PERSONALITY TRAITS/STATES THAT DETERMINE WOUND HEALING RATES

应激可以通过释放免疫抑制的激素来抑制对伤口早期愈合至关重要的炎症反应。因此，压力可能是伤口愈合率个体差异的重要决定因素。衰老也与伤口愈合所需的组织反应降低有关，例如新陈代谢减少、炎性细胞浸润和成纤维细胞功能。事实上，初步研究表明，在长期应激的照顾阿尔茨海默病患者的老年人中，实验性皮肤伤口愈合慢25%。应激考试时，口腔创伤愈合时间较非应激状态延迟40%。在这两项研究中，一种关键的促炎反应，IL-1β，在应激组的白细胞中显著减少。假设：衰老和心理困扰导致神经内分泌途径失调，尤其是糖皮质激素，抑制了对伤口早期愈合至关重要的炎症反应。如何感知压力源以及个体对感知到的压力源的反应差异可能与压力源的客观特征一样重要。因此，对影响事件评估的压力源和人格属性的分析是至关重要的，因为这些压力源和心理社会因素，如社会支持，增强/缓冲了压力源的感知后果。此外，外周血液反应将反映创伤愈合过程中组织反应的变化，并作为创伤愈合过程中应激下调炎性细胞功能的重要生物标志物。一种快速、愈合、无疤痕的标准化口腔伤口愈合模型将被用来评估压力和老化对伤口愈合的影响。

Stress can inhibit inflammatory responses critical to early wound healing by causing the release of hormones that are immunosuppressive. Thus, stress may be an important determinant in individual variance in wound healing rates. Aging has also been associated with decreased tissue responses required for wound healing, e.g., decreased metabolism, inflammatory cell infiltration and fibroblast function. Indeed, preliminary studies suggest that experimental skin wounds heal 25% slower in chronically stressed, older adults caring for Alzheimer's disease patients. The stress of taking examinations, delayed healing of oral wounds 40% as compared to non-stress conditions. In both of these studies, a key pro- inflammatory response, IL-1beta, was significantly reduced in leukocytes in stressed groups. Hypotheses: aging and psychological distress dysregulate neuroendocrine pathways, particularly glucocorticoids, that inhibit inflammatory responses critical to early wound healing. How stressors are perceived and individual differences in responsiveness to a perceived stressor can be as important as objective features of the stressor. Thus, analyses of the stressors as well as personality attributes that affect the appraisal of events as stressors and psychosocial factors, e.g., social support, that augment/buffer the perceived consequences of the stressor is essential. Furthermore, peripheral blood responses will reflect altered tissue responses during wound healing and serve as important biologic markers for stress down regulation of inflammatory cell function during wound healing. A rapidly, healing, non-scarring standardized oral wound healing model will be used to assess the affects of stress and aging in wound healing.