Abstract
Purpose Osteoporosis is a progressive systematic skeletal illness characterized by low bone mineral density and susceptibility to fracture caused by bone resorption. Aim of the Study. This study intended to evaluate the possible role of emdogain in combination with calcitonin on the healing of surgically induced mandibular defects performed on osteoporotic rats. Materials and Methods Forty healthy female white albino rats were included in this study and divided into four groups. In group I (negative control), 10 rats received a vehicle injection after which a unilateral mandibular defect was created in each rat of all groups. Three groups were subjected to induction of osteoporosis by subcutaneous injection of 0.1 mg/kg/day dexamethasone for 60 days. In group II, rats were kept without treatment. In group III, rats were treated with daily intramuscular injection of 2.5 IU/kg of synthetic salmon calcitonin. In group IV, rats were handled as group III, and the created cavity was filled with emdogain. Rats were euthanized at 2nd and 4th week postsurgically. Hematoxylin and eosin, Masson's trichrome, NF-κB (nuclear factor of activated B cells), and immunohistochemical stains were used, followed by statistical analysis. Results Group I showed normal stages of bone defects healing. Group II revealed the formation of granulation tissue with dilated blood vessels, while groups III and IV showed enhanced bone healing and proper collagen fibers. The percentage area of newly formed collagen fibers was significantly higher in group IV at 2nd week (13.96 ± 0.020%) and 4th week (16.95 ± 0.024%) than in group II (8.75 ± 0.015% and 10.29 ± 0.015%, respectively) and group III (12.93 ± 0.015% and 14.61 ± 0.021%, respectively), but was lower than that in group I (15.75 ± 0.015% and 17.49 ± 0.015%, respectively). Conclusion The local application of emdogain combined with systemically injected calcitonin improves bone healing in surgically induced bone defects in osteoporotic rats.
Highlights
Osteoporosis is a multifactorial skeletal disease characterized by disruption of the microarchitectural building of bone and reduction in bone mass that results in bone fragility and fast fracture with age, and described late in life, its origins can be traced back to childhood
E rats were surgically prepared for a mandibular bone defect, and the animals were divided into four groups (n 10): Group I: rats were injected with saline intramuscularly once a week for 60 days before a unilateral mandibular bone defect; this group of rats had surgery with a bone defect that was left to recover naturally without any treatment
Group III showed the woven bone filled with heavier bone trabeculae surrounded by large bone marrow cavities
Summary
Osteoporosis is a multifactorial skeletal disease characterized by disruption of the microarchitectural building of bone and reduction in bone mass that results in bone fragility and fast fracture with age, and described late in life, its origins can be traced back to childhood. Several reasons can play a role in the progress of osteoporosis, which include calcium levels in the diet throughout the bone growth stages, daily life, and hormones [1]. Cortisone’s action began with osteoblasts, which reduces reproduction and damages differentiation and growth, resulting in diminished bone construction [2]. Salmon calcitonin formed of a 32-amino acid peptide. It reduces the bone resorption via adhering and stimulating the International Journal of Dentistry calcitonin receptor on osteoclasts. The capability of salmon calcitonin to decrease breaks is debatable because of reports displaying an indistinct dose-response correlation [3]
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