Congenital cholesteatoma
Keratin-filled cysts that grow medial to the tympanic membrane are considered to be congenital if they fulfill the following criteria (Levensons criteria):
mass medial to the tympanic membrane
normal tympanic membrane
no previous history of ear discharge, perforation or ear surgeryCongenital cholesteatomas occur at three important sites: the middle ear, the Petrous apex, and the cerebropontinio angle. They are most often found deep to the anterior aspect of the ear drum, and a vestigial structure, the epidermoid formation, from which congenital cholesteatoma may originate, has been identified in this area.Not all middle ear epidermal cysts are congenital, as they can be acquired either by metaplasia of the middle ear mucosa or by traumatic implantation of ear canal or tympanic membrane skin. In addition, cholesteatoma inadvertently left by a surgeon usually regrows as an epidermal cyst. Some authors have also suggested hereditary factors. Acquired cholesteatoma
More commonly, keratin accumulates in a pouch of tympanic membrane which extends into the middle ear space. This abnormal folding or retraction of the tympanic membrane arises in one of the following ways:

Jackler’s theory : Mucosal coupling with traction generated by interaction of migrating opposing surfaces leading to formation of cholesteatoma.Wittmaacks theory : Invagination of tympanic membrane from the attic or part of pars tensa in the form of retraction pockets lead to the formation of cholesteatoma. Ruedis theory : The basal cells of germinal layer of skin proliferate under the influence of infection and lay down keratinising squamous epithelium.
Meibomian gland dysfunction (also known as MGD) is a chronic disease of the meibomian glands, which is commonly characterized by obstruction of the end of the duct that delivers the secretion produced by the glands (called meibum) to the eye surface,  which prevents the glandular secretion to reach the ocular surface. The dysfunction could be that the amount of secretion produced may be abnormal (either too little or too much meibum produced). Dysfunction could also be related to the quality of the meibum produced. MGD may result in evaporative dry eye, blepharitis, chalazion, unsealed lid during sleep, and meibomian gland atrophy.MGD causes the glands to be obstructed by thick, cloudy-to-yellow, more opaque and viscous-like, oily and waxy secretions, a change from the glands normal clear secretions. Besides leading to dry eyes, the obstructions can be degraded by bacterial lipases, resulting in the formation of free fatty acids, which irritate the eyes and sometimes cause punctate keratopathy. MGD has been described as "the most underrecognized, underappreciated and undertreated disease in ophthalmic care [...] so common as to be taken as ‘normal’ in many clinical practices".The dysfunction is more often seen in women, and is regarded as the main cause of dry eye syndrome. Factors that contribute to the dysfunction can include things such as a persons age and/or hormones, or severe infestation of Demodex brevis mites. Treatment can include warm compresses to thin the secretions and eyelid scrubs with baby shampoo or eyelid cleanser, or emptying ("expression") of the gland by a professional.