Ocular rosacea is the ocular type (subtype IV) of rosacea, a chronic inflammatory skin disease 1). It is characterized by telangiectasia, blepharitis, meibomian gland dysfunction (MGD), and keratitis, causing chronic inflammation of the ocular surface.
The global prevalence of rosacea is approximately 5.5%, and ocular symptoms are observed in 58–72% of patients 1). The typical age of onset is 25–55 years, and it is more commonly diagnosed in women. It is more frequent in Fitzpatrick skin types I–II (fair skin), but also occurs in individuals with darker skin 1).
Skin findings precede ocular symptoms in 53% of cases, simultaneous onset occurs in 27%, and ocular findings precede skin findings in 20% of cases 1). Therefore, it is important to recognize that ocular rosacea can develop even without skin symptoms. Pediatric cases (pediatric blepharokeratoconjunctivitis) have also been reported 1).
Ocular findings precede skin findings in about 20% of all cases 1). Even without typical skin symptoms such as facial erythema or telangiectasia, it can present as chronic blepharitis or meibomian gland dysfunction. If ocular surface symptoms persist, the possibility of ocular rosacea should be considered.
The subjective symptoms of ocular rosacea are nonspecific and require differentiation from dry eye 1).
Symptoms tend to progress over time with repeated exacerbations and remissions 1). The severity of skin symptoms does not necessarily correlate with the severity of ocular symptoms.
Eyelid Findings
Telangiectasia of the eyelid margin: Present in 50–94% of cases. Accompanied by erythema 1).
Meibomian gland dysfunction: Present in up to 92% of cases. Secretion of thickened, cloudy meibum. Obstruction of gland openings.
Recurrent chalazion and hordeolum: Secondary to meibomian gland dysfunction.
Conjunctival and Corneal Findings
Conjunctival injection: Redness of the bulbar conjunctiva. May be accompanied by follicular and papillary reactions 1).
Corneal lesions: Occur in 25–50% of cases. May progress from superficial punctate keratitis to marginal infiltration, neovascularization, ulceration, and perforation 1).
Corneal scarring: Persistent inflammation involving the visual axis can cause visual impairment.
Rare Findings
Morbihan syndrome: Indolent edema of the forehead, nose, glabella, cheeks, and periorbital area. Accompanied by lymphedema 5).
Rhinophyma: Late-stage skin finding. Thickening, nodularity, and fibrosis of the skin.
Non-invasive meibography is useful for morphological assessment of the meibomian glands. Meibography is the only method to observe meibomian gland structures in vivo using transillumination of the eyelids.
The exact cause of ocular rosacea is unknown, but it involves a combination of immune dysfunction, vascular dysregulation, microbial factors, and genetic predisposition 1).
Prolonged exposure to ultraviolet light, consumption of alcohol and caffeine, spicy foods and hot drinks, mental stress, intense exercise, and exposure to extreme temperatures and wind are typical exacerbating factors. These promote vasodilation and inflammation, triggering symptom recurrence. Since triggers vary by individual, keeping a daily log to identify personal triggers is recommended.
Ocular rosacea is a clinical diagnosis; there are no specific diagnostic tests1). The 2019 Global ROSacea COnsensus (ROSCO) panel recommends a comprehensive diagnostic approach1).
Differential diagnosis is necessary with dry eye syndrome, bacterial/allergic conjunctivitis, seborrheic blepharitis, herpes simplex keratitis, systemic lupus erythematosus, Sjögren’s syndrome, and others 1). Ocular rosacea should be suspected when there is poor response to standard blepharitis treatment 6).
Treatment of ocular rosacea is recommended with a stepwise approach based on severity 1). The ROSCO International Panel, the National Rosacea Society Expert Committee, and the Swiss treatment guidelines provide treatment recommendations.
Mild
Eyelid hygiene: Eyelid cleansing with non-irritating soap, warm compresses, massage 1).
Artificial tears: May contain preservatives.
Avoidance of exacerbating factors: UV protection, dietary guidance.
Omega-3 fatty acids: EPA 720 mg + DHA 480 mg/day 1).
Moderate
Azithromycin eye drops 1–1.5%: Twice daily for 2 days, or once daily for 5 days 1).
Cyclosporine eye drops 0.05–0.1%: Twice daily. Can be used long-term1).
Tacrolimus eye drops 0.03%: Twice daily1).
Steroid eye drops: Short-term use for active inflammation.
Severe
Oral doxycycline: Initial 100 mg 1–2 times/day → maintenance 40 mg/day. 12 weeks1).
Oral azithromycin: 500 mg once daily for 3 days, or once weekly for 3 weeks1).
Systemic cyclosporine: Reserved for refractory cases1).
IPL + MGX: Consider for moderate to severe cases.
In children, oral erythromycin or metronidazole is used1).
| Drug | Dosage | Notes |
|---|---|---|
| Doxycycline | 40–100 mg/day | First-line. Efficacy proven in RCTs1) |
| Azithromycin | 500 mg/day × 3 days | For tetracycline intolerance |
| Minocycline | 100 mg/day × 12 weeks | Alternative to doxycycline |
Demodex removal with eyelid wipes containing terpinen-4-ol (T4O) is effective.
Yin et al. (2021) reported a case of a 72-year-old woman with refractory rosacea-related blepharitis over 5 years, treated with T4O wipes 4). Facial and eyelid erythema markedly improved within 1 month, and telangiectasia disappeared within 2 months. The OSDI score improved from 37 to 15, and complete Demodex eradication and symptom resolution were maintained over 8 months of follow-up.
In a systematic review by Shergill et al. (2024), IPL + MGX combination resulted in partial response in 91% (89/98) of cases 3). No complete remission was observed, but the frequency and severity of dry eye symptoms and eyelid margin redness were reduced. The Toyos protocol, consisting of 3–4 sessions at 4–6 week intervals, is commonly used.
Deep anterior lamellar keratoplasty (DALK) is recommended when corneal scarring involves the visual axis 1). Full-thickness corneal transplantation often has poor prognosis due to corneal neovascularization and chronic inflammation. Conjunctival flap, Tenon patch graft, and tissue adhesive are used for corneal perforation 1).
IPL (Intense Pulsed Light) therapy is a treatment that uses pulsed light from a flash lamp applied to the face to improve meibomian gland secretion, reduce inflammation, and eliminate Demodex. It is performed with a protective shield placed over the eyelids, without direct irradiation of the eyelids. Typically, 3 to 4 sessions are conducted at intervals of 4 to 6 weeks. For details, refer to the IPL therapy section in Standard Treatments.
Ocular rosacea is a chronic disease, and complete cure is difficult. The goal of treatment is to control symptoms and prevent complications. With continued eyelid hygiene and avoidance of exacerbating factors, a stable condition can often be maintained, but flare-ups of inflammation require appropriate medication.
The pathophysiology of ocular rosacea is a chronic inflammation involving complex interactions of excessive activation of the innate immune system, neurovascular dysregulation, and meibomian gland dysfunction1)2).
Overexpression of TLR2 in keratinocytes plays a central role1)2). TLR2 activates the NF-κB signaling pathway, inducing the production of inflammatory cytokines such as IL-1β, TNF-α, IL-6, and IL-8. At the same time, it promotes the production of cathelicidin LL-37 via the serine protease KLK52).
LL-37 maintains chronic inflammation through the following combined actions:
In the tear fluid of patients with ocular rosacea, concentrations of IL-1α/β, MMP-8, and MMP-9 are elevated2). IL-1α promotes the production and activation of MMP-9, causing irritation symptoms of the eyelids and ocular surface, corneal epithelial defects, corneal ulcers, and corneal neovascularization2). The lower the tear clearance, the higher the concentration of these inflammatory factors.
MGD is defined as “a diffuse chronic abnormality of the meibomian glands, characterized by terminal duct obstruction and/or qualitative or quantitative changes in glandular secretion.” Obstruction occurs due to hyperkeratinization of the ductal epithelium and increased viscosity of meibum, leading to gland dropout, atrophy, and decreased secretion 2). Reduction of the lipid layer promotes tear evaporation, causing evaporative dry eye.
Meibomian gland dysfunction is broadly classified into hyposecretory and hypersecretory types, each with primary and secondary forms.
Demodex folliculorum and D. brevis parasitize sebaceous glands. In rosacea patients, they are present at higher densities than in normal skin, activating TLR2 and enhancing innate immune responses 4). Superantigens produced by the commensal bacterium Bacillus oleronius activate CD4+ T cells and macrophages via IL-8 and IL-12p70 production, promoting Langerhans cell infiltration 4). Demodex also increases the production of lipases and esterases, promoting lipid breakdown of meibum and worsening meibomian gland dysfunction.
A review by Mohamed-Noriega et al. (2025) reports that with advances in understanding immune dysregulation and microbiome changes, exploration of targeted therapies including biologics and small molecule inhibitors is progressing 1). Specific drug names and clinical trial results have not yet been sufficiently accumulated.
It has been suggested that gut dysbiosis may be involved in the exacerbation and recurrence of rosacea 1). Elucidation of inflammatory pathways via the gut-eye axis may lead to the discovery of new therapeutic targets.
Genome-wide association studies (GWAS) have reported that single nucleotide polymorphisms in HLA-DRA, BTNLA2, HLA-DRB1*03:01, etc., are associated with rosacea 1). Elucidation of genetic predisposition may form the basis for personalized treatment.
Anti-VEGF eye drops or subconjunctival injections are being considered for the management of corneal neovascularization 1). Fine-needle diathermy for existing telangiectasias has also been reported as an option.
