Dry eye disease (DED) is caused by tear film instability, ocular surface inflammation and damage, increased osmotic pressure, and neurosensory abnormalities

The meibomian glands are a type of sebaceous gland that is vertically arranged within the upper and lower tarsal plates (Miyake et al, 2017). Dry eye disease (DED) is caused by tear film instability, ocular surface inflammation and damage, increased osmotic pressure, and neurosensory abnormalities (Yu et al., 2021).

Meibomian is composed of phospholipids, cholesterol, wax esters, and cholesterol esters. The study further highlighted that meibomian is responsible for tear film stability and provides protection of the ocular surface against microbial agents. However, functional abnormalities may be experienced where the gland may not produce the required quantity and quality. Environmental stress, stem cell renewal, and aging lead to the risk of MGD (Chhadva et al., 2017). The abnormalities can lead to tear hyperosmolarity, tear evaporation, and ocular surface staining. Chhadva et al. (2017) found that the meibomian gland plays a significant role in the ocular surface. However, the authors did not highlight how to manage the dysfunction.

The quality of life of a patient is affected due to progressing disturbance in vision. Increase in disease prevalence is a major concern that should be addressed through interventions. Air pollution, dryness, allergy, smoke, and UV light are factors that affect tear osmolarity and tear film (Heidari et al., 2019).

Fakih et al. (2019) found that cornea injury is associated with inflammation and hypersensitivity because of the disturbances of the cornea nerves. However, the authors acknowledged that the study was limited in the efficient removal of functional glands for the model.

Rusciano et al. (2018) found that lactoferrin and mimetic lactobionic acid are effective in the management of dry eye among the aging. The authors highlighted that the treatment involves the etiology of the management of the ocular surface. Therefore, dry eye pathogenesis is paramount in avoiding adverse outcomes of the infection. Rusciano et al. (2018) reported that the damaged epithelial cells trigger the inflammatory mediators in the tear film. The instability may cause irritation, and the vicious cycle may start. The study suggested that lactobionic acid is used to prevent dry eye because of its high retention capacity and moisturizing ability. These benefits are effective towards enhancing the ocular surface towards the prevention of DED.

The pathospsychological mechanisms of DED are likely to be continuous, where the patient may experience adverse outcomes. Tear hyperosmolarity and tear film instability are the critical mechanisms in DED (Ganesalingam et al., 2019). These aspects induce the release of inflammatory mediators into the tear fluid, and inflammatory cascades are initiated. The authors found that Apoptosis death, goblet loss cell, and reduced mucus secretion are the factors that cause injury to the cornea. The stress on the immune system triggers the inflammatory mediators at the ocular surface. Chemokines and cytokines are the molecular mediators involved in the development of DED (Ganesalingam et al., 2019). The authors further argued that cytokines mediate intercellular communication while chemokine regulates the migration of immune cells.
Moreover, DED is associated with inflammation of the lacrimal glands, meibomian glands, cornea, aqueous tears, and conjunctiva (Yamaguchi, 2018). The inflammation is likely to be triggered by intrinsic and extrinsic factors.

Aragona et al. (2021) reported that transmembrane and secretory mucins facilitate the contact of tear fluid and epithelial cells, which may later cause instability. The study further argued that friction causes epithelial malfunction leading to the irritation of the ocular surface. These aspects enhance the continuation of the tear film stability, increased inflammation reaction, and reduced nerve-ending protections. However, the immunological process may be experienced because of the provocation of the inflammatory cells. Aragona et al. (2021) further suggested that adaptive immunological reaction is experienced because of prolonged exposure to the stimuli. The patient may experience chronic diseases because the immune system may have challenges in managing the infection.

Similarly, Matossian et al. (2019) argued that the loss of tear film is the central factor for DED pathogenesis. Hyperosmolarity occurs due to ocular discomfort, dryness, and visual disturbances that may lead to tearing film instability. The study further argued that hormonal cycles for women affect ocular function, structure, and health. The cycles are driven by the menstruation, pregnancy, and menopause that are likely to be experienced among women. The androgens and estrogens are sex steroids that affect the production of tears (Matossian et al., 2019). The immune system in the ocular surface is challenged because of the presence of sex steroids. Gender must be considered in the etiology of DED and may be enhanced through the pathogenesis process. The study suggested that the diagnosis of the disease at the early stages of life helps in improving the quality of life.
Eyelid notches are caused by the thickening and rounding of the lid margin (Aragona et al., 2021). Tear distribution and lipid layers are affected by the congruity leading to the impairments of the glands. The study further argued that the influence on tear lipids is one of the major causes of inflammation and infection. However, the study did not highlight the role of nerves in maintaining ocular surface homeostasis and inducing the inflammatory process. The factors that contribute to the vicious cycle must be treated towards enhancing individualized treatment approaches. On the other hand, Arita et al. (2021) proposed a strategy that can be used to manage MGD based on non-invasive meibography. The authors highlighted that the treatment should include ocular surface symptoms, meibum grade, lid margin abnormalities, and ocular surface staining. The understanding of these aspects may play a significant role in addressing the pathogenesis of DED. Arita et al. (2021) argued the non-pharmacological treatment of MGD includes thermal pulsation therapy, intraductal probing, and intense pulsed light. The treatment must be evaluated based on the non-invasive meibography grading. The authors acknowledged that the study did not consider the previous treatment of the patient. However, the understanding of the meiboscore can help enhance future treatments.
Antibiotics, non-steroids, essential fatty acids, steroids, intense pulsed light therapy, and hormonal therapy are effective in the treatment of MGD (Villani et al., 2020; Sabeti et al., 2020). MGD can lead to evaporative dry eye, and the eye care providers are likely to experience the condition. Increased meibum concentration in the sphingolipid metabolite ceramide leads to the instability of the tear film lipid layer (Sabeti et al., 2020). These aspects can affect the ocular surface because the vicious cycle may be experienced. However, medical management is vital and effective towards enhancing positive outcomes in the management of MGD. MGD diagnosis can help enhance the treatment of dysfunction towards enhancing the quality of life (Villani et al., 2020). These interventions are vital in the management of DED at the pathogenesis stage towards achieving the desired outcomes.
Baudouin et al. (2016) argued that Meibomian gland disfucintion (MGD) is the most common cause of DED. The dysfunction is associated with tear film instability and inflammation leading to the onset of DED. The study suggested that MGD is triggered by a deficiency in meibomian secretion and is often classified by obstruction. The changes affect the tear film, which may lead to inflammation and eye irritation. Eye surgery and hormonal therapy such as estrogen and anti-androgen are some of the factors that lead to the onset of MGD (Baudouin et al., 2016). The dysfunction involves pathophysiology mechanisms such as microbial factors, lipid deficiency, and inflammation. Baudouin et al. (2016) reported that meibomian absence leads to lipid content reduction in the tear film. The lipid deficiency promotes increased tear evaporation, inflammation, and hyperosmolarity.
Meibomian gland dysfunction is one of the causes of DED because it regulates the defense genes (Yu et al., 2021). The anti-inflammatory and anti-infection factors may be experienced, leading to adverse impacts on the eyes. Baudouin et al. (2016) reported that the pathophysiological mechanism of MGD can be used in treatment interventions. The treatment may play a significant impact in the reduction of the risk of dry eye disease. Lipid abnormalities associated with MGD can lead to tear instability, thus causing dry eye (Yamaguchi, 2018). Li et al. (2020) suggested that lipid layer thickness increases with age. Therefore, the elderly are likely to experience MGD that may later lead to dry eye.