Parathyroid hormone-related peptide (1-34) reduces alveolar bone loss in type 1 diabetic rats

- There was an exacerbated alveolar bone loss and inflammatory response in STZ-induced diabetic periodontitis in SD rats.
- Intermittent PTHrP administration exhibits an inhibitory effect on alveolar bone resorption and the gingival inflammation.
- Increased IL-1β and IL-6 protein levels in diabetic group were inhibited by treatment of PTHrP(1-34).
- The protective effect of PTHrP(1-34) may be attributed to downregulation of inflammatory responses, and in turn inhibiting alveolar bone loss.

ObjectiveTo investigate the role of parathyroid hormone related protein (PTHrP) in diabetic periodontitis.MethodsAfter injected with 55 mg/kg streptozotocin, diabetic rats were treated subcutaneously with low-dose (40 μg/kg, once daily for 5 days per week), middle-dose (80 μg/kg) or high-dose (160 μg/kg) PTHrP(1-34) peptide. Treatment continued for 12 weeks. Changes in periodontal tissues were confirmed by micro-computerized tomography assay and H&E analysis. We used tartrate resistant acid phosphatase (TRAP) staining to identify osteoclast cells. The expression of TNF-α, IL-1β and IL-6 was assessed by immunohistochemistry and Western blot.ResultsTooth-supporting structure loss was observed in periodontal tissues of diabetic rats. PTHrP (1-34) attenuated alveolar bone loss, especially in the middle-dose and high-dose group. Whereas TNF-α, IL-1β and IL-6 protein levels were increased in the diabetic gingival tissues, PTHrP (1-34) treatment inhibited the increase of IL-1β and IL-6, but had no effect on TNF-α.ConclusionType 1 diabetes increased the susceptibility to periodontal disease. Intermittent administration of PTHrP (1-34) exhibited an inhibitory effect on alveolar bone resorption and the gingival inflammation in periodontal tissues of diabetic rats.