Costal cartilage autografts to simulated degenerative intervertebral discs in the rat.

STUDY DESIGN: An autograft of costal cartilage was transplanted into the rat intervertebral space in the proximal tail following 2 weeks of simulated degeneration by chondroitinase ABC (CABC). OBJECTIVES: The purpose of this study was to evaluate costal cartilage transplantation into a degenerated disc as a possible therapy. SUMMARY OF BACKGROUND DATA: Reversal of degenerative disc dehydration is an attractive goal. Costal cartilage is plentiful, hydrophilic, and avascular, leading us to speculate that it would survive transplantation into the degenerated disc, increase proteoglycan content, and restore disc height. MATERIALS AND METHODS: Costal cartilage fragments were transplanted into a single proximal intervertebral disc in each of the rats' tails following a 2-week period of simulated degeneration. The intervertebral space was measured on radiographs under 2.5x magnification taken pretreatment and 21 days posttreatment. Each specimen was sagittally sectioned, mounted, and stained. The slides were graded for proteoglycan content. RESULTS: A 64% increase in intervertebral disc height was observed in the implant group compared with a 4% increase in sham operated group and a 39% increase in the CABC only group. Histology demonstrated a viable implant in 7 of 9 rats. The transplant group had significantly more proteoglycan staining than either the CABC group or sham group (P < 0.05). CONCLUSIONS: Costal cartilage transplantation may rehydrate degenerated intervertebral discs and might serve as a promising model for understanding and perhaps modifying this complex degenerative disease.

The effect of levodopa or levodopa-carbidopa (sinemet) on fracture healing.

OBJECTIVES: Levodopa (L-dopa) and L-dopa/carbidopa were evaluated to determine their effectiveness in the stimulation of bone healing of fractures at risk for nonunions. METHODS: Forty-two retired breeder female Sprague-Dawley rats were divided into 2 experimental groups and 1 control. Thirty-six rats were evaluated for results. The right femur of each rat was fractured and an intramedullary omega pin was inserted to create a 2 mm bone gap. The rats were administered either 0.2 g/kg/d of L-dopa, 0.2/0.02 g/kg/d L-dopa/carbidopa in their feed, or plain powdered chow (Sham control group). The rats were killed at 5 weeks postsurgery. The femurs were excised, radiographed, and mechanically tested. Bone healing was assessed. Bone stiffness, ultimate load, and energy to failure were determined under 3 point bending using an Instron materials testing system. RESULTS: The femurs of 30% of the Sham rats healed compared with 50% of the L-dopa/carbidopa and 84% of the L-dopa treated femurs. The healed L-dopa rat femurs had significantly greater ultimate load (P = 0.037) and energy to failure (P = 0.004) than the healed Sham rats. There were no significant differences between the L-dopa/carbidopa group and either the Sham or L-dopa group. CONCLUSIONS: These results confirm that L-dopa administration increases the healing in nonunion fractures. The combination of L-dopa/carbidopa did not significantly increase fracture healing.

Proinflammatory and Th1 cytokine alterations following ultraviolet radiation enhancement of disease due to influenza infection in mice.

Exposure of rodents to immunosuppressive agents such as ozone, dioxin, or ultraviolet radiation (UVR) leads to increased morbidity and mortality following influenza virus infection. However, these adverse effects are not related to the suppression of virus-specific immune responses. Our laboratory showed that UVR increased the morbidity, mortality, and pathogenesis of influenza virus without affecting protective immunity to the virus, as measured by resistance to reinfection, suggesting that UVR and other immunosuppressive pollutants such as dioxin and ozone may exacerbate early responses that contribute to the pathogenesis of a primary viral infection. In the present study, we examined the mechanism of UVR-enhanced mortality in the absence of effects on virus-specific immunity and tested the hypothesis that modulation of cytokine levels was associated with increased deaths and body weight loss. BALB/c mice were exposed to 8.2 kJ/m(2) UVR and were infected 3 days later with a sublethal influenza virus infection (LD(40) of mouse-adapted Hong Kong influenza A/68, H(3)N(2)). Influx of inflammatory cells, proinflammatory cytokines, and cytokines produced by T-helper lymphocytes (Th1 and Th2) were measured in lung homogenates (LH) as well as in bronchoalveolar lavage fluid (BAL). UVR preexposure decreased the influenza-induced lymphocytic influx 5 days after infection, but did not alter macrophage and neutrophil influx into the lung, or increase virus titers significantly. Although interferon (IFN)-gamma, total interleukin (IL)-12, IL-6, and TNF-alpha were altered in mice that received UVR exposure prior to infection, no clear association was made that correlated with the UVR-induced increase in body weight loss and mortality due to influenza infection.