Cummins Diane
Colgate-Palmolive Technology Center, Piscataway, NJ, USA.
J Clin Dent. 2009;20(1):1-9.
This paper provides an overview of the current knowledge of diagnosis, epidemiology, etiology, and clinical management of dentin hypersensitivity. It summarizes technical approaches to relieve sensitivity in professional and home-use products, with emphasis on the clinical evidence for the efficacy of desensitizing toothpaste, and introduces a new innovative dentifrice technology containing 8% arginine, calcium carbonate, and 1450 ppm fluoride. Dentin hypersensitivity is characterized by short, sharp pain arising from exposed dentin in response to external stimuli which cannot be ascribed to any other form of dental defect or disease. The hydrodynamic theory proposes that pain-producing stimuli cause a change in dentin fluid flow that activates intra-dental nerve fibers, via a mechanoreceptor response, to cause pain. To be hypersensitive, dentin must be exposed and dentin tubules must be open to external stimuli and patent at the pulp. Gingival recession is the primary cause of dentin exposure, and a major predisposing factor for dentin hypersensitivity. Dentin hypersensitivity is a prevalent condition. It has been reported to afflict 15-20% of the adult population, typically 20 to 50-year-olds, with peak incidence between 30 and 39 years. Some studies have reported higher prevalence levels of up to 57%. The incidence of dentin hypersensitivity is expected to rise with changing diets, and as caries and periodontal disease prevention result in improved oral health status, and retention and functionality of the dentition. Treatments to relieve dentin hypersensitivity are based on interruption of the neural response to pain stimuli or occlusion of open tubules to block the hydrodynamic mechanism. Effective and robust dentin occlusion offers the greatest prospect for instant and lasting relief of dentin hypersensitivity. In particular, materials which can coat exposed dentin surfaces, in addition to plugging and sealing open dentin tubules, offer the intriguing prospect of strengthening dentin and rendering it less susceptible to predisposing factors, while concurrently reducing dentin hypersensitivity. Clinical studies have shown that a new toothpaste containing 8% arginine, calcium carbonate, and 1450 ppm fluoride as sodium monofluorophosphate offers significantly increased efficacy in reducing sensitivity, compared to a market-leading toothpaste containing 2% potassium ion. Mechanism of action studies have shown that this technology physically seals dentin tubules with a plug that contains arginine, calcium carbonate, and phosphate. This plug, which is resistant to normal pulpal pressures and to acid challenge, effectively reduces dentin fluid flow and, thereby, reduces sensitivity.
本文概述了目前关于牙本质过敏症的诊断、流行病学、病因及临床管理的知识。总结了专业产品和家用产品中缓解牙本质过敏症的技术方法，重点阐述了脱敏牙膏疗效的临床证据，并介绍了一种含有8%精氨酸、碳酸钙和1450 ppm氟（以单氟磷酸钠形式存在）的新型创新牙膏技术。牙本质过敏症的特征是暴露的牙本质对外部刺激产生短暂、尖锐的疼痛，且这种疼痛不能归因于任何其他形式的牙齿缺损或疾病。流体动力学理论认为，产生疼痛的刺激会导致牙本质液流动发生变化，通过机械感受器反应激活牙髓内神经纤维，从而引起疼痛。要出现过敏症状，牙本质必须暴露，牙本质小管必须对外部刺激开放且与牙髓相通。牙龈退缩是牙本质暴露的主要原因，也是牙本质过敏症的一个主要诱发因素。牙本质过敏症是一种普遍存在的病症。据报道，它影响15%至20%的成年人口，通常为20至50岁人群，发病率高峰在30至39岁之间。一些研究报告的患病率更高，可达57%。随着饮食结构的变化，以及龋齿和牙周病预防措施使口腔健康状况改善、牙列保留及功能增强，牙本质过敏症的发病率预计会上升。缓解牙本质过敏症的治疗方法基于中断对疼痛刺激的神经反应或封闭开放的小管以阻断流体动力学机制。有效且稳固的牙本质封闭为即时且持久缓解牙本质过敏症提供了最大的可能性。特别是，除了堵塞和密封开放的牙本质小管外，还能覆盖暴露牙本质表面的材料，有望强化牙本质，使其不易受到诱发因素影响，同时降低牙本质过敏症。临床研究表明，与一种含2%钾离子的市场领先牙膏相比，一种含有8%精氨酸、碳酸钙和1450 ppm氟（以单氟磷酸钠形式存在）的新型牙膏在降低牙本质过敏症方面疗效显著提高。作用机制研究表明，该技术通过含有精氨酸、碳酸钙和磷酸盐的塞子物理性封闭牙本质小管。这种塞子能抵抗正常的牙髓压力和酸侵蚀，有效减少牙本质液流动，从而降低过敏症状。
