Burning mouth syndrome (BMS) is a distinct clinical entity characterized by a chief complaint of unremitting oral burning concomitant with no oral mucosal clinically observable lesions. Numerous causes of this condition have been suggested, including local factors, systemic factors, and psychogenic disorders. A total of 36 consecutive subjects, 32 women and 4 men, complaining of BMS, who had attended the Dental Clinic of the University of Ferrara during a period of 2 years, was studied. The method of assessment followed closely a strictly co-ordinated management protocol based on conventional guidelines, namely history, clinical examination and special investigations. A detailed history was taken of duration of the condition, site affected, and pattern of burning. The severity and the response to treatment were assessed with a Visual Linear Analogue Scale (VLAS). A full medical history was taken, with regard to xerostomia-inducing drug assumption. The presence and the severity of menopausal symptoms were explored. Inquiries were made on use of mouthwashes. For the denture-wearers, specific questioning was directed to the length of denture-wearing experience, temporal association of the symptom with the wearing of dentures, relationship to burning sensation of any relines or repairs, denture cleaning technique, and use of fixatives. A complete routine intraoral and extraoral examination was performed. The presence of parafunctional habits, such as tongue thrusting, clenching, grinding, lip and cheek biting, was investigated. If dentures were worn, their design and condition were examined. In particular, the relation between the vertical and horizontal components of the jaw and the denture base extension was assessed and the freeway space measured.(ABSTRACT TRUNCATED AT 250 WORDS)

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[Fibrous dysplasia. The clinico-therapeutic picture and new data on its etiology. A review of the literature].

In this paper the authors examine current findings on the etiology of fibrous dysplasia. Particular emphasized is the role of the biochemical pathways and the genetic mutations occurring in the disease. In fact it is demonstrated that the McCune-Albright syndrome, a variant of fibrous dysplasia, is caused by the mutations of the GNAS 1 gene that codify for the alfa-subunit of the stimulatory guanine-nucleotide binding protein (G-protein). This mutation activates adenylate cyclase and consequently increases intracellular concentrations of cAMP. The increased signaling through the cAMP is believed to be responsible for the clinical characteristic of the McCune-Albright syndrome. The cap is translocated to the nucleus where a family of transcription factors is phosphorylated. This group of factors regulates the expression of CAp responsive genes: one of them, the c-fos proto-oncogene, produces a nuclear protein that binds with other proteins encoded by c-jun proto-oncogene, to form a transcription factor, AP-1. Several studies have shown an increase of c-fos mRNA in the bone lesions of patients with fibrous dysplasia. It suggests that the overexpression of c-fos may represent the first step in the carcinogenesis of bone sarcomas. Finally, attention is focused on the intravenous use of pamidronate as medical management in the treatment of the lesions that are not susceptible to surgical treatment.

Facial Bones↗

PubMedDate not supplied

[Disinfection and sterilization of the dental outpatient office: a verification of efficacy].

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