Effects of Melatonin on Tibia Bone Defects in Rats

Koparal, Mahmut; İrtegün, Sevgi; Alan, Hilal; Deveci, Engin; Gülsün, Belgin; Pektanç, Gülsüm

doi:10.4067/s0717-95022016000200053

Cited by 7 publications

(5 citation statements)

References 17 publications

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“…In our study, the increase of osteocyte differentiation with decrease of osteoclastic activity at the end of 28 days accelerates the new bone development and the formation of bone trabeculae and explains the osteoinductive effect of Dexametazon with the graft. Osteonectin is a protein known to be involved in cell-matrix interactions, angiogenesis and important for normal ossification (Koparal et al, 2016). Osteonectin is secreted by osteoblast cells during bone formation.…”

Section: Discussionmentioning

confidence: 99%

Graft Application and Dexamethasone Treatment Influences New Bone Formation in Rat Tibial Bone Defects

Yigit

Deveci

2020

Int. J. Morphol.

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The objective of this study were bone defect complications that occur due to traumas or infections. Bone grafts are required to provide support, fill gaps and improve biological repair in skeletal damage. Dexamethasone plays role in calcium signaling modulation and used in diseases. Aim of this study was to evaluate osteonectin and osteopontin expressions in new bone development after dexamethasone application on tibial bone defects. Rats were divided into defect, defect+graft and defect+graft+dexamethasone treated groups. Tibial bone defect created, and rats were kept immobile for 28 days. Alloplastic material was placed in defect area in second and group third groups. 2.5 mg/kg Dex and normal saline were injected to dexamethasone and defect groups twice a week for 56 days. Inflammation and congestion were increased in defect and defect+graft groups. Defect+graft+dexamethasone group; increased number of osteoblast and osteocyte cells, dense bone matrix, formation of new bone trabeculae was observed. Defect+graft group; osteonectin expression in graft regions, osteoblast cells, some connective tissue cells and fibers were seen whereas in defect+graft+dexamethasone group; osteopontin expression in osteoblast and osteocyte cells of new bone trabeculae were observed. Dexamethasone may lead to formation of new bone trabeculae into the graft material resulting in increased osteoconduction and osteoinductive effect for differentiation of osteon.

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Section: Discussionmentioning

confidence: 99%

Graft Application and Dexamethasone Treatment Influences New Bone Formation in Rat Tibial Bone Defects

Yigit

Deveci

2020

Int. J. Morphol.

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“…Defect + graft group: a 6 mm defect was created on tibial bone, then allograft was applied and rats were kept immobilized for 28 days. Defect + graft + Melatonin(10mg/kg) group: a 6 mm defect was created on tibial bone, then allograft was applied, and rats were administered melatonine and kept immobilized for 28 days (Koparal et al, 2016). As part of this study, permission was obtained from the lead author, my thesis advisor, Engin Deveci, and peripheral nerve effects were studied.…”

Section: Methodsmentioning

confidence: 99%

Effect of Melatonin on Peripheral Nerve Damage Resulting from Tibial Defect in Rats

Yükselmis¹,

Ermiş

2022

Int. J. Morphol.

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Peripheral nerve damage (PNI) can cause demyelination, axonal degeneration and loss of motor and sensory function. Melatonin with its antioxidative effect, has been reported to reduce scar formation in nerve injury, take a role in repair process by suppressing fibroblast proliferation in the damaged area. It was aimed to investigate the effect of melatonin in the repair of peripheral nerve damage and the relationship between S100 proteins and angiogenic regulation. Wistar albino rats were divided into 3 groups. In the Defect group, 6 mm tibial bone defect using a motorized drill was created and kept immobile for 28 days . In Defect + graft group, tibial bone defect with allograft treatment was applied and kept immobile for 28 days. In Defect + graft + Melatonin group, melatonin was administered to defect + allograft group. All rats were sacrified by decapitation, skin and tibia bone were removed then fixed with 10 % neutral buffered formalin and embedded in paraffin, sections were examined under light microscopy. In the Defect+Graft group, enlargement and occlusion of the vessels with degeneration of the epineural sheath, thickening of the endoneural sheath and mild hyperplasia of schwannocytus (Schwann cells) were remarkable. In the Defect+Graft+Melatonin group, the epineural sheath was tight and regular, the axonal structures were prominent in the endoneural area. Mild S100 expression was observed in Defect+Graft group in fibers of the endoneural region with a prominent expression in schwannocytus. In Defect+Graft+Melatonin group (10mg/kg), S100 expression was moderate in areas where schwannocytus proliferated and nerve-connective tissue sheaths were reconstructed. VEGF expression was moderate in endoneural, perineural and epineural connective tissue sheaths in the Defect+Graft+Melatonin group, with negative expression in blood vessel endothelial cells, but with a positive expression in schwannocytus. We conclude that with the application of melatonin; oxidative stress decreases, schwannocytus proliferation increases, having positive influence on nerve repair with the regulation of S100 signaling and angiogenetic structuring.

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“…It is connected with type I collagen, calcium, and hydroxyapatite and therefore prevents mineralisation (27). Osteopontin (also called BSP-1) protein located in the extracellular bone matrix is non-collagenous and acts in bone cell functions (28). Osteopontin participates in the upregulation of cell adhesion and differentiation in osteoblast cells, and concomitantly in the upregulation of cell adhesion and bone resorption in osteoclast cells (29).…”

Section: Introductionmentioning

confidence: 99%

Effects of alloplastic graft material combined with a topical ozone application on calvarial bone defects in rats

et al. 2020

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Background:The present study presents the evaluation of the damage in the bone tissue resulting from a calvarial defect in rats and the efficiency of exposure to an ozone application with an alloplastic bone graft on the calvarial bone damage. Materials and methods:Wistar male rats (n = 56) were divided into four groups: a control group (n = 14), defect and ozone group (n = 14), defect and graft group (n = 14), and defect, graft, and ozone group (n = 14). Under anaesthesia, a circular full-thickness bone defect was created in all groups, and the experimental groups were further divided into two sub-groups, with seven rats in each group sacrificed at the end of the 4 th and 8 th weeks. Bone samples were dissected, fixed in 10% formalin solution, and decalcified with 5% ethylene-diaminetetraacetic acid (EDTA). After the routine follow-up on tissues, immunostaining of osteopontin and osteonectin antibodies was applied to sections and observed under a light microscope. Results:The control group exhibited osteopontin and osteonectin expression in fibroblasts and inflammatory cells at the end of the 4 th week with an acceleration at the 8 th week. Ozone administration elucidated new trabecular bone formation by increasing osteoblastic activity.Lastly, our observations underscore that a combination of allograft and ozone application increased the osteoblast, osteocyte, and bone matrix development at the 4 th and 8 th weeks. Conclusions:Exposure to an ozone application with an alloplastic bone graft on calvarial bone damage may induce osteoblastic activity, matrix development, mature bone cell formation, and new bone formation in rats.

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Effects of Melatonin on Tibia Bone Defects in Rats

Cited by 7 publications

References 17 publications

Graft Application and Dexamethasone Treatment Influences New Bone Formation in Rat Tibial Bone Defects

Graft Application and Dexamethasone Treatment Influences New Bone Formation in Rat Tibial Bone Defects

Effect of Melatonin on Peripheral Nerve Damage Resulting from Tibial Defect in Rats

Effects of alloplastic graft material combined with a topical ozone application on calvarial bone defects in rats

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