Dextrose prolotherapy and corticosteroid injection into rat Achilles tendon.

PURPOSE: To assess the mechanical behavior and the histology of collagen fibers after prolotherapy with 12.5% dextrose into rat Achilles tendons and to compare with those of corticosteroid treatment. METHODS: Out of 60 adult female Wistar rats (70 tendons), 15 received 12.5% dextrose (group I); 15 were treated with corticosteroid injection (group II); and 15 were given 0.9% saline injection (group III), all into the right Achilles tendon, whereas 13 animals received no injections (group IV). Three doses of each substance (groups I, II, and III) were given at a 5-day interval. Collagen fiber color was quantitatively assessed in three samples from each group and in five samples from the control group using picrosirius red staining under polarized and nonpolarized light. Twelve tendons from each group treated with the test substance and 20 tendons from the control group were submitted to the tensile strength test. RESULTS: There was no statistical difference across the groups with respect to maximum load at failure (n.s.) and absorbed energy (n.s.). With respect to tendon rupture, there was no difference between the myotendinous and the tendinous regions (n.s.). However, hematoxylin-eosin staining revealed statistical significance in lymphocytic inflammatory infiltrate (P = 0.008) and in parallel fiber orientation (P = 0.003) when comparing groups to the control group, without significance for either neovascularization (n.s.) or the presence of fibroblasts (n.s.). Likewise, there was no significant difference between the percentage of mature (n.s.) and immature (n.s.) fibers. CONCLUSIONS: Dextrose was not deleterious to the tendinous tissue, as it did not change the mechanical and histological properties of Achilles tendons in rats. The data obtained in this study may help clinicians in their daily work as they suggest that injections of 12.5% dextrose caused no harm to the tendons, although the clinical importance in humans still needs to be defined.

Interação das enterotoxinas estafilocócicas com o sistema imune do hospedeiro / Interaction of staphylococcal exterotoxins with the immmune system of the host

As enterotoxinas estafilocócicas estão entre as principais causas de intoxicação alimentar e, possivelmente, da síndrome do choque tóxico não menstrual. Essas enterotoxinas são também denominadas de superantígenos, pela capacidade de serem potentes ativadores de células T e macrófagos. Os superantígenos ligam-se diretamente às moléculas classe II do complexo de histocompatibilidade principal sobre as células apresentadoras de antígenos e estimulam células T que expressam os elementos VB do seu receptor. A produção excessiva de citocinas por essas células e pelos macrófagos é responsável pela patôgenese da intoxicação alimentar. Essas citocinas incluem o fator de necrose tumoral-a (TNF-a), o interferon-y (IFN-y), a interleucina-l (IL-1) e mediadores proinflamatórios com potentes efeitos no sistema imune, com o óxido nítrico (NO), que apresenta tanto efeito cintotóxico como regulador.