Effect of tenoxicam on fracture healing in rat tibiae

Giordano, Vincenzo; Giordano, Mario; Knackfuss, Irocy Guedes; Apfel, Mara Ibis Rodrigues; Gomes, Renato das C

doi:10.1016/s0020-1383(02)00199-7

Cited by 36 publications

(24 citation statements)

References 32 publications

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“…Many factors, such as the use of NSAIDs for the prevention of bone fracture pain, can affect this process. Recent studies have shown that these drugs affect the process of bone fracture healing [29][30][31]. NSAIDs interfere with the arachidonic acid mechanism by blocking the formation of PGs through the inhibition of the cyclooxygenase pathway, which plays a fundamental role in the bone healing process [32][33][34][35].…”

Section: Discussionmentioning

confidence: 99%

Comparison of the effects of dexketoprofen trometamol, meloxicam and diclofenac sodium on fibular fracture healing, kidney and liver: An experimental rat model

İnal

Kabay

Çaycı

et al. 2014

Injury

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Section: Discussionmentioning

confidence: 99%

Comparison of the effects of dexketoprofen trometamol, meloxicam and diclofenac sodium on fibular fracture healing, kidney and liver: An experimental rat model

İnal

Kabay

Çaycı

et al. 2014

Injury

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“…Many studies have shown that traditional NSAIDS (nonspecific) such as aspirin, indomethacin, and ibuprofen (our definition of NSAID does not include acetaminophen) impede bone healing in various animal models (see Table 1) [20,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48]. …”

Section: Nsaid Effects On Experimental Models Of Bone Healingmentioning

confidence: 99%

Effect of Non-Steroidal Anti-Inflammatory Drugs on Bone Healing

Cottrell

O’Connor

2010

Pharmaceuticals

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Nonspecific and COX-2 selective nonsteroidal anti-inflammatory drugs (NSAIDs) function by inhibiting the cyclooxygenase isoenzymes and effectively reduce pain and inflammation attributed to acute or chronic musculoskeletal pathologies. However, use of NSAIDs as an analgesic is thought to negatively contribute to bone healing. This review strived to provide a thorough unbiased analysis of the current research conducted on animals and humans regarding NSAIDs and their effect on bone healing. Specifically, this review discusses the role of animal models, dosing regiments, and outcome parameters when examining discrepancies about NSAIDS and their effects on bone regeneration. The role of COX-2 in bone regeneration needs to be better defined in order to further elucidate the impact of NSAIDs on bone healing.

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“…Results of these studies are variable. For example, treatment with aspirin, diclofenac, ibuprofen, indomethacin, and tenoxicam, was associated with impaired bone healing in rats and rabbits [69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87]. The main effects observed in those models included inhibition of Haversian (cortical bone) remodeling, alterations in spinal fusions, poor mineralization of bone matrix, decreased osteoid formation and callus bone formation, decreased bone mineral content, reduced mechanical strength of replacement tissue, decreased amounts of cortical bone and inhibition of new bone formation [73,77,[80][81][82][88][89][90][91][92].…”

Section: Effects Of Non-selective Nsaids On Bone Healingmentioning

confidence: 99%

Effects of cyclooxygenase inhibition on bone, tendon, and ligament healing

Radi

Khan

2005

Inflamm. res.

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Cyclooxygenases (COX-1 and COX-2) catalyze the conversion of arachidonic acid to prostaglandins (PGs). PGs play a significant role in bone metabolism in health and disease. Conventional non-selective, non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors (COXIBs) are widely used in patients with musculoskeletal conditions and as a post-surgical analgesics. Due to their effects on PG synthesis, these drugs have been hypothesized to affect the healing process of bone fractures and orthopedic surgical sites. A variety of experimental models of bone, ligament, and tendon repair have assessed the effects of these selective and non-selective COX inhibitors in animals, but with variable outcomes. At this time, large-scale, robust clinical study data do not exist, limiting the relevant assessment of experimental animal data to humans. Here, we provide a critical review of available data on the role of PGs and the effect of COX inhibitors on bone, tendon, and ligament repair. Collectively, this assessment suggests potential involvement of PGs in the healing process of these tissues via modulation by non-selective NSAIDs and selective COX-2 inhibitors.

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Effect of tenoxicam on fracture healing in rat tibiae

Cited by 36 publications

References 32 publications

Comparison of the effects of dexketoprofen trometamol, meloxicam and diclofenac sodium on fibular fracture healing, kidney and liver: An experimental rat model

Comparison of the effects of dexketoprofen trometamol, meloxicam and diclofenac sodium on fibular fracture healing, kidney and liver: An experimental rat model

Effect of Non-Steroidal Anti-Inflammatory Drugs on Bone Healing

Effects of cyclooxygenase inhibition on bone, tendon, and ligament healing

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