Oral manifestations of Parry-Romberg syndrome: A review of literature

Abstract

Parry–Romberg syndrome (PRS) or progressive facial hemiatrophy is a developmental craniofacial disorder of unknown etiology characterized by a slowly progressive unilateral facial atrophy. It is associated with different systemic manifestations particularly, maxillofacial, neurologic and ophthalmologic abnormalities. Dentists must be aware of PRS to identify this invalidating disorder. In this article, we review the etiology, clinical features (especially craniofacial and dental manifestations) and treatment of PRS. We searched in PubMed line using specific words such as PRS from 2008 to 2014 (August). We identify 14 papers have described oral manifestations of this syndrome. We excluded all the article papers that did not indicate to oral manifestations of PRS.

Bone Resorption of the Jaws and Occlusal Disturbances in Parry-Romberg Syndrome

“…Parry-Romberg Syndrome is a rare disease that encompasses aesthetics and functionality of the involved tissues. Considered differential diagnosis for Parry-Romberg Syndrome are Rasmussen Syndrome, circumscribed scleroderma and hemifacial dystrophy [6], [7]. It is a self-limiting condition and there is no developed cure for such disease [8].…”

“…Partial anodontia, delayed eruption and morphological root disturbances including root resorption are the most common teeth conditions found in this syndrome. There is no genetic component able to explain this disease [5], [6].…”

Treatment of hemifacial spasm in patient with hemifacial atrophy using combination therapy (ultrasound therapy and TENS): a case report

“…The incidence of HFA is higher in women. The left side is commonly affected [ 5 ]. Disturbance in fat metabolism, endocrine disturbances, autoimmunity, heredity, and local facial trauma are believed to be associated with its pathogenesis.…”

“…Disturbance in fat metabolism, endocrine disturbances, autoimmunity, heredity, and local facial trauma are believed to be associated with its pathogenesis. Some inherent relationship between HFA and the disorder of malformation or disturbed migration of neural crest cells might also be associated [ 5 ]. This syndrome mostly onsets in the first and second decades of life, with the atrophy progressing gradually and then stabilizing on its own [ 2 ].…”

“…This syndrome mostly onsets in the first and second decades of life, with the atrophy progressing gradually and then stabilizing on its own [ 2 ]. The salient features of HFA have been described by Wartenbergand Nader [ 2 5 ]. HFA may overlap with various clinical entities like atrophy of the tongue, hemi-facial/hemi-masticatory spasm (HMS), linear scleroderma, vitiligo, and hyperpigmentation [ 6 ].…”