Dextrose injection directly in
tendon is safe
tendon is safe
Can dextrose be safely injected directly into ligaments or tendons?
Dextrose is often injected directly in ligament or tendon tissue. Steroids may weaken ligaments of tendons and result in a rupture upon direct injection but that has not be reported with dextrose injection. To further investigate for risk of of loading a tendon after intratendinous, the following study was performed.
Martins et al. Martins CA, Bertuzzi RT, Tisot RA, et al. Dextrose prolotherapy and corticosteroid injection into rat Achilles tendon. Knee Surg Sports Traumatol Arthrosc 2012;20:1895-900.
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 corticosteroidinjection (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.
SUMMARY: A transient reduction in tensile strength of the healthy rat Achilles tendon was not demonstrable at 0, 5 or 10 days by Martins et al after masked injection of 12.5% dextrose compared to normal saline injection or no injection. The rupture site of the tendons in the dextrose group was predominantly the myotendinous region, demonstrating good strength of the tendinous region into which the substance was injected. One of the limitations of our study was the short time period for the analyses. This might have influenced the results, especially regarding the effects of intratendinous
corticosteroid injection. In addition the tendons did not have previous injuries. However, these results suggest that
injections of 12.5% dextrose caused no harm to the tendons. Thus, animal data suggests there are not acute decreases in tendon strength of injection with dextrose.
Dextrose is often injected directly in ligament or tendon tissue. Steroids may weaken ligaments of tendons and result in a rupture upon direct injection but that has not be reported with dextrose injection. To further investigate for risk of of loading a tendon after intratendinous, the following study was performed.
Martins et al. Martins CA, Bertuzzi RT, Tisot RA, et al. Dextrose prolotherapy and corticosteroid injection into rat Achilles tendon. Knee Surg Sports Traumatol Arthrosc 2012;20:1895-900.
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 corticosteroidinjection (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.
SUMMARY: A transient reduction in tensile strength of the healthy rat Achilles tendon was not demonstrable at 0, 5 or 10 days by Martins et al after masked injection of 12.5% dextrose compared to normal saline injection or no injection. The rupture site of the tendons in the dextrose group was predominantly the myotendinous region, demonstrating good strength of the tendinous region into which the substance was injected. One of the limitations of our study was the short time period for the analyses. This might have influenced the results, especially regarding the effects of intratendinous
corticosteroid injection. In addition the tendons did not have previous injuries. However, these results suggest that
injections of 12.5% dextrose caused no harm to the tendons. Thus, animal data suggests there are not acute decreases in tendon strength of injection with dextrose.