Tears play a fundamental role in maintaining ocular surface health, ensuring clear vision, and facilitating emotional expression. They are classified into four major types: basal tears, which provide continuous lubrication and protection of the ocular surface; reflex tears, produced in response to external irritants; emotional tears, triggered by strong emotional states; and closed-eye tears, secreted during sleep to remove debris and support ocular homeostasis[1, 2].

The tear film is uniformly spread over the cornea through blinking and ocular movements and comprises four 

anatomical regions: (1) the marginal tear film along the moist eyelid margin posterior to the lipid strip, (2) the portion overlying the palpebral conjunctiva, (3) the portion covering the bulbar conjunctiva, and (4) the precorneal tear film directly covering the cornea. Total tear volume ranges from 5–10 μl with a secretion rate of 1–2 μl/min, of which approximately 95% is produced by the lacrimal gland, with additional contributions from conjunctival goblet cells and accessory lacrimal glands[3].

Structurally, the precorneal tear film consists of three layers:

According to the TFOS DEWS II Definition and Classification Report (2017), dry eye disease (DED) is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, accompanied by ocular symptoms, in which tear film instability, hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles. DED is broadly classified into aqueous-deficient dry eye (ADDE), evaporative dry eye (EDE), or a mixed form[6, 7]. DED is defined as a multifactorial disorder of the tears and ocular surface characterized by tear film instability, visual disturbance, discomfort, elevated tear osmolarity, and ocular surface inflammation. Patients commonly experience irritation, burning, itching, fluctuating vision, foreign-body sensation, redness, and excessive tearing, all of which contribute to impaired visual performance and reduced quality of life[8-10].

This review aims to consolidate current knowledge on tear physiology, dry eye disease, contrast sensitivity impairment, and their collective impact on quality of life, providing an updated and comprehensive understanding of these interrelated concepts.

Study Design

This study was conducted as a narrative review to provide a comprehensive and up-to-date overview of dry eye disease (DED), focusing on tear film stability, contrast sensitivity, and quality of life (QoL). The review aimed to synthesize current evidence regarding the physiology of the tear film, pathophysiology and classification of DED, diagnostic investigations, epidemiology, visual function impairment, and their clinical implications.

Literature Search Strategy

A comprehensive literature search was performed using four electronic databases: PubMed, Web of Science, Google Scholar, and ResearchGate. The search included articles published between January 2017 and March 2025, corresponding to the publication of the Tear Film and Ocular Surface Society Dry Eye Workshop II (TFOS DEWS II) reports and subsequent advances in dry eye research.

The search strategy combined Medical Subject Headings (MeSH) and free-text terms using Boolean operators. The primary search terms included "Dry Eye Disease" OR "DED", "Tear Film", "Tear Film Stability", "TFOS DEWS II", "Contrast Sensitivity", "Visual Function", "Quality of Life" OR "QoL", "Schirmer Test", "Tear Break-Up Time" OR "TBUT", "Non-Invasive Tear Break-Up Time" OR "NIBUT", "Tear Osmolarity", "Ocular Surface Disease", "Dry Eye Epidemiology", "Dry Eye Diagnosis", and "Dry Eye Management".

A representative PubMed search strategy was:

("Dry Eye Disease" OR DED) AND ("Tear Film" OR "Tear Film Stability") AND ("Contrast Sensitivity" OR "Visual Function") AND ("Quality of Life" OR QoL).

Manual screening of the reference lists of selected articles was also performed to identify additional relevant studies that were not retrieved through the electronic database search.

Eligibility Criteria

Inclusion Criteria:

Studies were included if they met the following criteria:

Exclusion Criteria:

The following publications were excluded:

Study Selection

The electronic database search identified 268 records. After removing duplicate records, 214 unique articles remained for title and abstract screening. Following the initial screening, 92 full-text articles were assessed for eligibility based on the predefined inclusion and exclusion criteria. After full-text evaluation, 54 studies met the eligibility criteria and were included in the final narrative review. Reference lists of the included studies were also manually searched to identify additional relevant publications.

Data Extraction

The following information was extracted from each included study:

The extracted data were organized and summarized to facilitate comparison of study characteristics and outcomes.

Data Synthesis

As this was a narrative review, no quantitative meta-analysis or statistical pooling of results was performed. Instead, the evidence was synthesized descriptively under the following themes:

Priority was given to high-quality evidence, including the TFOS DEWS II reports, systematic reviews, meta-analyses, multicenter studies, and recent peer-reviewed clinical research to ensure scientific accuracy and clinical relevance.

Quality Assessment

Since this study was designed as a narrative review, a formal methodological quality assessment or risk-of-bias evaluation of the included studies was not undertaken. However, preference was given to evidence derived from internationally recognized consensus reports, systematic reviews, meta-analyses, and well-designed observational and clinical studies.

Literature Selection Flow

To improve methodological transparency, the study selection process followed the general principles of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The literature identification, screening, eligibility assessment, and final inclusion of studies are illustrated in [Fig. 1].

Tear Physiology and Tear Film Structure

The tear film is essential for maintaining ocular surface homeostasis, providing lubrication, protecting against environmental insults, and maintaining optical quality of the eye. Tears are broadly classified into basal, reflex, emotional, and closed-eye tears, each contributing to ocular surface protection and physiological regulation[1].

Basal tears provide continuous lubrication and nourishment to the corneal epithelium, whereas reflex tears are produced in response to external stimuli such as irritants or foreign bodies and contain increased concentrations of antimicrobial components. Emotional tears are associated with psychological responses, while closed-eye tears contribute to ocular surface maintenance during sleep.

The tear film is distributed over the ocular surface through blinking and consists of marginal tear film, palpebral conjunctival tear film, bulbar conjunctival tear film, and precorneal tear film. The precorneal tear film maintains corneal transparency and consists of three interacting components.

The lipid component, secreted primarily by the meibomian glands, reduces tear evaporation, improves tear film stability, and facilitates smooth eyelid movement. Dysfunction of the meibomian glands contributes significantly to evaporative dry eye disease.

The aqueous component, produced mainly by the lacrimal glands, contains water, electrolytes, proteins, immunoglobulins, lysozyme, lactoferrin, and other protective molecules. Reduced aqueous secretion results in increased tear osmolarity, inflammation, and ocular surface damage.

The mucin component, secreted mainly by conjunctival goblet cells, crypts of Henle, and glands of Manz, transforms the hydrophobic corneal epithelial surface into a hydrophilic surface, allowing uniform tear distribution and lubrication. Alterations in mucin expression contribute to tear film instability and ocular surface disease[1, 3].

Definition and Classification of Dry Eye Disease

According to the TFOS DEWS II Definition and Classification Report (2017), dry eye disease (DED) is defined as a multifactorial disease of the ocular surface characterized by loss of tear film homeostasis, accompanied by ocular symptoms. Tear film instability, hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities are important mechanisms involved in DED development[2].

DED is broadly classified into:

Many patients demonstrate overlapping features of both subtypes. Clinical manifestations include dryness, burning, foreign body sensation, redness, photophobia, fluctuating vision, and excessive tearing. These symptoms may significantly affect visual performance and daily activities such as reading, driving, and digital device use[2, 9, 10].

Clinical Investigations of Dry Eye Disease

Diagnosis of DED requires assessment of both symptoms and objective signs because clinical findings may not always correlate with patient-reported severity.

Tear Film Stability Assessment

Tear film stability is commonly evaluated using Tear Break-Up Time (TBUT) and Non-Invasive Tear Break-Up Time (NIBUT).

Fluorescein-based TBUT measures the interval between a complete blink and the appearance of the first dry spot on the ocular surface. A value of less than 10 seconds generally indicates tear film instability.

NIBUT provides a dye-free assessment of tear stability using technologies such as corneal topography and interferometry. It minimizes the influence of fluorescein application and provides a more physiological assessment of tear dynamics[14].

Tear Secretion Assessment

The Schirmer test remains one of the commonly used methods for evaluating aqueous tear production[27].

Schirmer I measures combined basal and reflex tear secretion, whereas Schirmer II evaluates reflex tearing following nasal stimulation. Schirmer testing with anesthesia primarily assesses basal secretion. Lower Schirmer values indicate reduced aqueous tear production and are associated with aqueous-deficient DED[27, 28].

Ocular Surface Integrity Assessment

Ocular surface damage is assessed using vital dyes including fluorescein, rose bengal, and lissamine green. These tests detect epithelial disruption, punctate epithelial erosions, and areas of increased ocular surface staining, providing important information regarding disease severity[3].

Accurate diagnosis of dry eye disease requires assessment of both patient-reported symptoms and objective clinical signs, as symptoms alone may not always correlate with ocular surface changes. Various diagnostic modalities are used to evaluate tear film stability, aqueous tear production, ocular surface integrity, tear homeostasis, and functional visual impairment. [Table. 1] summarizes the commonly used diagnostic tests for dry eye disease and their clinical significance.

Impact of Dry Eye Disease on Quality of Life

DED affects multiple domains of quality of life, including physical functioning, psychological well-being, independence, and social functioning. The impact of DED extends beyond ocular discomfort and influences daily activities, occupational performance, and emotional health[22].

Patients with DED commonly experience ocular discomfort, burning, foreign body sensation, photophobia, blurred vision, visual fluctuation, eye fatigue, and contact lens intolerance. These symptoms interfere with reading ability, computer use, driving, and other visually demanding activities[11, 22].

Persistent symptoms and visual disturbances associated with DED contribute to psychological stress, frustration, anxiety, and reduced emotional well-being. The chronic nature of the disease and incomplete symptom relief may further increase the emotional burden among affected individuals[23].

DED requires long-term management involving artificial tears, medications, follow-up visits, and lifestyle modifications. Healthcare costs and reduced work 

productivity contribute to a significant socioeconomic burden. Studies indicate that DED negatively affects vision-related mental health and overall quality of life[9, 20, 23, 31].

Contrast Sensitivity and Visual Function in Dry Eye Disease

Contrast sensitivity (CS) represents the ability of the visual system to distinguish differences in luminance between an object and its background. It is essential for functional vision, particularly under low illumination conditions and during activities such as night driving and navigation[25, 26].

DED reduces contrast sensitivity through several mechanisms, including tear film instability causing transient optical degradation, increased higher-order aberrations, and irregular corneal surfaces due to epithelial damage and superficial punctate keratopathy (SPK).

Patients with central corneal staining demonstrate greater reduction in contrast sensitivity due to increased light scattering and optical irregularity. These findings indicate that visual impairment in DED extends beyond conventional visual acuity measurements and contributes to reduced functional vision and quality of life[10, 15, 30, 35].

Prevalence of Dry Eye Disease

The prevalence of dry eye disease (DED) varies widely worldwide, ranging approximately from 5% to 50%, depending on diagnostic criteria, population characteristics, environmental exposure, and study methodology[32-35].

Global estimates suggest considerable variation, with pooled prevalence reported around 11.59% in population-based analyses[36].

Studies from India demonstrate substantial regional variation:

The variability in prevalence reflects differences in diagnostic methods, age distribution, environmental factors, lifestyle patterns, and population characteristics.

Summary of Reviewed Studies

A summary of the included studies is presented in [Table. 2]. The table provides an overview of the key characteristics of the selected literature, including author, year of publication, country, study design, major findings, and clinical significance. The included studies represent evidence related to dry eye disease classification, epidemiology, diagnostic evaluation, contrast sensitivity changes, tear film alterations, and quality-of-life outcomes. This summary facilitates comparison of findings across different populations and highlights the clinical relevance of dry eye disease in terms of visual function and patient-reported outcomes.

Dry eye disease (DED) is a multifactorial ocular surface disorder characterized by disruption of tear film homeostasis, ocular surface inflammation, tear hyperosmolarity, and neurosensory abnormalities. The current understanding of DED has evolved from the traditional classification of aqueous-deficient and evaporative dry eye to a more comprehensive concept described by the TFOS DEWS II report, which emphasizes loss of tear film homeostasis as the central mechanism of disease development and progression[7, 24]. The present narrative review highlights the complex interaction between tear film alterations, visual function impairment, particularly contrast sensitivity reduction, and deterioration in quality of life (QoL).

The tear film plays an essential role in maintaining corneal transparency, lubrication, and optical quality. Alterations in the lipid, aqueous, or mucin components of the tear film can compromise tear distribution and stability, resulting in ocular surface damage and visual disturbances[1, 4, 5]. Tear film instability produces an irregular optical surface that increases light scatter and optical aberrations, leading to fluctuating vision and reduced visual quality[30, 37]. Therefore, patients with DED may experience significant functional visual impairment despite having relatively preserved conventional visual acuity[10, 28].

According to the TFOS DEWS II pathophysiology report, tear hyperosmolarity and inflammation contribute to a self-perpetuating cycle of epithelial damage and further tear film instability[24]. Reduced aqueous secretion, increased evaporation, and meibomian gland dysfunction may initiate this cycle, resulting in inflammatory mediator release, goblet cell dysfunction, and ocular surface compromise[15, 24]. This explains why DED symptoms and clinical signs may persist even when individual diagnostic parameters show variable results.

Tear film instability has a direct influence on optical performance. Studies have demonstrated that ocular surface irregularity in DED patients is associated with increased straylight, reduced contrast sensitivity, and impaired visual quality[34, 37]. Contrast sensitivity represents the ability to detect differences in luminance between objects and their background and is essential for practical visual tasks such as driving, reading, and navigating under low illumination[32, 33]. Reduction in 

contrast sensitivity has been reported in DED patients and correlates with ocular surface damage severity, particularly in individuals with corneal epithelial abnormalities[34-36].

The effect of DED extends beyond ocular discomfort and significantly influences quality of life. Patients commonly report pain, burning sensation, foreign-body sensation, photophobia, fluctuating vision, and difficulty performing daily activities[16, 18]. Chronic symptoms may contribute to psychological stress, frustration, anxiety, and reduced emotional well-being[19]. Previous studies have demonstrated associations between DED, reduced work productivity, impaired reading ability, and decreased vision-related quality of life[20, 22, 23]. These findings indicate that DED should be considered a functional disorder affecting multiple aspects of daily living rather than merely a tear deficiency condition.

The epidemiological burden of DED varies considerably worldwide due to differences in diagnostic criteria, environmental exposure, lifestyle factors, and population characteristics. Age and female sex are consistently identified as important risk factors, possibly due to age-related lacrimal gland dysfunction and hormonal influences on ocular surface homeostasis. Indian studies have reported variable prevalence across different geographical regions, including North India and Western India, suggesting the contribution of environmental conditions, occupational exposure, and lifestyle-related factors.

Diagnosis of DED requires integration of symptoms, clinical signs, and objective investigations. Tear break-up time (TBUT), non-invasive tear break-up time (NIBUT), Schirmer testing, ocular surface staining, and meibomian gland evaluation are commonly used methods for assessing tear film stability and ocular surface status[11, 13, 15]. However, because DED is a heterogeneous disease, no single diagnostic test is sufficient to represent the complete disease profile. A combination of structural, functional, and patient-reported assessments provides a more comprehensive evaluation[7, 21].

Management strategies for DED should be individualized according to underlying mechanisms and disease severity. Current approaches include tear supplementation, lipid-based lubricants, anti-inflammatory therapy, meibomian gland-directed treatments, punctal occlusion, and lifestyle modification[15, 24]. Assessment of functional outcomes such as contrast sensitivity and QoL may provide additional information regarding treatment effectiveness beyond improvement in clinical signs alone[10, 23, 28].

Despite advances in understanding DED, several challenges remain, including variability in diagnostic criteria, limited availability of objective biomarkers, and differences in treatment response among patients. Future research should focus on molecular biomarkers, advanced ocular surface imaging, and long-term evaluation of treatment effects on visual function and quality of life[2, 15]. Large-scale studies using standardized TFOS DEWS II criteria are required to better define disease burden and improve preventive and therapeutic strategies.

Overall, DED represents a complex ocular surface disorder affecting tear film stability, visual performance, and patient well-being. Integration of tear film evaluation, contrast sensitivity assessment, and QoL measurement provide a more complete understanding of disease severity and supports a patient-centered approach to diagnosis and management.

Dry eye disease (DED) is a multifactorial ocular surface disorder involving loss of tear film homeostasis, ocular surface inflammation, tear instability, and visual dysfunction. The present review highlights that DED affects not only ocular comfort but also functional vision, particularly contrast sensitivity, which plays an important role in real-world visual activities despite relatively preserved conventional visual acuity.

Tear film instability, increased tear evaporation, ocular surface irregularity, and inflammatory changes contribute to optical degradation and reduced visual performance. These alterations significantly influence daily activities such as reading, computer use, driving, and occupational tasks, ultimately reducing quality of life. The burden of DED is further increased by psychological stress, reduced productivity, and limitations in daily functioning.

Accurate diagnosis requires a comprehensive approach integrating symptom evaluation, tear film stability assessment, ocular surface examination, and functional visual tests. Early identification and appropriate management targeting tear film stabilization, inflammation control, and modification of risk factors are essential to improve clinical outcomes.

Future research focusing on objective biomarkers, advanced diagnostic technologies, and long-term evaluation of treatment outcomes will further improve understanding and management of DED. Considering its impact on visual function and overall well-being, DED should be recognized as a significant ocular and public health concern requiring a holistic, patient-centered approach.

Authors’ Contributions: Ms. Rashmi conceptualized the study, Dr. R.K. conducted the literature review, drafted the manuscript, and approved the final version Mr. Singh supported during all works.

Funding and Financial Support: No funding was received for this work.

Conflict of Interest: The author declares no conflict of interest.

Informed Consent: Not applicable.