The pineal hormone melatonin was recently shown to have a free radical scavenging ability which reduces lipid peroxidation and has also been shown to scavenge the hydroxyl radical and other reactive oxygen species. Melatonin stimulates several antioxidative enzymes, which increases its efficiency as an antioxidant. Also, melatonin stimulates osteoblast differentiation and mineralization of matrix and it may regulate osteoclastic activity via superoxide dismutase in vitro. Therefore, the effect of melatonin in fracture healing depends in part on the free radical scavenging and osteoblastic-osteoclastic regulatory properties of melatonin.

In this study the effect of melatonin (MEL) on fracture healing in rat tibia model was studied by using biochemical, radiological and histopathologic methods.

Male Sprague-Dawley rats (n=80) were randomized into control and melatonin groups with 8 rats per group according to the day of sacrifice (Days 1, 3, 7, 14, 28). Group B (melatonin group) received 30 mg/kg melatonin intraperitoneally (i.p.) for the duration of the experiment.

Malondialdehyde (MDA) levels in MEL group decreased at days 3, 7, 14, and 28 compared to control values (p< 0.05). Superoxide dismutase (SOD) activity in MEL group decreased at days 3, 7, and 14, and returned to the first day value after 28 days. Myeloperoxidase (MPO) values in MEL group decreased at days 1, 3, and 7 (p< 0.001). Both radiologically and histopathologically fracture healing was significantly more advanced in the MEL group (p< 0.05, p< 0.05 respectively).

We conclude that exogenously administering a pharmacological dose of melatonin has a positive effect on fracture healing and may be beneficial as a supportive agent in fracture cases.

Aims: Immature articular cartilage has a different celularity from mature articular cartilage. Thus, the healing response may be different between these tissues. In this study, we investigated the role of IGF-I in full-thickness articular cartilage defects between immature and mature rabbits. Methods: This study used 36 immature and 36 mature New Zealand rabbits. Full-thickness articular cartilage defects in the medial femoral condyle were created. Spontaneous evolution occurred in 36 animals (18 immature and 18 mature). The other 36 animals were treated with a locally administrated IGF-I. The animals were killed in groups of eight at 4th, 8th and 12th weeks. Macroscopic, histopathologic and biochemical results were evaluated and analyzed statistically. Results: Serum IGF-I levels were signiþcantly higher in the immature group than the mature group (p< 0.001). Serum IGFBP-3 levels were signiþcantly higher in the mature group than the immature group (p< 0.05). Immunuhistochemical investigation showed chondrcyte proliferation in both groups, but duration of cell proliferation and healing process were shorter in the immature groups. The cell morphology was different between the groups. Local IGF-I treated groups had better histological scores than the control groups at all weeks (p< 0.001). Conclusions: The healing response in mature and immature cartilage were similar but the duration of this healing process was shorter in the immature group and repairing cell morphology was similar to that of the normal chondrocyte.