Dyskeratosis is abnormal keratinization occurring prematurely within individual cells or groups of cells below the stratum granulosum.

Dyskeratosis congenita is congenital disease characterized by reticular skin pigmentation, nail degeneration, and leukoplakia on the mucous membranes associated with short telomeres.

Osteophytes form because of the increase in a damaged joint's surface area. This is most common from the onset of arthritis. Osteophytes usually limit joint movement and typically cause pain.

Osteophytes form naturally on the back of the spine as a person ages and are a sign of degeneration in the spine. In this case, the spurs are not the source of back pains, but instead are the common symptom of a deeper problem. However, bone spurs on the spine can impinge on nerves that leave the spine for other parts of the body. This impingement can cause pain in both upper and lower limbs and a numbness or tingling sensations in the hands and feet because the nerves are supplying sensation to their dermatomes.

Spurs can also appear on the feet, either along toes or the heel, as well as on the hands. In extreme cases, bone spurs have grown along a person's entire skeletal structure: along the knees, hips, shoulders, ribs, arms and ankles. Such cases are only exhibited with multiple exostoses.

Osteophytes on the fingers or toes are known as Heberden's nodes (if on the distal interphalangeal joint) or Bouchard's nodes (if on the proximal interphalangeal joints).

Osteophytes may also be the end result of certain disease processes. Osteomyelitis, a bone infection, may leave the adjacent bone with a spur formation. Charcot foot, the neuropathic breakdown of the feet seen primarily in diabetics, can also leave bone spurs that may then become symptomatic.

Zenker's degeneration is a severe glassy or waxy hyaline degeneration or necrosis of skeletal muscles in acute infectious diseases ;a prototype of coagulative necrosis.

The condition was named by Friedrich Albert von Zenker. It is a hyaline degeneration of skeletal muscles such as rectus abdominis and diaphragm, and occurs in severe toxaemia as typhoid fever. It is also seen in electrical burns. Grossly the muscles appear pale and friable; microscopically, the muscle fibres are swollen, have a loss of cross striations, and show a hyaline appearance. Rupture and small hemorrhage may complicate the lesion. Coagulative necrosis occurs here.

Osteophytes, commonly referred to as bone spurs are bony projections that form along joint margins. They should not be confused with enthesophytes, which are bony projections that form at the attachment of a tendon or ligament. Osteophytes are not always distinguished from exostoses in any definite way, although in many cases there are a number of differences. Osteophytes are typically intra-articular (within the joint capsule).

CCCA usually begins at the central (sagittal) midline of the scalp. It is symmetric and exhibits scarring as the name suggests. It involves solely the top of the scalp or may progress to Hamilton–Norwood scale Type VI or VII. Early symptoms may include pruritus, dysesthesias and tenderness. On examination the skin is thin with few follicular ostia and later in the disease the scalp may appear shiny.

The median palatal cyst is a rare cyst that may occur anywhere along the median palatal raphe. It may produce swelling because of infection and is treated by excision or surgical removal.

Some investigators now believe that this cyst represents a more posterior presentation of a nasopalatine duct cyst, rather than a separate cystic degeneration of epithelial rests at the line of fusion of the palatine shelves.

Blue nails, or more formally azure lunula, are characterized by a blue discoloration of the lunulae, seen in argyria and cases of hepatolenticular degeneration (Wilson's disease), also having been reported in hemoglobin M disease and hereditary acrolabial telangiectases.

In Wilson's disease the blue color involves the lunula (most intense pigmentation) and fades proximally. In argyria, the nail is permanently pigmented a slate-blue color and is most evident in the lunula. Minocycline and Zidovudine can also turn the nail plate blue-gray. There are also reports of hydroxyurea as a rare cause.

Central centrifugal cicatricial alopecia (CCCA), also referred to as hot comb alopecia and follicular degeneration syndrome, is a type of alopecia first noticed in African Americans in the 1950s and reported by LoPresti et al. in 1968 as a result of application of petrolatum followed by a stove-heated iron comb. The original theory was that the hot petrolatum would travel down to the hair root, burn the follicle, and after repetitive injury scarring would result. Later CCCA was realized to affect men and women without a history significant for use of such styling techniques. Consequently, the terms "follicular degeneration syndrome" per Sperling and Sau in 1992 and then CCCA per Olsent et al. in 2003 were evolved. Plausible contributing factors may include other African-American styling techniques such as relaxers, tight braids, heavy extensions, certain oils, gels or pomades.

Familial thoracic aortic aneurysm is an autosomal dominant disorder of large arteries.

There is an association between familial thoracic aortic aneurysm, Marfan syndrome and massive baclofen overdose as well as other hereditary connective tissue disorders.

It is sometimes called "Erdheim cystic medial necrosis of aorta", after Jakob Erdheim.

The term "cystic medial degeneration" is sometimes used instead of "cystic medial necrosis", because necrosis is not always found.

In season 6 of House MD in the episode 12 titled Remorse, House diagnoses his patient with Wilson's Disease in absence of Kayser-Fleischer rings by removing the nail polish to note the blue nails.

Lev's disease (or Lenegre-Lev syndrome) is an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. Lev's disease is most commonly seen in the elderly, and is often described as senile degeneration of the conduction system.

One form has been associated with SCN5A.

Stokes-Adams attacks can be precipitated by this condition. These involve a temporary loss of consciousness resulting from marked slowing of the heart when the atrial impulse is no longer conducted to the ventricles. This should not be confused with the catastrophic loss of heartbeat seen with ventricular fibrillation or asystole.

Vacuolar interface dermatitis (VAC, also known as liquefaction degeneration, vacuolar alteration or hydropic degeneration) is a dermatitis where degenerative changes occur at the dermoepidermal junction, with lymphophatic inflammation at the epidermis and dermis. This change is frequently found in lupus erythematosis, erythema multiforme and lichen sclerosis.

Distal hereditary motor neuronopathies (distal HMN, dHMN), sometimes also called distal hereditary motor neuropathies, are a genetically and clinically heterogeneous group of motor neuron diseases that result from genetic mutations in various genes and are characterized by degeneration and loss of motor neuron cells in the anterior horn of the spinal cord and subsequent muscle atrophy.

Although they can hardly be distinguished from hereditary motor and sensory neuropathies on the clinical level, dHMNs are considered a separate class of disorders.

Terrien marginal degeneration is a noninflammatory, unilateral or asymmetrically bilateral, slowly progressive thinning of the peripheral corneal stroma.

The cause of Terrien marginal degeneration is unknown, its prevalence is roughly equal between males and females, and it usually occurs in the second or third decade of life.

In 1993, A. E. Hardnig proposed to classify hereditary motor neuropathies into seven groups based on age at onset, mode of inheritance, and presence of additional features. This initial classification has since been widely adopted and expanded and currently looks as follows:

Note: Acronym "HMN" is also used interchangeably with "DHMN".

Degenerative disc disease (DDD) describes the natural breakdown of an intervertebral disc of the spine. Despite its name, DDD is not considered a disease, nor is it progressively degenerative. On the contrary, disc degeneration is often the effect of natural daily stresses and minor injuries that cause spinal discs to gradually lose water as the anulus fibrosus, or the rigid outer shell of a disc, weakens. As discs weaken and lose water, they begin to collapse. This can result in pressure being put on the nerves in the spinal column, causing pain and weakness.

While not always symptomatic, DDD can cause acute or chronic low back or neck pain as well as nerve pain depending on the location of the affected disc and the amount of pressure it places on the surrounding nerve roots.

The typical radiographic findings in DDD are black discs, disc space narrowing, vacuum disc, end plate sclerosis, and osteophyte formation.

DDD can greatly affect quality of life. Disc degeneration is a disease of micro/macro trauma and of aging, and though for most people is not a problem, in certain individuals a degenerated disc can cause severe chronic pain if left untreated.

Degenerative disc disease can result in lower back or upper neck pain, but this isn't always true across the board. In fact, the amount of degeneration does not correlate well with the amount of pain patients experience. Many people experience no pain while others, with exactly the same amount of damage have severe, chronic pain. Whether a patient experiences pain or not largely depends on the location of the affected disc and the amount of pressure that is being put on the spinal column and surrounding nerve roots.

Nevertheless, degenerative disc disease is one of the most common sources of back pain and affects approximately 30 million people every year. With symptomatic degenerative disc disease, the pain can vary depending on the location of the affected disc. A degenerated disc in the lower back can result in lower back pain, sometimes radiating to the hips, as well as pain in the buttocks, thighs or legs. If pressure is being placed on the nerves by exposed nucleus pulposus, sporadic tingling or weakness through the knees and legs can also occur.

A degenerated disc in the upper neck will often result in pain to the neck, arm, shoulders and hands; tingling in the fingers may also be evident if nerve impingement is occurring.

Pain is most commonly felt or worsened by movements such as sitting, bending, lifting and twisting.

After an injury, some discs become painful because of inflammation and the pain comes and goes. Some people have nerve endings that penetrate more deeply into the anulus fibrosus (outer layer of the disc) than others, making discs more likely to generate pain. In the alternative, the healing of trauma to the outer anulus fibrosus may result in the innervation of the scar tissue and pain impulses from the disc, as these nerves become inflamed by nucleus pulposus material. Degenerative disc disease can lead to a chronic debilitating condition and can have a serious negative impact on a person's quality of life. When pain from degenerative disc disease is severe, traditional nonoperative treatment may be ineffective.

Symptoms typically are onset in the adult years, although, childhood cases have also been observed. Common symptoms include a loss of coordination which is often seen in walking, and slurred speech. ADCA primarily affects the cerebellum, as well as, the spinal cord. Some signs and symptoms are:

Most cases of back pain are related to issues in human musculoskeletal system and are not related to severe diseases. Musculoskeletal problems also called mechanical because many of them linked to vertebrae physical motions. Back pain itself is not considered a diagnosis, but rather a symptom of underlying (in most cases musculoskeletal) problems.

following:

- Vertebrae misalignment, which can cause nerve interference (also called subluxation), muscle tension, or muscle spasm

- Strained muscles

- Sprained ligaments

- Ruptured disks, which also called "slipped", or herniated disks

- Degenerative discs (lose their cushioning ability). The degeneration usually caused by repetitive strain, or injury, or aging.

- Irritated joints

FHM signs overlap significantly with those of migraine with aura. In short, FHM is typified by migraine with aura associated with hemiparesis and, in FHM1, cerebellar degeneration. This cerebellar degeneration can result in episodic or progressive ataxia. FHM can also present with the same signs as benign familial infantile convulsions (BFIC) and alternating hemiplegia of childhood. Other symptoms are altered consciousness (in fact, some cases seem related to head trauma), gaze-evoked nystagmus and coma. Aura symptoms, such as numbness and blurring of vision, typically persist for 30–60 minutes, but can last for weeks and months. An attack resembles a stroke, but unlike a stroke, it resolves in time. These signs typically first manifest themselves in the first or second decade of life.

A pinguecula is a common type of conjunctival degeneration in the eye.

BVVL is marked by a number of cranial nerve palsies, including those of the motor components involving the 7th and 9th-12th cranial nerves, spinal motor nerves, and upper motor neurons. Major features of BVVL include facial and neck weakness, fasciculation of the tongue, and neurological disorders from the cranial nerves. The neurological manifestations develop insidiously: they usually begin with sensorineural deafness, progress inexorably to paralysis, and often culminate in respiratory failure. Most mortality in patients has been from either respiratory infections or respiratory muscle paralysis. Pathological descriptions of BVVL include injury and depletion of 3rd-7th cranial nerves, loss of the spinal anterior horn cells, degeneration of Purkinje cells, as well as degeneration of the spinocerebellar and pyramidal tracts. The first symptoms in nearly all cases of BVVL is progressive vision loss and deafness, and the first initial symptoms are seen anywhere from one to three years.

Most cases of deafness are followed by a latent period that can extend anywhere from weeks to years, and this time is usually marked by cranial nerve degeneration. Neurological symptoms of BVVL include optic atrophy, cerebellar ataxia, retinitis pigmentosa, epilepsy and autonomic dysfunction. Non-neurological symptoms can include diabetes, auditory hallucinations, respiratory difficulties, color blindness, and hypertension.

Corneal ectatic disorders or corneal ectasia are a group of uncommon, noninflammatory, eye disorders characterised by bilateral thinning of the central, paracentral, or peripheral cornea.

- Keratoconus, a progressive, noninflammatory, bilateral, asymmetric disease, characterized by paraxial stromal thinning and weakening that leads to corneal surface distortion.

- Keratoglobus, a rare noninflammatory corneal thinning disorder, characterised by generalised thinning and globular protrusion of the cornea.

- Pellucid marginal degeneration, a bilateral, noninflammatory disorder, characterized by a peripheral band of thinning of the inferior cornea.

- Posterior keratoconus, a rare condition, usually congenital, which causes a nonprogressive thinning of the inner surface of the cornea, while the curvature of the anterior surface remains normal. Usually only a single eye is affected.

- Post-LASIK ectasia, a complication of LASIK eye surgery.

- Terrien's marginal degeneration, a painless, noninflammatory, unilateral or asymmetrically bilateral, slowly progressive thinning of the peripheral corneal stroma.