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Schwarting and colleagues use an In Vitro coculture model to investigate the effect of cyclooxygenase (COX) inhibition during anterior cruciate ligament regeneration on tendon-bone healing. Schwarting and colleagues used selective COX-2 and non-selective COX inhibitions to study the tendon-bone interface and associations between osteoblasts and fibroblasts. The tests included an MC3T3-E1 coculture model containing both osteoblasts and fibroblasts. The cultures were then put through a cell-viability analysis, microscopic proliferation and migration at the interface region, determining quantitative polymerase chain reaction and statistical analysis of the results using SPSS. The results show that COX-2 is useful to some extent in improving tendon-bone healing but are not superior to non-selective COX. From the findings, it is evident cyclooxygenase inhibition aids tendon healing if conducted in In Vitro. This implies that for orthopedic surgeons to be successful in treating knee injuries, they should tendon bone integration is facilitated by ibuprofen and parecoxib analgesic regimes are administered.
Nagano, A., Arioka, M., Yanaga, F.T., Matsuzaki, E., & Sasaguri, T. (2017). Celecoxib inhibits osteoblast maturation by suppressing the expression of Wnt target genes. Journal of Pharmacological Sciences, 133, pp.18-24. Retrieved from http:\/\/ac.els-cdn.com\/S1347861316301591\/1-s2.0-S1347861316301591-main.pdf?_tid=a119810a-9d10-11e7-baa8-00000aacb361&acdnat=1505808220_e072143281c7060d25adb714d2ca4c47
The article explores how Celecoxib prevents the healing of bone fractures. The authors point out that Non-Steroidal Anti-Inflammatory drugs (NSAIDs) hinder bone healing, but the mechanism in which it is done has not been grasped fully. Although Celecoxib helps to treat arthritis and other acute and chronic pains that affect bones, it also degrades the Wnt pathways and target genes used to facilitate differentiation and maturation of bone tissues.
To determine how Celecoxib suppresses Wnt target genes, leading to inhibition of osteoblast maturation, Nagano and other researchers conducted experiments. The research used TOP flash and FOP flash in MC3T3-E1 cell culture from bones derived from mice. Then von Kossa staining of cell culture, western blotting analysis, reporter plasmids, measurement of phosphate alkaline activity and statistical analysis. The findings showed that celecoxib suppressed osteoblast-mediated mineralization, Wnt pathway in M3T3-E1, and suppression of expression of ALP (Nagano et al. 2017, p.21). The findings concluded that indeed, celecoxib inhibited osteoblast maturation and therefore affected bone healing. This implies that NSAIDs prevent bone healing although selective COX-2 and CoX-1 play conflicting role in the maturation of osteoblasts. Despite Celecoxib reducing pain after surgery, they may impair healing of the bones.
Puontos, I., Georgouli, T., Calori, G.M., & Giannoudis, P.V. (2012). Do Non-steroidal Anti-Inflammatory Drugs Affect Bone Healing? A Critical Analysis. The Scientific World Journal, pp.1-14. Retrieved from https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3259713\/pdf\/TSWJ2012-606404.pdf
This article examines the aspect of bone healing and the factors that affect the physiological process of healing fractures. Anti-inflammatory drugs and steroids have been found to reduce pain in patients but in the process delay bone healing. The article explores NSAIDs and the extent to which they hamper fracture healing. Puontos and his colleagues assert that prostaglandins (PGs) are usually released by cells to respond to inflammation after an injury and kick-start the process of fracture healing.
The authors conducted a literature review of database search to look for information regarding NSAIDs and bone healing. The journals included in the report were written from 1980-2011, specifically in the English language and search words included bone healing, bone marrow, NSAIDs bone healing in vitro and in vivo in both humans and animals. The results showed that NSAIDs in vitro models inhibited the ability of osteoblasts to differentiate. Both animal and clinical models also proved that steroids and other drugs affected the ability of bones to heal. This implies that patients using NSAIDs immediately after surgery or injury will experience prolonged fracture healing.
All the research from the three articles points to the fact that NSAIDs inhibit fracture healing. Furthermore, it is clear that tendon bone interface offers a challenge to orthopedic surgeons in conducting successful surgeries without follow up with minor operations. Doctors should delay the administration of NSAIDs like celecoxib to boost the chances of healing while looking for alternatives to reduce pain.
Nagano, A., Arioka, M., Yanaga, F.T., Matsuzaki, E., & Sasaguri, T. (2017). Celecoxib inhibits osteoblast maturation by suppressing the expression of Wnt target genes. Journal of Pharmacological Sciences, 133, pp.18-24. Retrieved from http://ac.els-cdn.com/S1347861316301591/1-s2.0-S1347861316301591-main.pdf?_tid=a119810a-9d10-11e7-baa8-00000aacb361&acdnat=1505808220_e072143281c7060d25adb714d2ca4c47
Puntos, I., Georgouli, T., Calori, G.M., & Giannoudis, P.V. (2012). Do Non-steroidal Anti-Inflammatory Drugs Affect Bone Healing? A Critical Analysis. The Scientific World Journal, pp.1-14. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259713/pdf/TSWJ2012-606404.pdf
Schwarting, T., Pretzsch, S., Debus, F., Ruchholtz, S., & Lechler, P. (2015). The Effect of Cyclooxygenase Inhibition on Tendon-Bone healing an In Vitro Coculture Model. Mediators of Inflammation, pp. 1-10. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438175/pdf/MI2015-926369.pdf
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