Some examples of this in practice are that if a patient whose endoscopy did not detect dysplasia on biopsy during screening for Barretts esophagus, then research shows that there is little chance of any test detecting dysplasia for that patient within three years.Individuals at average-risk for colorectal cancer should have another screening after ten years if they get a normal result and after five years if they have only one or two  adenomatous polyps removed. Microscopic changes
Dysplasia is characterised by four major pathological microscopic changes:

Anisocytosis (cells of unequal size)
Poikilocytosis (abnormally shaped cells)
Hyperchromatism (excessive pigmentation)
Presence of mitotic figures (an unusual number of cells which are currently dividing).Other changes that occur in epithelial dysplasia include:

Drop-shaped rete processes
Basal cell hyperplasia
Irregular epithelial stratification
Increased nuclear-cytoplasmic ratio
Increased normal and abnormal mitosis
Enlarged nucleoli
Individual cell keratinization
Loss or reduction of cellular cohesion
Cellular pleomorphism
Loss of basal cell polarity
KoilocytosisEpithelial cell dysplasia is divided into three categories of severity: mild, moderate, and severe. Epithelial dysplasia becomes microinvasive squamous cell carcinoma once the tumor begins to invade nearby tissue. Dysplasia vs. carcinoma in situ vs. invasive carcinoma
These terms are related since they represent three stages in the progression of many malignant tumors of the epithelium. The likelihood of the development to cancer is related to the degree of dysplasia. Dysplasia is the earliest form of precancerous lesion which pathologists can recognize in a pap smear or in a biopsy. Dysplasia can be low grade or high grade. The risk of low-grade dysplasia transforming into high-grade dysplasia, and eventually cancer, is low. Treatment is usually straightforward.
Herpetic simplex keratitis is a form of keratitis caused by recurrent herpes simplex virus (HSV) infection in the cornea.It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the cornea. Primary infection typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the corneal surface. The effect of the lesions varies, from minor damage to the epithelium (superficial punctate keratitis), to more serious consequences such as the formation of dendritic ulcers. Infection is unilateral, affecting one eye at a time. Additional symptoms include dull pain deep inside the eye, mild to acute dryness, and sinusitis. Most primary infections resolve spontaneously in a few weeks. Healing can be aided by the use of oral and topical antivirals. Subsequent recurrences may be more severe, with infected epithelial cells showing larger dendritic ulceration, and lesions forming white plaques. The epithelial layer is sloughed off as the dendritic ulcer grows, and mild inflammation (iritis) may occur in the underlying stroma of iris. Sensation loss occurs in lesional areas, producing generalised corneal anaesthesia with repeated recurrences. Recurrence can be accompanied by chronic dry eye, low grade intermittent conjunctivitis, or chronic unexplained sinusitis. Following persistent infection  the concentration of viral DNA reaches a critical limit. Antibody responses against the viral antigen expression in the stroma can trigger a massive immune response in the eye.