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The article presents information on the microdontic pin system (MPS) in dentistry, which is a specially designed pin and applicator system for dental restorations. It is stated that the MPS system is designed in such a way that it prevents trauma to the dentin and reduces the risk of crazing and cracking of dentin and enamel. The MPS pin is made of bioinert titanium. It is stated that the use of a noncorrosive material such as titanium prevents the corrosion and discoloration of the retentive pin.

Fibrous dysplasia (FD) is a non-malignant condition caused by post-zygotic, activating mutations of the GNAS gene that results in inhibition of the differentiation and proliferation of bone-forming stromal cells and leads to the replacement of normal bone and marrow by fibrous tissue and woven bone. The phenotype is variable and may be isolated to a single skeletal site or multiple sites and sometimes is associated with extraskeletal manifestations in the skin and/or endocrine organs (McCune-Albright syndrome). The clinical behavior and progression of FD may also vary, thereby making the management of this condition difficult with few established clinical guidelines. This paper provides a clinically-focused comprehensive description of craniofacial FD, its natural progression, the components of the diagnostic evaluation and the multi-disciplinary management, and considerations for future research. [ABSTRACT FROM AUTHOR]

The human nicotinic acetylcholine receptor (nAChR) subunit α9 gene (CHRNA9) codes for a component of the AChR in hair cells of the inner ear. While no direct evidence presently links this gene to known hearing disorders, it may underlie individual susceptibility to acoustic inner ear injury, and is associated with the autoimmune skin disorder Pemphigus vulgaris. Future studies will depend upon a thorough characterization of the nAChR α9 gene. CHRNA9 was localized to chromosome 4p15.1→p14 by FISH analysis. Radiation hybrid mapping further localized the gene between markers D4S405 and D4S496 (Stanford G3 panel), and between markers WI-3875 and D4S1231 (Genebridge 4 panel), representing a distance of approximately 3.1 cR. The D4S405 marker has been linked to a non-syndromic form of hereditary hearing loss, DFNB-25. The gene contains five exons, separated by four introns. Exons 1–5 are 78, 145, 154, 532 and 877 bases, respectively. Introns 1–4 are 294, 1239, 11517, and 4571 bases, respectively. The intron-exon splice junction sites correlate identically with those of the rat α9 gene and are nearly identical to those of the human α10 gene. Sequence promoter analysis reveals a number of potential regulatory elements, including several in common with the nAChR α10 gene, whose expressed protein is assumed to combine with α9 in the inner ear. Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]