The concept of ocular surface disease (OSD) refers to diseases that damage the normal structure and function of the ocular surface of the cornea. Since the ocular surface is a holistic concept, the ocular surface changes caused by any cause should be considered from the ocular surface component system in order to achieve the desired effect in diagnosis and treatment of the disease. The maintenance of ocular surface health is achieved through exogenous factors that provide a stable tear film on the ocular surface and endogenous factors such as the subepithelial stromal microenvironment, which together regulate the function of epithelial stem cells. Lesions in any of these components will cause abnormalities in the corneal and conjunctival surfaces or the tear film, i.e., the ocular surface. Severe tear film instability can lead to lesions of the corneal and conjunctival epithelium and squamous epithelial metaplasia. Lesions of the ocular surface epithelium will also cause abnormalities of the tear film, even in the absence of conjunctival cupped cells in the presence of normal tear volume, which will lead to dry eye. The health of the corneal and conjunctival epithelium depends on the health of the underlying stromal microenvironment and the stability of the tear film covering its surface, and the various influences that lead to corneal conjunctival changes and tear film changes will all lead to ocular surface damage. Thus, ocular surface disease and tear disease need to be functionally integrated and summarized as ocular surface & tear disease. In general, ocular surface tear disease includes all superficial keratoconjunctival, conjunctival and external eye diseases, as well as lacrimal gland and lacrimal tract diseases affecting the tear film. Classification of ocular surface diseases With the increasing understanding of the cells and functions of the ocular surface, it is possible to diagnose some ocular surface abnormalities at the level of living cells. By examining the terminal phenotype of epithelial cells by blot cytology, corneal and conjunctival epithelial lesions can be classified into two main types of ocular surface abnormalities. The first type presents with pathologic non-keratinizing epithelial metaplasia, called squamous metaplasia. This group has a clear etiology and can be diagnosed by a history of previous stem cell damage to the corneal limbus, including chemical injury, Stevens-Johnson syndrome, and ocular aspergillosis. Decreased tear film stability or local concomitant keratoconjunctival inflammation is the main causative factor for corneal epithelial chemosis, while it can lead to loss of cupped cells in the conjunctiva, thereby exacerbating tear film instability. The second type of ocular surface abnormality is characterized by the invasion and replacement of the normal corneal epithelium by the conjunctival epithelium, i.e. “limbal stem cells deficiency”. It does not have a clear past history like the first type of ocular surface dysfunction, but still shows a gradual decrease of limbal stem cells over time. It is thought that the limbal stem cells may be affected by the stromal microenvironment (developmental, hormonal, vascular and inflammatory) in which they are located, leading to abnormal regulation. The main manifestations are varying degrees of conjunctival epithelial ingrowth, vascularization, chronic inflammation, persistent ulceration, destruction of the basement membrane, and invasion of fibroblasts. Clinically, there are two conditions: corneal limbal stem cell deficiency due to injury, such as Stevens-Johnson syndrome or toxic epidermal necrolysis, multiple surgeries or condensation of the corneal limbus, toxicity of antimetabolic drugs, keratoconus due to corneal contact lenses, severe microbial infections, etc. Corneal limbal stem cell deficiency due to abnormal stromal microenvironment, such as congenital absence of iris, genetic endocrine keratoconus due to abnormalities, keratoconus due to neuropathy, keratoconus due to radiation, limbal keratitis or ulceration, chronic keratoconus, pterygium or pseudopterygium, etc. The classification of tear film abnormalities is detailed in section III (dry eye). Principles of treatment of ocular surface diseases The normalcy and stability of the ocular surface is an important guarantee for maintaining corneal transparency. Since the 1980s, as the mechanisms of ocular surface epithelial cell differentiation and trauma healing have been studied, ocular surface reconstruction (ocular surface reconstruction), which aims to restore the integrity of the ocular surface and the normal phenotype of its epithelial cells to facilitate the recovery of vision in the affected eye, has received attention. Ocular surface reconstruction (ocular surface reconstruction) is beginning to receive attention. In a narrow sense, ocular surface reconstruction refers only to the surgical restoration of the epithelial phenotype and stability of the ocular surface, but in fact there are five inseparable factors that maintain the normal function of the ocular surface: normal phenotype of the conjunctival and corneal epithelium; normal anatomy and function of the stem cells of both epithelium; the ability to produce and maintain a normal and stable tear film; normal anatomy and physiological function of the eyelid to protect the ocular surface and maintain normal fluid dynamics of the tear film; and the associated innervation and reflexes. The associated innervation and reflexes must be normal. Therefore, reconstructive surgery of the ocular surface in the broadest sense should include the following: reconstructing the epithelium or stem cells of the ocular surface; reconstructing tear production or tear film stability; protecting or restoring the associated innervation of the ocular surface; and reconstructing the anatomy and function of the eyelid. The corresponding therapeutic measures are derived from this: blepharoplasty – to restore normal eyelid closure; corneal limbal grafting or corneal limbal stem cell transplantation – to restore normal limbal stem cell function; conjunctival capsuloplasty (including amniotic membrane graft, amniotic membrane graft plus conjunctival graft, and allogeneic conjunctival graft) – to formation of a normal conjunctival capsule. With the restoration of normal ocular surface structure through these comprehensive measures, the success rate of rejuvenating corneal transplantation is greatly improved. Reconstructive ocular surface surgery can be divided into four categories: conjunctival ocular surface reconstruction, corneal ocular surface reconstruction, tear film reconstruction, and eyelid reconstruction, depending on the purpose of the surgery. When performing ocular surface reconstruction surgery, the indications should be correctly grasped, and healthy ocular surface epithelium, especially the source site of ocular surface stem cells, should be preserved as much as possible to avoid medical source damage; at the same time, necrotic or inflammatory reactive diseased tissues should be completely removed to provide a healthy growth environment for epithelial cells. Another important prerequisite for corneal and conjunctival reconstruction is the general normalization of the tear film. In severe dry eye and tear film instability, the ocular surface epithelium is dry and detached, squamous epithelialization, delayed regeneration, or even corneal thinning and corneal stromal ulceration, and any corneal and conjunctival transplantation reconstructive surgery will face a failed fate. Therefore, dry eyes should be improved by certain therapeutic measures first in order to prepare for later corneal and conjunctival reconstructions. In conclusion, the cornea, conjunctiva and tear film and their corresponding influencing elements should be considered as a holistic concept in the process of ocular surface reconstruction. When reconstructing the ocular surface, the interplay between the cornea, conjunctiva and tear film, the origin of the ocular surface epithelium, the microenvironmental condition of the graft bed and the stability or otherwise of the tear film should be fully considered. Any mishandling and delay may affect the success of ocular surface reconstruction.