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We report a case of Gongylonema infection of the mouth, which caused a migrating, serpiginous tract in a resident of Massachusetts. This foodborne infection, which is acquired through accidental ingestion of an infected insect, such as a beetle or a roach, represents the 11th such case reported in the United States.

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Massive cortical autografts and allografts have been found to incorporate into host bone very slowly and thus are subject to complications such as fatigue fracture and infection. In order to understand and improve the process of osteogenesis in these types of bone grafts, a new experimental model was developed using bone discs from rat calvaria prepared by demineralization and drilling of 0.5 mm diameter holes with a pulsed, 2.94 microns wavelength Erbium:Yttrium-Aluminum-Garnet laser. Four types of bone discs were analyzed: untreated (Type I), demineralized (Type II), laser-ablated (Type III), and laser-ablated then demineralized (Type IV). The discs were transplanted into a subcutaneous site in adult Sprague-Dawley rats and followed for as long as 6 weeks. Histologic analysis of the discs at weekly intervals with use of hematoxylin and eosin staining confirmed the presence of new bone growth in Type-II and Type-IV discs. The amount of new bone growth in each disc was estimated by determining the mineral x-ray attenuation coefficient, which is proportional to mineral density, from digitized radiographs of the discs. The results showed that the processes of demineralization (P < 0.001) and laser ablation with demineralization (p < 0.05) were both significant in enhancing new bone growth in this model. This study demonstrated that osteoinduction can be fostered in cortical bone through the processes of demineralization and laser ablation. To the extent that laser ablation may allow maintenance of structural integrity while altering the surface geometry in such a way as to promote ingrowth of new bone, this experimental model represents an advance in understanding how osteogenesis in cortical bone grafts might be improved.

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A model system of the irradiated rat mandible has been developed and used in conjunction with a non-spontaneously healing mandibular defect. The contribution of the tissue components in the healing of bony defects was studied using demineralized bone powder (DBP) prepared from unirradiated or in vivo irradiated rat long bones. Better bony fill of the defects occurred in the irradiated beds filled with unirradiated DBP than in the unirradiated beds containing irradiated DBP. This suggests that, at least in the early postirradiation period, the bed is not the limiting factor in healing of bony defects and the osteogenic components of bone in the DBP may be most affected by irradiation. In the irradiated bed, the defects grafted 2 weeks after irradiation healed better than those grafted at 4 weeks. Thus, the timing of surgery after irradiation also plays a role in the healing process, with early surgery producing better results.

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Microvascular and free rib grafts were placed in 4.5 cm defects in an edentate mandibular body defect 18 to 28 days after completion of 50 Gy of irradiation from a 60Co source. The animals were sacrificed from two to forty weeks postoperatively and evaluated clinically, radiographically, and histologically. There was a marked difference in the alveolar mucosal viability with the two grafts. Mucosal dehiscence was not observed over any of the microvascular grafts, but was present in seven-eighths of the free grafts. Union of the microvascular bone graft to the host bone occurred within six weeks. In contrast, after six weeks the free graft was sequestered in all the animals. An unexpected finding with both types of graft was the marked subperiosteal bone formation. This bone appeared to be derived from the host bed, stabilizing and bridging the defects bilaterally. The results suggest that radiated periosteum may play an important role in osteogenesis.

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An animal model system has been established which reproduces some of the features of the Fetal Hydantoin Syndrome. This pattern of altered growth and development includes growth retardation, craniofacial anomalies, distal phalangeal hypoplasia, and mental deficiency. Rats exposed in utero to phenytoin on gestational days 9, 11, and 13 exhibited fetal onset growth retardation, abnormalities of the craniofacial region and axial skeleton. In addition, the exposed offspring had significantly lower fetal weights, a shortened snout and a high-arched, irregular palate, and significant delays in skeletal maturation. These abnormalities resemble those reported for the Fetal Hydantoin Syndrome and provide a means to study the effect of phenytoin on the morphological and biochemical development of the fetus.

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Retinoic acid or retinyl acetate was administered to pregnant rats in doses sufficient to induce a 90% incidence of cleft palate. In another study, a delay in the reorientation of the palatal shelves was observed to be longer with the more potent teratogen, retinoic acid. On day 16 of gestation, 24 hours after final dosage with vitamin A, the synthesis of DNA and protein was studied in fetal carcass, mandible, and palate, and that of sulfated mucopolysaccharides (S-MPS) and glycoproteins (GP) in fetal head, mandible, and palate. Increases in DNA synthesis in fetal palate and in GP synthesis in fetal palate were found; thus, the mechanism of action of vitamin A in inducing cleft palates in rats may be caused by interference with the normal biochemical synthetic pattern of the palatal shelves.

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Both retinoic acid and retinyl acetate, administered in high doses on days 13--15 of gestation, are capable of causing a 90 per cent incidence of cleft palate in Charles River rats. However, an attempt to develop as in vivo rabbit model system for the induction of clefts via hypervitaminosis A was unsuccessful. In the rat, the retinoic acid form of vitamin A is the more potent teratogen, inducing clefts at less than half the dose required to produce them with retinyl acetate. Histologic examination of fetal rat heads confirmed the biochemical evidence that retinoic acid is the more potent teratogen. Both forms of vitamin A prevented palatal shelf reorientation from occurring at the correct gestational age. The retinyl acetate treatment delayed the rotation for approximately 12 hours, the retinoic acid for at least 48 hours.

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Pregnant rats and rabbits were given excess vitamin A, in the form of retinyl acetate or retinoic acid, for the 3-day period just prior to palatal closure in the fetuses. Twenty-four hours later, the various forms of vitamin A, and their levels, were determined in fetal liver and carcass and in maternal liver and serum by thin-layer chromatography. The predominant forms of vitamin A found in both fetal and maternal tissues were retinyl palmitate, retinol and retinoic acid. In both species, the tissues from the groups treated with retinoic acid contained levels of vitamin A similar to those found in control tissues. After retinyl acetate treatment in the rat, both of the maternal tissues studied had elevated vitamin A, whereas in the rabbit only maternal liver levels increased. In the groups treated with retinyl acetate, the ratio of the vitamin A levels in fetal liver: maternal serum reflected a species difference: the ratio was lower than the control value in the rabbit and higher than controls in the rat. Radiotracer studies in the rat, using either 3H-retinol or 14C-retinoic acid, demonstrated vitamin A transport across the placenta, with vitamin A concentrating in the fetal liver.

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