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The Effect of Parathyroid Hormone on Osseointegration in Insulin-Treated Diabetic Rats
Tina Rybaczek1, Stefan Tangl, Toni Dobsak
1*Assistant Doctor, Department of Oral Surgery, Medical University of Vienna, Vienna, Austria; Scientific Assistant, Karl Donath Laboratory for Hard Tissue and Biomaterial Research, Vienna, Austria; Austrian Cluster for Tissue Regeneration, Austria. †Head, Karl Donath Laboratory for Hard Tissue and Biomaterial Research, Vienna, Austria. ‡Scientific Assistant, Karl Donath Laboratory for Hard Tissue and Biomaterial Research, Vienna, Austria. §Head, Department of Oral Biology, Medical University of Vienna, Vienna, Austria; Scientific Associate, Department of Preventive, Restorative, and Pediatric Dentistry, University of Bern, Bern, Switzerland. ¶Assistant Professor, Department of Oral Surgery, Medical University of Vienna, Vienna, Austria; Assistant Doctor, Department of Oral Surgery and Stomatology, University of Bern, Bern, Switzerland.
Objectives:
Uncontrolled diabetes mellitus is associated with impaired osseointegration. Diabetic individuals might benefit from bone anabolic therapies. Intermittent administration of 1-34 parathyroid hormone (PTH) stimulates bone formation in rodent models. However, this anabolic effect fails in diabetic rats. Whether the anabolic effect of PTH can be achieved in insulin-controlled diabetic rats has not been investigated yet.
Materials And Methods:
After diabetes induction with streptozotocin in 40 female Wistar rats, the animals were randomly divided into 4 groups: diabetes, diabetes plus PTH, insulin-treated diabetes, and insulin-treated diabetes plus PTH. After 1 week, miniscrews were inserted in the tibiae. Osmotic pumps with insulin or saline solution were implanted. Animals received 60 mg/kg PTH or saline solution. Histomorphometric analysis was performed.
Results:
In diabetic rats, no changes of medullary periimplant bone area or bone-to-implant contacts (BICs) were achieved with or without treatment with PTH. However, also animals treated with insulin failed to response significantly to PTH regarding bone area (7.4 ± 4.1% and 8.1 ± 4.1%) and BICs (33.7 ± 16.9% and 49.9 ± 11.9%).
Conclusion:
These results demonstrate that the metabolic characteristics of the diabetic rats produced a condition unable to respond to PTH treatment, even when hyperglycemia was controlled with insulin.
