Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK; Vision and Eye Research Unit, Anglia Ruskin University, Cambridge, UK.
Department of Ophthalmology, Baylor College of Medicine, Houston, TX, USA.
Ocul Surf. 2017 Jul;15(3):438-510. doi: 10.1016/j.jtos.2017.05.011. Epub 2017 Jul 20.
The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease. Its central mechanism is evaporative water loss leading to hyperosmolar tissue damage. Research in human disease and in animal models has shown that this, either directly or by inducing inflammation, causes a loss of both epithelial and goblet cells. The consequent decrease in surface wettability leads to early tear film breakup and amplifies hyperosmolarity via a Vicious Circle. Pain in dry eye is caused by tear hyperosmolarity, loss of lubrication, inflammatory mediators and neurosensory factors, while visual symptoms arise from tear and ocular surface irregularity. Increased friction targets damage to the lids and ocular surface, resulting in characteristic punctate epithelial keratitis, superior limbic keratoconjunctivitis, filamentary keratitis, lid parallel conjunctival folds, and lid wiper epitheliopathy. Hybrid dry eye disease, with features of both aqueous deficiency and increased evaporation, is common and efforts should be made to determine the relative contribution of each form to the total picture. To this end, practical methods are needed to measure tear evaporation in the clinic, and similarly, methods are needed to measure osmolarity at the tissue level across the ocular surface, to better determine the severity of dry eye. Areas for future research include the role of genetic mechanisms in non-Sjögren syndrome dry eye, the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation.
TFOS DEWS II 病理生理学小组委员会审查了与干眼发病和持续相关的机制。其中心机制是蒸发导致的水丢失，从而导致高渗组织损伤。人类疾病和动物模型的研究表明，这种机制无论是直接的还是通过诱导炎症，都会导致上皮细胞和杯状细胞的丧失。由此导致的表面润湿性降低会导致泪膜早期破裂，并通过恶性循环放大高渗性。干眼疼痛是由泪液高渗、润滑丧失、炎症介质和神经感觉因素引起的，而视觉症状则是由泪液和眼表不规则引起的。摩擦力增加会导致眼睑和眼表受损，导致特征性点状上皮角膜炎、上象限性边缘性角膜结膜炎、丝状角膜炎、睑缘平行性结膜皱褶和睑缘擦拭上皮病。混合性干眼，具有水液缺乏和蒸发增加的特征，很常见，应努力确定每种形式对总体情况的相对贡献。为此，需要在临床上测量泪液蒸发的实用方法，同样，也需要测量眼表组织水平的渗透压，以更好地确定干眼的严重程度。未来的研究领域包括遗传机制在非干燥综合征性干眼中的作用、睑板腺疾病终末导管的靶向以及注视动态和闭眼状态对泪液稳定性和眼表炎症的影响。
