Histological changes in the bone structure induced at 12 weeks by experimental administration of bisphosphonates

Histological changes in bone structure were induced at 12 weeks by experimental administration of bisphosphonates, which have been associated with osteonecrosis of the jaws. The purpose of this study was to determine the effect of local administration of bisphosphonate on bone formation in rats. Surgically created bone defects were evaluated at 12 weeks by histological examination after bisphosphonate administration. Fifteen Wistar rats that underwent surgery to create a bone defect at the right femur were divided in 3 groups: 2 experimental groups and a control group. The 1st experimental group received bisphosphonate as a single 1-mL dose into the bone defect, the 2nd experimental group received 1 mL of bisphosphonate as a 10-day fractionated dose, and the control group comprised rats who did not receive any bisphosphonate. At 12 weeks after the injection, new bone tissue was collected and a histological examination was performed. At 12 weeks after the bisphosphonate administration, bone repair processes were found in both the experimental and control groups. The bone continuity in the intervention area was ensured by a continuous layer of bone tissue. Compared with the control, the repair processes were significantly more advanced in the experimental groups, the layer of bone tissue covering the bone defect being thicker and more consolidated and the trabeculae from the Haversian canal being thicker and denser. External and internal consolidation structures were present in animals from all of the groups. Bisphosphonate had a positive influence on bone formation. The stimulatory effect of the bisphosphonate increased with the number of administered doses.

Histological changes in the bone structure induced at 12 weeks by experimental administration of bisphosphonates

Histological changes in bone structure were induced at 12 weeks by experimental administration of bisphosphonates, which have been associated with osteonecrosis of the jaws. The purpose of this study was to determine the effect of local administration of bisphosphonate on bone formation in rats. Surgically created bone defects were evaluated at 12 weeks by histological examination after bisphosphonate administration. Fifteen Wistar rats that underwent surgery to create a bone defect at the right femur were divided in 3 groups: 2 experimental groups and a control group. The 1st experimental group received bisphosphonate as a single 1-mL dose into the bone defect, the 2nd experimental group received 1 mL of bisphosphonate as a 10-day fractionated dose, and the control group comprised rats who did not receive any bisphosphonate. At 12 weeks after the injection, new bone tissue was collected and a histological examination was performed. At 12 weeks after the bisphosphonate administration, bone repair processes were found in both the experimental and control groups. The bone continuity in the intervention area was ensured by a continuous layer of bone tissue. Compared with the control, the repair processes were significantly more advanced in the experimental groups, the layer of bone tissue covering the bone defect being thicker and more consolidated and the trabeculae from the Haversian canal being thicker and denser. External and internal consolidation structures were present in animals from all of the groups. Bisphosphonate had a positive influence on bone formation. The stimulatory effect of the bisphosphonate increased with the number of administered doses.

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  • Boonyapakorn, T., Schirmer, I., Reichart, P.A., Sturm, I., Massenkeil, G.: Bisphosphonate-induced osteonecrosis of the jaws: prospective study of 80 patients with multiple myeloma and other malignancies. Oral. Oncol., 2008; 44: 857–869. Marx, R.E.: Pamidronate (Aredia) and zoledronate (Zometa) induced avascular necrosis of the jaws: a growing epidemic. J. Oral. Maxillofac. Surg., 2003; 1: 1115–1117.
  • Feller, L., Wood, N.H., Khammissa, R.A., Chikte, U.M., Bouckaert, M., Lemmer, J.: Bisphosphonate-related osteonecrosis of the jaw. SADJ, 2011; 66(1): 30–32.
  • Wutzl, A., Pohl, S., Sulzbacher, I., Seemann, R., Lauer, G., Ewers, R., Drach, J., Klug, C.: Factors influencing surgical treatment of bisphosphonate-related osteonecrosis of the jaws. Head Neck, 2011; 33: e1–7.
  • Borromeo, G.L., Tsao, C.E., Darby, I.B., Ebeling, P.R.: A review of the clinical implications of bisphosphonates in dentistry. Aust. Dent. J., 2011; 56(1): 2–9.
  • Patel, V., McLeod, N.M., Rogers, S.N., Brennan, P.A.: Bisphosphonate osteonecrosis of the jaw--a literature review of UK policies versus international policies on bisphosphonates, risk factors and prevention. Br. J. Oral. Maxillofac. Surg., 2011; 49(4): 251–257.
  • Vitté, C., Fleisch, H., Guenther, H.L.: Bisphosphonates induce osteoblasts to secrete an inhibitor of osteoclast-mediated resorption. Endocrinology, 1996; 137: 2324–2333.
Turkish Journal of Veterinary and Animal Sciences-Cover
  • ISSN: 1300-0128
  • Yayın Aralığı: Yılda 6 Sayı
  • Yayıncı: TÜBİTAK
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