Determination of the optimal diabetes duration for bone regeneration experiments in an alloxan-induced diabetic rabbit calvarial defect model
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Purpose: The purpose of this study was to evaluate the optimal diabetes duration for bone regeneration experiments in an alloxan monohydrate (ALX)–induced diabetic rabbit calvarial defect model by evaluating the association between diabetes duration and bone healing capacity. Methods: Twenty-four New Zealand white rabbits were used. Twenty-two rabbits were injected with 100 mg/kg of ALX to induce experimental diabetes. These rabbits were divided into 4 groups, including a control group and groups with diabetes durations of 1 week (group 1), 2 weeks (group 2), and 4 weeks (group 3). Calvarial defects were created at 1, 2, and 4 weeks after ALX injection and in the control rabbits. Cone-beam computed tomography (CBCT) scanning was performed on the day of surgery and at 2 and 4 weeks after surgery. The rabbits were sacrificed 4 weeks after surgery, followed by histological and immunofluorescence analysis. Results: The diabetic state of all diabetic rabbits was well-maintained throughout the experiment. Reconstructed 3-dimensional CBCT imaging showed more rapid and prominent bone regeneration in the control group than in the experimental groups. Histological staining showed notable bone regeneration in the control group, in contrast to scarce bone formation in the experimental groups. The appearance and immunoreactivity of receptor activator of nuclear factor-kappa B and osteoprotegerin did not show notable differences among the groups. Conclusion: ALX administration at 100 mg/kg successfully induced experimental diabetes in rabbits. The effect of diabetes on bone healing was evident when the interval between diabetes induction and the intervention was ≥1 week.
Abstract
Purpose: The purpose of this study was to evaluate the optimal diabetes duration for bone regeneration experiments in an alloxan monohydrate (ALX)–induced diabetic rabbit calvarial defect model by evaluating the association between diabetes duration and bone healing capacity. Methods: Twenty-four New Zealand white rabbits were used. Twenty-two rabbits were injected with 100 mg/kg of ALX to induce experimental diabetes. These rabbits were divided into 4 groups, including a control group and groups with diabetes durations of 1 week (group 1), 2 weeks (group 2), and 4 weeks (group 3). Calvarial defects were created at 1, 2, and 4 weeks after ALX injection and in the control rabbits. Cone-beam computed tomography (CBCT) scanning was performed on the day of surgery and at 2 and 4 weeks after surgery. The rabbits were sacrificed 4 weeks after surgery, followed by histological and immunofluorescence analysis. Results: The diabetic state of all diabetic rabbits was well-maintained throughout the experiment. Reconstructed 3-dimensional CBCT imaging showed more rapid and prominent bone regeneration in the control group than in the experimental groups. Histological staining showed notable bone regeneration in the control group, in contrast to scarce bone formation in the experimental groups. The appearance and immunoreactivity of receptor activator of nuclear factor-kappa B and osteoprotegerin did not show notable differences among the groups. Conclusion: ALX administration at 100 mg/kg successfully induced experimental diabetes in rabbits. The effect of diabetes on bone healing was evident when the interval between diabetes induction and the intervention was ≥1 week.
참고문헌 (37)
- Stavropoulos A, "Pre-clinical in vivo models for the screening of bone biomaterials for oral", craniofacial indications: focus on small-animal models, 2015, pp.68, 55~65
- Kantarci A, "Animal models for periodontal regeneration and peri-implant responses", Periodontol 2000, 68, pp.66~82 (2015)
- Expert Committee on the Diagnosis, "Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus", Diabetes Care, 20, pp.1183~1197 (1997)
- "Korean diabetes fact sheet 2015" (2011)[URL]
- Goodman WG, "Diminished bone formation in experimental diabetes. Relationship to osteoid maturation and mineralization", Diabetes, 33, pp.825~831 (1984)
- Nyomba BL, "Bone mineral homeostasis in spontaneously diabetic BB rats. I. Abnormal vitamin D metabolism and impaired active intestinal calcium absorption", Endocrinology, 124, pp.565~572 (1989)
- Shires R, "The effect of streptozotocin-induced chronic diabetes mellitus on bone and mineral homeostasis in the rat", J Lab Clin Med, 97, pp.231~240 (1981)
- Morris HF, "Implant survival in patients with type 2 diabetes: placement to 36 months", Ann Periodontol, 5, pp.157~165 (2000)
- Moy PK, "Dental implant failure rates and associated risk factors", Int J Oral Maxillofac Implants, 20, pp.569~577 (2005)
- Nevins ML, "Wound healing around endosseous implants in experimental diabetes", Int J Oral Maxillofac Implants, 13, pp.620~629 (1998)
- Giglio MJ, "Histomorphometric study of bone healing around laminar implants in experimental diabetes", Implant Dent, 9, pp.143~149 (2000)
- Lalla E, "Hyperglycemia, glycoxidation and receptor for advanced glycation endproducts: potential mechanisms underlying diabetic complications, including diabetes-associated periodontitis", Periodontol 2000, 23, pp.50~62 (2000)
- Taylor GW, "Non-insulin dependent diabetes mellitus and alveolar bone loss progression over 2 years", J Periodontol, 69, pp.76~83 (1998)
- Balint E, "Glucose-induced inhibition of in vitro bone mineralization", Bone, 28, pp.21~28 (2001)
- Terada M, "Growth-inhibitory effect of a high glucose concentration on osteoblast-like cells", Bone, 22, pp.17~23 (1998)
- Brownlee M, "Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications", N Engl J Med, 318, pp.1315~1321 (1988)
- Santana RB, "A role for advanced glycation end products in diminished bone healing in type 1 diabetes", Diabetes, 52, pp.1502~1510 (2003)
- Lalla E, "Enhanced interaction of advanced glycation end products with their cellular receptor RAGE: implications for the pathogenesis of accelerated periodontal disease in diabetes", Ann Periodontol, 3, pp.13~19 (1998)
- Brussee V, "Distal degenerative sensory neuropathy in a long-term type 2 diabetes rat model", Diabetes, 57, pp.1664~1673 (2008)
- Diabetes Control, "The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus", N Engl J Med, 329, pp.977~986 (1993)
- Kamiya H, "Degeneration of the Golgi and neuronal loss in dorsal root ganglia in diabetic BioBreeding", Worcester rats, 2006, pp.49, 2763~2774
- UK Prospective Diabetes Study (UKPDS) Group, "Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)", Lancet, 352, pp.837~853 (1998)
- Follak N, "Histomorphometric evaluation of the influence of the diabetic metabolic state on bone defect healing depending on the defect size in spontaneously diabetic BB", OK rats, 2004, pp.35, 144~152
- Shyng YC, "The effect of streptozotocin-induced experimental diabetes mellitus on calvarial defect healing and bone turnover in the rat", Int J Oral Maxillofac Surg, 30, pp.70~74 (2001)
- Lenzen S, "The mechanisms of alloxan- and streptozotocin-induced diabetes", Diabetologia, 51, pp.216~226 (2008)
- Lackey RW, "Glycogen in alloxan-treated rats", Proc Soc Exp Biol Med, 57, pp.191~194 (1944)
- Zhao ZH, "Variations of susceptibility to alloxan induced diabetes in the rabbit", Horm Metab Res, 19, pp.534~537 (1987)
- Nath MC, "Studies on alloxan diabetes. I. Increase of susceptibility caused by acetoacetate", Biochem J, 53, pp.481~483 (1953)
- Hadour G, "Improved myocardial tolerance to ischaemia in the diabetic rabbit", J Mol Cell Cardiol, 30, pp.1869~1875 (1998)
- Mah P, "Deriving Hounsfield units using grey levels in cone beam computed tomography", Dentomaxillofac Radiol, 39, pp.323~335 (2010)
- Greenwald JA, "Biomolecular mechanisms of calvarial bone induction: immature versus mature dura mater", Plast Reconstr Surg, 105, pp.1382~1392 (2000)
- Hsu H, "Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand", Proc Natl Acad Sci U S A, 96, pp.3540~3545 (1999)
- Horowitz MC, "Control of osteoclastogenesis and bone resorption by members of the TNF family of receptors and ligands", Cytokine Growth Factor Rev, 12, pp.9~18 (2001)
- Crotti T, "Receptor activator NF kappaB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis", J Periodontal Res, 38, pp.380~387 (2003)
- Rees DA, "Animal models of diabetes mellitus", Diabet Med, 22, pp.359~370 (2005)
- Wang J, "Creating a long-term diabetic rabbit model", Exp Diabetes Res, 2010, pp.289614~ (2010)
- Mir SH, "Histopathological abnormalities of prolonged alloxan-induced diabetes mellitus in rabbits", Int J Exp Pathol, 90, pp.66~73 (2009)
