TFOS DEWS III Advancing the understanding and management of dry eye disease

September 3, 2025 Professor Jennifer Craig and Jordan Cooper

The 2007 Tear Film & Ocular Surface Society Dry Eye Workshop (TFOS DEWS)¹ marked a major milestone in standardising the understanding and management of dry eye disease (DED). A decade later, TFOS DEWS II (2017)² expanded on this foundation, supported by widespread global research. Now, TFOS DEWS III represents the next step in this evolution, reflecting the significant scientific advancements since DEWS II, in refining the definition, classification, diagnosis and management of DED.

 

Definition

 

TFOS DEWS III redefines DED as: a multifactorial, symptomatic disease characterised by a loss of homeostasis of the tear film and/or ocular surface, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage and neurosensory abnormalities are aetiological factors.

 

This updated definition acknowledges that tear film and ocular surface homeostasis may be disrupted by various pathophysiological mechanisms, any of which can be present in an individual.

 

Diagnostic methodology

 

Diagnosing DED has long been a clinical challenge. Differential diagnosis is essential to rule out conditions that mimic DED, and a combination of both symptoms and signs should be used to confirm a diagnosis.

 

Symptoms

 

To standardise symptom assessment, TFOS DEWS III recommends use of a single, validated screening tool. While multiple questionnaires have previously been used, a shortened form of the Ocular Surface Disease Index (OSDI), the OSDI-6³ has been selected for its sensitivity, simplicity and practicality in routine care. A score of ≥4 indicates further diagnostic testing is warranted⁴. See https://heiko-pult.de/media/files/OSDI-6-EN-NEW.pdf

 

Signs

 

 

Fig 1. TFOS DEWS III Diagnostic criteria for dry eye

 

 

If symptoms are present, objective markers of tear film homeostasis support a positive diagnosis. An abnormal result in any one of the following three tests confirms DED (Fig 1):

 

1. Non-invasive tear breakup time <10 seconds (or fluorescein tear break up time <5 seconds)
2. Osmolarity (≥308 mOsm/L in either eye or an interocular difference of >8 mOsm/L)
3. Ocular surface staining:  
   1. Cornea: >5 punctate spots and/or
   2. Conjunctiva: >9 punctate spots and/or
   3. Lid margin: ≥2mm length and ≥25% width.

 

Contrasting with TFOS DEWS II – which required all three of these tests to be confident a patient did not have DED – TFOS DEWS III allows for the absence of DED to be confirmed by performing only two clinical tests, provided one of them is comprehensive ocular surface staining (that includes corneal, conjunctival and lid margin staining). Additionally, where non-invasive testing is unavailable, fluorescein tear film breakup time may be used as a proxy, the diagnostic cut-off reduced from 10 to 5 seconds due to better understanding of fluorescein’s impact on tear film stability⁴.

 

TFOS DEWS III Digest

 

The TFOS DEWS III Digest summarises interdisciplinary research across several key areas of DED including epidemiology, pathophysiology, pain and sensation, and sex, gender and hormones. These inform both diagnostic and therapeutic frameworks.

 

Epidemiology

 

DED prevalence varies significantly across populations, reaching up to 62.9% in certain populations⁵. DEWS III classifies risk factors as conclusive or probable risks for DED, categorising them as either modifiable or non-modifiable. Broad categories include demographics, lifestyle/environment, systemic disorders, ocular disorders, medications and iatrogenic factors⁵. Identifying these factors is crucial in both preventing and managing DED.

 

Pathophysiology

 

TFOS DEWS III solidifies distinctions between aqueous deficient and evaporative dry eye. While inflammation is a recognised driver, evaporative dry eye often presents with minimal or no inflammatory markers present in tears⁶. Inflammation should therefore not be assumed to be present in all DED cases, although it may emerge secondarily from stress on the ocualr surface induced by triggering the vicious circle of dry eye. Immune-mediated aetiologies eg. Sjögren’s disease, Stevens-Johnson syndrome and ocular graft versus host disease (GVHD) are associated with more severe disease presentation⁷, where inflammation is a primary mechanism.

 

Pain and sensation

 

The ocular surface is densely innervated with sensory nerves. The TFOS DEWS II pain and sensation report⁸ outlined how trauma, surgery, systemic disease and aging can disrupt corneal nerve architecture, impairing protective reflexes such as blinking and tearing. TFOS DEWS III explores recent findings in corneal nerve modelling and the relevance of the anatomical and functional status of corneal nerves in diagnosing and managing DED⁵.

 

Sex, gender and hormones

 

Sex- and gender-related differences influence susceptibility to DED, as highlighted in TFOS DEWS II⁹ and expanded upon in DEWS III⁵.These differences are attributed to hormones, sex chromosomes, sex-specific autosomal factors, epigenetics, care-seeking behaviours and service utilisation. New findings reveal that androgens, progesterone, thyroid eye disease and insulin/insulin-like growth factor pathways can significantly affect lacrimal gland, meibomian gland, corneal and eyelid function.

 

Subclassification

 

 

Fig 2. After dry eye diagnosis, nine subtypes representing tear film deficiencies, eyelid anomalies and ocular surface abnormalities, are checked and managed as required, to restore tear film and ocular surface homeostasis

 

 

DED commonly arises as a downstream consequence of a range of aetiologies. TFOS DEWS III classifies DED based on aetiological subtypes, aiding targeted management⁴. Broadly, these include tear film component deficiencies, eyelid anomalies, ocular surface abnormalities and systemic conditions. Assessment techniques for each subtype of DED are outlined in the TFOS DEWS III Diagnostic Methodology report.

 

Tear film component deficiencies

 

The tear film consists of lipid, aqueous and mucin components. Deficiencies in lipid or aqueous lead to the well-established evaporative and aqueous deficient dry eye subtypes, respectively. Mucins play a critical role in tear film spread and ocular surface protection¹⁰ and likely arise from secondary ocular surface inflammation leading to cellular damage¹¹.

 

Eyelid anomalies

 

Blinking plays a critical role in tear distribution and debris removal⁴. Abnormal blinking patterns due to lifestyle factors or conditions influencing eyelid function have been implicated in DED development and exacerbation^12,13. Diseases of the eyelid, such as anterior blepharitis and meibomian gland dysfunction (MGD), remain widely recognised as common drivers of DED through microbial overgrowth and impaired lipid secretion, respectively⁴.

 

Ocular surface abnormalities

 

Ocular surface abnormalities include anatomical misalignment (eg. due to pterygium, pinguecula and conjunctivochalasis), abnormal corneal sensitivity and cellular damage, which can hinder tear film production, spread and blinking, leading to a loss of tear film and/or ocular surface homeostasis⁴.

 

Systemic diseases

 

Systemic conditions (eg. autoimmune, inflammatory, metabolic and neural) can significantly impact ocular surface health through inflammation, metabolic dysregulation and ocular surface exposure. This underscores the need for interdisciplinary collaboration where systemic disease drives DED⁴.

 

Management and therapy

 

DED management is rapidly evolving; the TFOS DEWS III Management and Therapy¹⁴ report outlines evidence-based strategies in three concise tables. Management spans low-risk, at-home interventions through to more invasive medical or surgical options, aligned with individual aetiologies.

 

Lifestyle modifications remain paramount across all dry eye subtypes, as outlined in the TFOS Lifestyle reports¹⁵, where they influence not only ocular health, but overall wellbeing and quality of life. Their consideration remains critical in both the development and management of DED.

 

Tear supplementation and stabilisation remain the mainstays of therapy, with growing options to restore, stimulate or stabilise tear film components.

 

TFOS DEWS III discussed the use of artificial tears, where more novel ingredients, such as trehalose and perfluorohexyloctane, offer broader options for tear film stabilisation and ocular surface protection, healing and lubrication. Neurostimulation/neuromodulation targeting the sensory nerves has also been demonstrated to increase tear production^6,16, potentially providing an alternative to artificial tears. Blinking therapy may help to improve spontaneous blinking behaviour and promote lipid secretion and tear film spread¹⁷.

 

A range of pharmacological and naturally derived agents, including anti-inflammatories, blood-derived products and amniotic membrane products, show promise in managing more severe DED.

 

MGD is recognised as a common driver of DED, with many treatments designed to specifically target the eyelids and meibomian glands. Various heat-based, light-based and electrotherapeutic devices increase treatment options available to clinicians¹⁴.

 

In more severe DED that is non-responsive to other management approaches, surgical options may help to address anatomical misalignment, eyelid abnormalities and severe aqueous deficient dry eye¹⁴.

 

Summary

 

TFOS DEWS III represents a significant evidence-based resource and advance in DED clinical care recommendations. By updating definitions, refining diagnostic criteria, describing advances in our understanding of pathophysiological mechanisms and emphasising personalised, evidence-based management, it sets a new benchmark for improving patient outcomes and reducing the global burden of DED.

 

 

References

 

1. Lemp MA, Baudouin C, Baum J, Dogru M, Foulks GN, Kinoshita S, et al. The definition and classification of dry eye disease: Report of the Definition and Classification Subcommittee of the international Dry Eye WorkShop (2007). Ocular Surface. 2007;5:75-92.

2. Craig JP, Nelson JD, Azar DT, Belmonte C, Bron AJ, Chauhan SK, et al. TFOS DEWS II Report Executive Summary. Ocul Surf. 2017;15:802-12.

3. Pult H, Wolffsohn JS. The development and evaluation of the new Ocular Surface Disease Index-6. The ocular surface. 2019;17:817-21.

4. Wolffsohn JS, Benítez-Del-Castillo J, Loya-Garcia D, Inomata T, Iyar G, Liang L, et al. TFOS DEWS III Diagnostic Methodology. American journal of ophthalmology. 2025.

5. Stapleton F, Argüeso P, Asbell P, Azar D, Bosworth C, Chen W, et al. TFOS DEWS III Digest Report. American journal of ophthalmology. 2025.

6. Perumal N, Funke S, Pfeiffer N, Grus FH. Proteomics analysis of human tears from aqueous-deficient and evaporative dry eye patients. Scientific reports. 2016;6:29629.

7. Chotikavanich S, de Paiva CS, Chen JJ, Bian F, Farley WJ, Pflugfelder SC. Production and activity of matrix metalloproteinase-9 on the ocular surface increase in dysfunctional tear syndrome. Investigative ophthalmology & visual science. 2009;50:3203-9.

8. Belmonte C, Nichols JJ, Cox SM, Brock JA, Begley CG, Bereiter DA, et al. TFOS DEWS II pain and sensation report. The ocular surface. 2017;15:404-37.

9. Sullivan DA, Rocha EM, Aragona P, Clayton JA, Ding J, Golebiowski B, et al. TFOS DEWS II Sex, Gender, and Hormones Report. Ocul Surf. 2017;15:284-333.

10. Hori Y. Secreted mucins on the ocular surface. Investigative ophthalmology & visual science. 2018;59:DES151-DES6.

11. You Y, Chen J, Chen H, Wang J, Xie H, Pi X, et al. Investigation of Conjunctival Goblet Cell and Tear MUC5AC Protein in Patients With Graves’ Ophthalmopathy. Translational vision science & technology. 2023;12:19-.

12. Su Y, Liang Q, Su G, Wang N, Baudouin C, Labbé A. Spontaneous eye blink patterns in dry eye: clinical correlations. Investigative ophthalmology & visual science. 2018;59:5149-56.

13. Mitchell T, Murri M, Pflugfelder SC. Video viewing blink rate in normal and dry eyes. Eye & contact lens. 2021;47:442-4.

14. Jones L, Craig JP, Markoulli M, Karpecki P, Akpek EK, Basu S, et al. TFOS DEWS III Management and Therapy Report. American journal of ophthalmology. 2025.

15. Craig JP, Alves M, Wolffsohn JS, Downie LE, Efron N, Galor A, et al. TFOS lifestyle report executive summary: a lifestyle epidemic-ocular surface disease. The ocular surface. 2023;30:240-53.

16. Gumus K, Pflugfelder SC. Intranasal tear neurostimulation: an emerging concept in the treatment of dry eye. International ophthalmology clinics. 2017;57:101-8.

17. Ashwini D, Ramesh SV, Nosch D, Wilmot N. Efficacy of blink software in improving the blink rate and dry eye symptoms in visual display terminal users–A single-blinded randomized control trial. Indian journal of ophthalmology. 2021;69:2643-8.

 

 

Professor Jennifer Craig is head of the Ocular Surface Laboratory in the University of Auckland’s Department of Ophthalmology, was the former chair of the TFOS Lifestyle Workshop and is now the chair (formerly called president) of TFOS DEWS II.

 

Jordan Cooper is a former optometry graduate and current PhD candidate with the OSL, working under the supervision of Professor Jennifer Craig.