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

Zhang, Wen; Wu, Suzhen; Zhou, Jian; Chen, Hongmin; Gong, Yeli; Peng, Fei; Zhang, Baifang

doi:10.1016/j.archoralbio.2017.06.013

Cited by 9 publications

(13 citation statements)

References 32 publications

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“…Furthermore, our study showed that although systemic oxidative stress was aggravated in diabetic rats, no significant difference in oxidative stress level was detected in the local periodontal tissues between the D and C groups. Previous animal studies have demonstrated that when DM is induced in rats for 3, 6, 9, and 12 months, marked alveolar bone loss is observed in periodontal tissues [18, 19]; thus, we inferred that the 1-month duration in our study might not be long enough for DM to affect either bone loss or periodontal oxidative stress level in rats without periodontitis. Regarding DP, both local and systemic oxidative stress levels were enhanced, as reflected by higher expression of 3-NT, 4-HNE, and 8-OHdG in periodontal tissues, accompanied by elevated serum level of MDA and decreased serum SOD activity.…”

Section: Discussionmentioning

confidence: 67%

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Sun

Zhang

et al. 2018

Oxidative Medicine and Cellular Longevity

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Diabetes mellitus is a well-recognized risk factor for periodontitis. The goal of the present study was to elucidate whether oxidative stress and nuclear factor erythroid 2-related factor 2 (Nrf2) participate in the aggravation of periodontitis by diabetes. For this purpose, we assigned Wistar rats to control, periodontitis, diabetes, and diabetic periodontitis groups. Two weeks after induction of diabetes by streptozotocin, periodontitis was induced by ligation. Two weeks later, periodontal tissues and blood were harvested and analyzed by stereomicroscopy, immunohistochemistry, and real-time polymerase chain reaction. We found that ligation induced more severe bone loss and periodontal cell apoptosis in diabetic rats than in normal rats (p < 0.05). Compared with the control group, periodontitis significantly enhanced local oxidative damage (elevated expression of 3-nitrotyrosine, 4-hydroxy-2-nonenal, and 8-hydroxy-deoxyguanosine), whereas diabetes significantly increased systemic oxidative damage and suppressed antioxidant capacity (increased malondialdehyde expression and decreased superoxide dismutase activity) (p < 0.05). Simultaneous periodontitis and diabetes synergistically aggravated both local and systemic oxidative damage (p < 0.05); this finding was strongly correlated with the more severe periodontal destruction in diabetic periodontitis. Furthermore, gene and protein expression of Nrf2 was significantly downregulated in diabetic periodontitis (p < 0.05). Multiple regression analysis indicated that the reduced Nrf2 expression was strongly correlated with the aggravated periodontal destruction and oxidative damage in diabetic periodontitis. We conclude that enhanced local and systemic oxidative damage and Nrf2 downregulation contribute to the development and progression of diabetic periodontitis.

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Section: Discussionmentioning

confidence: 67%

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Sun

Zhang

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Besides, a recent study, showed that adding PTH1-34 to a xenograft increased the hardness of regenerated bone and accelerated bone mineralization in reconstructing mandible defects of pigs (Emam et al, 2020). Also, PTH1-34 may prevent alveolar bone resorption in type 1 diabetic rats, and that its intermittent administration could play an anabolic role in alveolar bone (Zhang et al, 2017).…”

Section: Parathyroid Hormone-related Peptidesmentioning

confidence: 99%

Bioactive Synthetic Peptides for Oral Tissues Regeneration

et al. 2021

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Regenerative therapy in oral tissues has gained relevance since tissue loss due to congenital or acquired diseases as well as trauma is a major health problem worldwide. Regeneration depends on the natural capacity of the body and the use of biomaterials and bioactive molecules that can module the processes to replace lost or damaged tissues and restore function. The combined use of scaffolds, cells, and bioactive molecules such as peptides is considered the best approach to achieve tissue regeneration. These peptides can induce diverse cellular processes as they can influence cell behavior and also can modify scaffold properties, giving as a result the enhancement of cell adhesion, proliferation, migration, differentiation, and biomineralization that are required given the complex nature of oral tissues. Specifically, synthetic peptides (SP) have a positive influence on scaffold biocompatibility since in many cases they can mimic the function of a natural peptide or a full-length protein. Besides, they are bioactive molecules easy to produce, process, and modify, and they can be prepared under well-defined and controlled conditions. This review aims to compile the most relevant information regarding advances in SP for dental and periodontal tissue regeneration, their biological effects, and their clinical implications. Even though most of the SP are still under investigation, some of them have been studied in vitro and in vivo with promising results that may lead to preclinical studies. Besides there are SP that have shown their efficacy in clinical trials such as P11-4 for enamel regeneration or caries prevention and ABM/P-15 for cementum, periodontal ligament (PDL), and alveolar bone on a previously calculus- and biofilm-contaminated zone. Also, some SP are commercially available such as PTH1-34 and PepGen P-15 which are used for bone defects treatment.

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“…[ 45 , 46 ] Analogs of parathyroid hormone directly stimulate bone formation through parathyroid hormone type-1 receptors and regulation of osteocytic sclerostin expression. [ 47 – 49 ] Tumor necrosis factor-α antagonist inhibits expression of pro-inflammatory cytokines in periodontitis to attenuate alveolar bone loss and diminishes osteocytic RANKL and sclerostin expression in periodontitis to mediate bone formation. [ 50 , 51 ] WP9QY (W9) peptide, a RANKL-binding peptide, restores alveolar bone loss by inhibiting RANKL signaling to suppress osteoclastogenesis and attenuates sclerostin expression to enhance osteoblastogenesis.…”

Section: Periodontitis and Potential Therapiesmentioning

confidence: 99%

Sclerostin regulation: a promising therapy for periodontitis by modulating alveolar bone

Wang²,

Li³

et al. 2020

Chinese Medical Journal

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Periodontitis is one of the most prevalent epidemics affecting human health and life recently, and exploration of the pathogenesis and treatment of periodontitis has been valued by scholars. In recent years, sclerostin, a new factor on bone resorption and reconstruction caused by inflammation and mechanical stimulation, has been a research hotspot. This article summarizes the researches on sclerostin in periodontitis development in recent years. Among them, sclerostin has been shown to be a critical negative regulator of bone formation, thereby inhibiting bone remodeling in periodontitis development, and is closely associated with tooth movement. Besides, evidence indicates that the removal of sclerostin seems to reasonably protect the alveolar bone from resorption. Regulation of sclerostin expression is a novel, promising treatment for periodontitis and addresses several complications seen with traditional therapies; accordingly, many drugs with similar mechanisms have emerged. Moreover, the application prospect of sclerostin in periodontal therapy combined with orthodontic treatment is another promising approach. There are also a lot of drugs that regulate sclerostin. Anti-sclerostin antibody (Scl-Ab) is the most direct one that inhibits bone resorption caused by sclerostin. At present, drugs that inhibit the expression of sclerostin have been applied to the treatment of diseases such as multiple myeloma and osteoporosis. Therefore, the application of sclerostin in the oral field is just around the corner, which provides a new therapeutic bone regulation strategy in oral and general health.

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

Cited by 9 publications

References 32 publications

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Enhanced Oxidative Damage and Nrf2 Downregulation Contribute to the Aggravation of Periodontitis by Diabetes Mellitus

Bioactive Synthetic Peptides for Oral Tissues Regeneration

Sclerostin regulation: a promising therapy for periodontitis by modulating alveolar bone

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