A study conducted in November of 2017, conveyed a correlation between blepharitis and early onset metabolic syndrome (MetS). To investigate the relationship between blepharitis and MetS, researchers used the Longitudinal Health Insurance Database in Taiwan. Results indicated that hyperlipidaemia and coronary artery disease were significantly correlated with the prior development of blepharitis. Therefore, blepharitis was shown to be significantly related to MetS and can serve as an early indication of the condition.

In another recent study, the presence of Demodex has been unveiled as a common cause of blepharitis. However, the pathogenesis of demodicosis is still unclear. In this study, researchers provide a diagnosis of the disease and propose diagnostic criteria of Demodex blepharitis.

Trichiasis in dogs is hair from the eyelid growing in the wrong direction and rubbing on the eye, causing irritation. It usually occurs at the lateral upper eyelid, especially in the English Cocker Spaniel. Trichiasis also refers to hair from a nasal fold rubbing on the eye. This type of trichiasis can be flattened by rubbing petroleum jelly onto it, but surgery is sometimes necessary for permanent correction.

Trichiasis (, or , ) a medical term for abnormally positioned eyelashes that grow back toward the eye, touching the cornea or conjunctiva. This can be caused by infection, inflammation, autoimmune conditions, congenital defects, eyelid agenesis and trauma such as burns or eyelid injury. It is the leading cause of infectious blindness in the world.

Standard treatment involves removal or destruction of the affected eyelashes with electrology, specialized laser, or surgery. In many cases, removal of the affected eyelashes with forceps resolves the symptoms, although the problem often recurs in a few weeks when the eyelashes regrow. Severe cases may cause scarring of the cornea and lead to vision loss if untreated. Mild cases may not require treatment.

Repeated cases of trachoma infection may cause trichiasis.

Posterior misdirection of normal lashes most frequently affects lower lid.

The mechanism by which the bacteria causes symptoms of blepharitis is not fully understood and may include direct irritation of bacterial toxins and/or enhanced cell-mediated immunity to S. aureus.

Staphylococcal blepharitis is caused by an infection of the anterior portion of the eyelid by Staphylococcal bacteria. In a study of ocular flora, 46% to 51% of those diagnosed with staphylococcal blepharitis had cultures positive for Staphylococcus aureus in comparison to 8% of normal patients. Staphylococcal blepharitis may start in childhood and continue into adulthood. It is commonly recurrent and it requires special medical care. The prevalence of Staphylococcus aureus in the conjunctival sac and on the lid margin varies among countries, likely due to differences in climate and environment. Seborrheic blepharitis is characterized by less inflammation than Staphylococcal blepharitis; however, it causes more excess oil or greasy scaling. Meibomian Gland Dysfunction is a result of abnormalities of the meibomian glands and altered secretion meibum, which plays an imperative role in lagging the evaporation of tear films and smoothing of the tear film to produce an even optical surface. Posterior blepharitis is an inflammation of the eyelids, secondary to dysfunction of the meibomian glands. Like anterior blepharitis, it is a bilateral chronic condition and may be associated with skin rosacea. There is growing evidence that, in some cases, it is caused by Demodex mites.

Punctate epithelial erosions may be seen with different disorders:

- Rosacea

- Dry-eye syndrome

- Blepharitis

- Acute bacterial conjunctivitis

- Trauma

- Exposure keratopathy from poor eyelide closure

- Ultraviolet or chemical burn

- Contact lens-related disorder such as toxicity or tight lens syndrome

- Trichiasis

- Entropion or ectropion

- Floppy eyelid syndrome

- Chemotherapy i.e. cytosine arabinoside

- Thygeson's Superficial Punctate Keratopathy

Trachoma is caused by "Chlamydia trachomatis", serotypes (serovars) A, B, and C. It is spread by direct contact with eye, nose, and throat secretions from affected individuals, or contact with fomites (inanimate objects that carry infectious agents), such as towels and/or washcloths, that have had similar contact with these secretions. Flies can also be a route of mechanical transmission. Untreated, repeated trachoma infections result in entropion—, the inward turning of the eyelids, which may result in blindness due to damage to the cornea. Children are the most susceptible to infection due to their tendency to get dirty easily, but the blinding effects or more severe symptoms are often not felt until adulthood.

Blinding endemic trachoma occurs in areas with poor personal and family hygiene. Many factors are indirectly linked to the presence of trachoma including lack of water, absence of latrines or toilets, poverty in general, flies, close proximity to cattle, crowding, and so forth. However, the final common pathway seems to be the presence of dirty faces in children, facilitating the frequent exchange of infected ocular discharge from one child’s face to another. Most transmission of trachoma occurs within the family.

Due to the different underlying causes, proper diagnosis, treatment, and prognosis can only be determined by an eye care professional. Punctate epithelial erosions may be treated with artificial tears. In some disorders, topical antibiotic is added to the treatment. Patients should discontinue contact lens wear until recovery.

Environmental improvement: Modifications in water use, fly control, latrine use, health education, and proximity to domesticated animals have all been proposed to reduce transmission of "C. trachomatis". These changes pose numerous challenges for implementation. It seems likely that these environmental changes ultimately impact on the transmission of ocular infection by means of lack of facial cleanliness. Particular attention is required for environmental factors that limit clean faces.

A systematic review examining the effectiveness of environmental sanitary measures on the prevalence of active trachoma in endemic areas showed that usage of insecticide spray resulted in significant reductions of trachoma and fly density in some studies. Health education also resulted in reductions of active trachoma when implemented. Improved water supply did not result in a reduction of trachoma incidence.

Causes of epiphora are any that cause either overproduction of tears or decreased drainage of tears, resulting in tearing onto the cheek. This can be due to ocular irritation and inflammation (including trichiasis and entropion) or an obstructed tear outflow tract which is divided according to its anatomical location (i.e. ectropion, punctal, canalicular or nasolacrimal duct obstruction). The latter is often due to aging (a spontaneous process), conjunctivochalasis, infection (i.e. dacryocystitis), rhinitis, and in neonates or infants, failure of the nasolacrimal duct to open. Another cause could be poor reconstruction of the nasolacrimal duct system after trauma to the area. Cause of trauma could be facial fractures (including nasoethmoid fractures or maxillary Le Fort fractures), and soft tissue trauma involving the nose and/or the eyelid.

This condition is often frustrating or irritating. A systematic review studying the usage of punctal plugs for treatment of dry eye reported a few cases of epiphora among participants.

Corneal ulcers are a common human eye disease. They are caused by trauma, particularly with vegetable matter, as well as chemical injury, contact lenses and infections. Other eye conditions can cause corneal ulcers, such as entropion, distichiasis, corneal dystrophy, and keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa, and chlamydia:

- Bacterial keratitis is caused by "Staphylococcus aureus", "Streptococcus viridans", "Escherichia coli", "Enterococci", "Pseudomonas", "Nocardia", "N. Gonorrhoea" and many other bacteria.

- Fungal keratitis causes deep and severe corneal ulcer. It is caused by "Aspergillus" sp., "Fusarium" sp., "Candida" sp., as also "Rhizopus", "Mucor", and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen.

- Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual.

- Protozoa infection like "Acanthamoeba keratitis" is characterized by severe pain and is associated with contact lens users swimming in pools.

- "Chlamydia trachomatis" can also contribute to development of corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and trichiasis (inturning of eyelashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.

Epiphora is an overflow of tears onto the face. A clinical sign or condition that constitutes insufficient tear film drainage from the eyes in that tears will drain down the face rather than through the nasolacrimal system.

Topical antibiotics are used at hourly intervals to treat infectious corneal ulcers. Cycloplegic eye drops are applied to give rest to the eye. Pain medications are given as needed. Loose epithelium and ulcer base can be scraped off and sent for culture sensitivity studies to find out the pathogenic organism. This helps in choosing appropriate antibiotics. Complete healing takes anywhere from about a few weeks to several months.

Refractory corneal ulcers can take a long time to heal, sometimes months. In case of progressive or non-healing ulcers, surgical intervention by an ophthalmologist with corneal transplantation may be required to save the eye. In all corneal ulcers it is important to rule out predisposing factors like diabetes mellitus and immunodeficiency.

The mortality for toxic epidermal necrolysis is 25-30%. People with SJS or TEN caused by a medications have a better prognosis the earlier the causative medication is withdrawn. Loss of the skin leaves patients vulnerable to infections from fungi and bacteria, and can result in sepsis, the leading cause of death in the disease. Death is caused either by infection or by respiratory distress which is either due to pneumonia or damage to the linings of the airway. Microscopic analysis of tissue (especially the degree of dermal mononuclear inflammation and the degree of inflammation in general) can play a role in determining the prognosis of individual cases.

Of note, this scoring system is most valuable when used on the first and third day of hospitalization, and it may underestimate mortality in patients with respiratory symptoms.

Acquired hypertrichosis lanuginosa is commonly present with cancer. This condition is also linked to metabolic disorders, such as anorexia, hormone imbalances, such as hyperthyroidism, or as a side effect of certain drugs.

Acquired generalized hypertrichosis may be caused by cancer. The resulting hair growth is known as malignant down. The mechanism behind cancer induced hypertrichosis is unknown. Oral and topical minoxidil treatments are also known to cause acquired generalized hypertrichosis.

Congenital hypertrichosis lanuginosa may be caused by an paracentric inversion mutation of the q22 band of chromosome 8; however, it could also be possibly the result of a spontaneous genetic mutation rather than inheritance. This form is an autosomal dominant (not located on the sex chromosomes) cutaneous disorder, that affects the skin.

- Generalized hypertrichosis

Congenital generalized hypertrichosis has a dominant pattern of inheritance and has been linked to chromosome Xq24-27.1. An affected female (carrying the hypertrichosis gene) has a 50% chance of passing it to her offspring. An affected male will pass this form of hypertrichosis to his daughters, but never the sons.

- Generalized hypertrichosis terminalis

Congenital generalized hypertrichosis terminalis is thought to be caused by genetic changes on chromosome 17 resulting in the addition or removal of millions of nucleotides. The gene MAP2K6 may be a factor contributing to this condition. This condition may also be due to the change in the chromosome affecting the transcription of genes.

Other hypertrichosis patterns

Porphyria cutanea tarda may manifest in some patients as hypertrichosis on the face (mainly on top of the cheeks).