Oral Cavity J Clin Endocrinol Metab 2006; 91: 3439-3445 [Abstract] [Full text] [PDF]

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Primary hyperparathyroidism and mandible

Akira Taguchi   (20 September 2006)

Primary hyperparathyroidism and mandible 20 September 2006
Akira Taguchi, Assistant Professor Department of Oral and Maxillofacial Radiology, Hiroshima University Hospital Send letter to journal: Re: Primary hyperparathyroidism and mandible akiro{at}hiroshima-u.ac.jp Akira Taguchi	I was interested in the recent article by Padbury et al. (1) describing two new oral cavity findings in patients with primary hyperparathyroidism (HPT): an increased incidence of oral tori (a mandibular torus) and an association between periodontal ligament space and PTH level. White and Pharoah have already summarized the decreased density of alveolar bone and the thinning of the cortex in patients with hyperparathyroidism in the textbook (2); however, no information about an increased prevalence of a mandibular torus and the positive periodontal ligament space- PTH level association have been described. I have several concerns and questions for the authors. First, the authors hypothesized that cortical bone loss and trabecular expansion resulted in an increased incidence of a mandibular torus. Usually, a mandibular torus appears as a radiopaque, homogeneous, knobby protuberance from the lingual surface of the mandible. If the hypothesis of the authors is true, can patients with HPT be distinguished from others by the internal structure of a mandibular torus on cross-sectional occlusal radiography, conventional tomography or computed tomography? The inner structure of a mandibular torus in patients with HPT should mainly consist of a trabeculation, whereas those without HPT should represent cortex. Second, the general changes in osseous structure in HPT patients (Figure 5) are characterized by surrounding cortices appearing to become thinner. However, the authors only found a significant difference in cortical thickness at gonial angle (gonial index: GI) between subjects with and without HPT, but not in cortical thickness below the mental foramen (mental index: MI) and antegonial cortical thickness (antegonial index: AI). Since major muscles (masetter and internal pterygoid muscles) attach at the gonial angle, it seems to me that bite force may retain the cortex in the gonial angle than in antegonial part and below the mental foramen. Consequently, can the authors clarify why only the cortex of gonial angle was influenced by HPT. Furthermore, an instable horizontal magnification of dental panoramic radiographs may largely influence GI measurement. How did the authors correct for this influence? Third, although the authors measured the periodontal ligament space in this study, it is very difficult to measure it accurately because this space is considerably narrowed. Further, the projection angle of x-ray in the radiographs may influence the ligament space, especially in patients with a mandibular torus. It would be informative for readers if the authors can report the periodontal ligament space of control subjects. References 1. Padbury AD Jr, Tozum TF, Taba M Jr, Ealba EL, West BT, Burney RE, Gauger PG, Giannobile WV, McCauley LK. 2006. The impact of primary hyperparathyroidism on the oral cavity. J Clin Endocrinol Metab 91:3439-3445 2. White SC, Pharoah MJ. 2000. Systemic diseases manifested in the jaws. In White SC, Pharoah MJ, eds. Oral Radiology- Principles and Interpretation. 4th ed. St. Louis: Mosby; 472-449