Safe and Durable Treatment of Dentin Hypersensitivity via Nourishing and Remineralizing Dentin Based on β-Chitooligosaccharide Graft Derivative.
Bailei LiJiren XuRuixue AiHaixing ZhangMingjun WeiRongqing ZhangChunling BaoWen-Hui WuPublished in: Small (Weinheim an der Bergstrasse, Germany) (2023)
Dentin hypersensitivity (DH) is a common symptom of various dental diseases that usually produces abnormal pain with external stimuli. Various desensitizers are developed to treat DH by occluding dentine tubules (DTs) or blocking intersynaptic connections of dental sensory nerve cells. However, the main limitations of currently available techniques are the chronic toxic effects of chemically active ingredients and their insufficiently durable efficacy. Herein, a novel DH therapy with remarkable biosafety and durable therapeutic value based on β-chitooligosaccharide graft derivative (CAD) is presented. Particularly, CAD indicates the most energetic results, restoring the amino polysaccharide protective membrane in DTs, significantly promoting calcium and phosphorus ion deposition and bone anabolism, and regulating the levels of immunoglobulin in saliva and cellular inflammatory factors in plasma. Exposed DTs are occluded by remineralized hydroxyapatite with a depth of over 70 µm, as shown in in vitro tests. The bone mineral density of Sprague-Dawley rats' molar dentin increases by 10.96%, and the trabecular thickness of bone improves to about 0.03 µm in 2 weeks in the CAD group compared to the blank group. Overall, the ingenious concept that modified marine biomaterial can be a safe and durable therapy for DH is demonstrated by nourishing and remineralizing dentin.
Keyphrases
- bone mineral density
- postmenopausal women
- body composition
- coronary artery disease
- induced apoptosis
- optical coherence tomography
- drug induced
- oxidative stress
- chronic pain
- pain management
- oral health
- stem cells
- spinal cord
- neuropathic pain
- tissue engineering
- signaling pathway
- bone marrow
- endoplasmic reticulum stress
- cell cycle arrest