Critical Reviews in Oral Biology & Medicine

The Official Publication of the American Association of Oral Biologists

A Publication of the International/American Associations for Dental Research
Table of Contents for Volume 6, 1995

Volume 6, Issue 1
Volume 6, Issue 2
Volume 6, Issue 3
Volume 6, Issue 4

Volume 6, Issue 1

• Enwonwu CO; Meeks VI
• Department of Biochemistry, College of Dental Surgery, University of Maryland, Baltimore 21201, USA.
• Pages 5-17.

Tobacco (smoking and smokeless) use and excessive consumption of alcohol are considered the main risk factors for oral cancer (ICD9 140-149). Conspicuous national and international variations in oral cancer incidence and mortality rates, as well as observations in migrant populations, raise the possibility that diet and nutritional status could be an important etiologic factor in oral carcinogenesis. As shown in this report, abuse of alcohol and tobacco has serious nutritional implications for the host, and generates increased production of reactive free radicals as well as eliciting immunosuppression. Maintenance of optimal competence of the immune system is critical for cancer surveillance. Active oxygen species and other reactive free radicals mediate phenotypic and genotypic alterations that lead from mutation to neoplasia. Consequently, the most widely used chemopreventive agents against oral cancer (e.g., vitamins A, E, C, and beta-carotene) are anti-oxidants/free radical scavengers. These anti-oxidants, both natural and synthetic, neutralize metabolic products (including reactive oxygen species), interfere with activation of procarcinogens, prevent binding of carcinogens to DNA, inhibit chromosome aberrations, restrain replication of the transformed cell, suppress actions of cancer promoters, and may even induce regression of precancerous oral lesions such as leukoplakia and erythroplakia. Malnutrition is characterized by marked tissue depletion of anti-oxidant nutrients, including GSH (gamma-glutamyl-cysteinyl-glycine), a key cellular anti-oxidant as well as a modulator of T-cell activation. GSH or its precursor cysteine inhibits activation of the nuclear transcription factor kB(NFkB), and has been shown to be protective against chemically induced oral cancer and leukoplakia. Alcohol-, tobacco-, and/or malnutrition-induced immunosuppression promotes impaired salivary gland function and oral mucosal immunity, a prominent reduction in the number of helper CD4 cells with less marked changes in number of suppressor T-cells, and depressed NK cell activity, among others. These suggest a breakdown in capacity or the malnourished to mount effective tumor surveillance. This review article underscores the compounding but important roles of nutritional/dietary factors in the long-established causal link between abuse of alcohol and tobacco (smoking and smokeless) and oral cancer.

• Donoff RB
• Harvard School of Dental Medicine, Boston, Massachusetts 02115, USA.
• Pages 18-24.

Increased knowledge is shedding new light on our understanding of central and peripheral nerve anatomy and molecular biology and function. New tools and methods provide important methods for the study of the behavior of cells, axons, and receptors. This review discusses the current state of that knowledge, with particular regard to the efficacy of the Seddon classification of nerve injury. The correlation of that new information to damage and repair of the peripheral sensory nerve, especially the inferior alveolar and lingual nerves, serves to highlight the progress and problems that exist.

• Johnston MC; Bronsky PT
• Dental Research Center, University of North Carolina, Chapel Hill 27599, USA.
• Pages 25-79. [published erratum appears in Crit Rev Oral Biol Med 1995; 6(4):368]

Technical advances are radically altering our concepts of normal prenatal craniofacial development. These include concepts of germ layer formation, the establishment of the initial head plan in the neural plate, and the manner in which head segmentation is controlled by regulatory (homeobox) gene activity in neuromeres and their derived neural crest cells. There is also a much better appreciation of ways in which new cell associations are established. For example, the associations are achieved by neural crest cells primarily through cell migration and subsequent cell interactions that regulate induction, growth, programmed cell death, etc. These interactions are mediated primarily by two groups of regulatory molecules: "growth factors" (e.g., FGF and TGFalpha) and the so-called steroid/thyroid/retinoic acid superfamily. Considerable advances have been made with respect to our understanding of mechanisms involved in primary and secondary palate formation, such as growth, morphogenetic movements, and the fusion/merging phenomenon. Much progress has been made on the mechanisms involved in the final differentiation of skeletal tissues. Molecular genetics and animal models for human malformations are providing many insights into abnormal development. A mouse model for the fetal alcohol syndrome(FAS), a mild form of holoprosencephaly, demonstrates a mid-line anterior neural plate deficiency which leads to olfactory placodes being positioned too close to the mid-line, and other secondary changes. Work on animal models for the retinoic acid syndrome (RAS) shows that there is major involvement of neural crest cells. There is also major crest cell involvement in similar syndromes, apparently including hemifacial microsomia. Later administration of retinoic acid prematurely and excessively kills ganglionic placodal cells and leads to a malformation complex virtually identical to the Treacher Collins syndrome. Most clefts of the lip and/or palate appear to have a multifactorial etiology. Genetic variations in TGF alpha s, RAR alpha s, NADH dehydrogenase, an enzyme involved in oxidative metabolism, and cytochrome P-450, a detoxifying enzyme, have been implicated as contributing genetic factors. Cigarette smoking, with the attendant hypoxia, is a probable contributing environmental factor. It seems likely that few clefts involve single major genes. In most cases, the pathogenesis appears to involve inadequate contact and/or fusion of the facial prominences or palatal shelves. Specific mutations in genes for different FGF receptor molecules have been identified for achondroplasia and Crouzon's syndrome, and in a regulatory gene (Msx2) for one type of craniosynostosis.

Volume 6, Issue 2

• Fincham AG; Simmer JP
• Pages 84-108.

• Graves DT; Jiang Y
• Pages 109-118.

• Purushotham KR; Humphreys-Beher MG
• Pages 119-131.

• Barnum SR
• Pages 132-146.

• Sciubba JJ
• Pages 147-160.

• Schenkels LCPM; Veerman ECI; Nieuw Amerongen AV
• Pages 161-175.

Volume 6, Issue 3

• Ignelzi, MA Jr.; Liu Y-H; Maxson, RE Jr.; Sjnead, ML
• Pages 181-201.

• Shuler, CF
• Pages 202-217.

• Rutherford B; Fitzgerald M
• Pages 218-229.

• Polverini PJ
• Pages 230-247.

• Haskin CL; Milam SB; Cameron IL
• Pages 248-277.

Volume 6, Issue 4

• Fisher C; Blumenberg M; Tomic-Canic M
• Pages 284-301.

• Ferracane JL
• Pages 302-318.

• Hassell TM; Harris EL
• Pages 319-342.

• Rudney JD
• Pages 343-367.

• Johnston MC; Bronsky PT
• Pages 368-422.