Bleeding canker of horse chestnut is a common canker of horse chestnut trees ("Aesculus hippocastanum", also known as conker trees) that is known to be caused by infection with several different pathogens.

Infections by the gram-negative fluorescent bacterium "Pseudomonas syringae" pathovar "aesculi" are a new phenomenon, and have caused most of the bleeding cankers on horse chestnut that are now frequently seen in Britain.

Dead arm, sometimes grape canker, is a disease of grapes caused by a deep-seated wood rot of the arms or trunk of the grapevine. As the disease progresses over several years, one or more arms may die, hence the name "dead arm". Eventually the whole vine will die. In the 1970s, dead-arm was identified as really being two diseases, caused by two different fungi, "Eutypa lata" and "Phomopsis viticola" (syn. "Cryptosporella viticola").

Adult walnut twig beetles carry spores of the "Geosmithia morbida" fungus, which grows profusely around the pupal chamber of the beetles. Following emergence from trees the beetles subsequently tunnel into branches and trunks of walnut for production of egg galleries or overwintering shelters. The fungus is introduced into the tree during this wounding where it subsequently germinates and grows.

The fungal mycelium initially colonize tissue immediately surrounding the beetle galleries. However, in less than a month black, oval-shaped, inky cankers extend considerably beyond the galleries and may reach more than 3 cm in length in susceptible hosts (e.g., black walnut). In the beginning these cankers develop in phloem and tissues formed by the cork cambium. The affected area is very shallow and never show the ‘open-faced’, perennial, target-shape typical of many canker diseases of trees (e.g., Nectria canker). Instead in TCD the bark remains firmly attached to the canker face making the necrotic areas very difficult to observe. Branch cankers usually are not visible until the outer bark is shaved to expose the beetle tunnels, although during late stages of the disease a dark amber stain may form on the bark surface in association with the cankers.

Each time a beetle tunnels into a tree a canker is initiated. Cankers also may continue to expand and penetrate into the cambium of the tree. Each such injury destroys the phloem and robs the tree of its ability to store and move nutrients. As TCD progresses cankers coalesce to further girdle branches greatly restricting nutrient movement. As the tree declines, more bark beetles are attracted and more cankers are formed.

Eventually the enormous number of beetle attacks and subsequent canker formation overwhelms and kills the tree. Thousand cankers is a progressive disease and its effects result from the culmination of a large number of relatively small cankers over a period of time. Just as a thousand cuts was once used as a form of human execution in Imperial China, black walnuts are subjected to death by thousands of branch and trunk cankers produced by infection from the "Geosmithia" fungus.

In end stages of the disease external symptoms become visible. Leaf yellowing on the exterior of the crown is often the first symptom and may originally be restricted to a single branch. However, as the cumulative effects of the girdling progress increasingly large areas of the tree are affected. Sudden leaf wilting, ultimately involving large limbs, characterizes end stage thousand cankers disease. In susceptible hosts, trees are almost always killed within 2–3 years after external symptoms of leaf yellowing are first observed.

The progress of thousand cankers will vary due to several factors, notably the susceptibility of the host. There appears to be a considerable range of TCD susceptibility among various "Juglans" species with "Juglans nigra" (black walnut) being particularly susceptible. Conversely, Arizona walnut ("Juglans major") appears to be quite resistant to the disease, with bark beetle attacks largely limited to small diameter branches, the fungus growing to a very limited extent, and effects of the disease rarely, if ever, progressing to involve large areas of the tree. Similarly southern California walnut ("Juglans californica") and little walnut ("Juglans microcarpa") may show fairly high resistance. Northern California walnut ("Juglans hindsii") and the commercial nut-producing Persian (English) walnut ("Juglans regia") apparently show various degrees of intermediate TCD susceptibility.

Leucostoma canker is a fungal disease that can kill stone fruit ("Prunus" spp.). The disease is caused by the plant pathogens "Leucostoma persoonii" and "Leucostoma cinctum" (teleomorph) and "Cytospora leucostoma" and "Cytospora cincta" (anamorphs). The disease can have a variety of signs and symptoms depending on the part of the tree infected. One of the most lethal symptoms of the disease are the Leucostoma cankers. The severity of the Leucostoma cankers is dependent on the part of the plant infected. The fungus infects through injured, dying or dead tissues of the trees. Disease management can consist of cultural management practices such as pruning, late season fertilizers or chemical management through measures such as insect control. Leucostoma canker of stone fruit can cause significant economic losses due to reduced fruit production or disease management practices. It is one of the most important diseases of stone fruit tree all over the world.

Dead arm is a disease that causes symptoms in the common grapevine species, "vitis vinifera", in many regions of the world. This disease is mainly caused by the fungal pathogen, "Phomopsis viticola", and is known to affect many cultivars of table grapes, such as Thompson Seedless, Red Globe, and Flame Seedless. Early in the growing season, the disease can delay the growth of the plant and cause leaves to turn yellow and curl. Small, brown spots on the shoots and leaf veins are very common first symptoms of this disease. Soil moisture and temperature can impact the severity of symptoms, leading to a systemic infection in warm, wet conditions. As the name of this disease suggests, it also causes one or more arms of the grapevine to die, often leading to death of the entire vine.

Canker and anthracnose generally refer to many different plant diseases of such broadly similar symptoms as the appearance of small areas of dead tissue, which grow slowly, often over years. Some are of only minor consequence, but others are ultimately lethal and therefore of major economic importance in agriculture and horticulture. Their causes include such a wide range of organisms as fungi, bacteria, mycoplasmas and viruses. The majority of canker-causing organisms are bound to a unique host species or genus, but a few will attack other plants. Weather and animals can spread canker, thereby endangering areas that have only slight amount of canker.

Although fungicides or bactericides can treat some cankers, often the only available treatment is to destroy the infected plant to contain the disease.

Thousand cankers disease is a recently recognized disease of certain walnuts ("Juglans" spp.). The disease results from the combined activity of the walnut twig beetle ("Pityophthorus juglandis") and a canker producing fungus, "Geosmithia morbida". Until July 2010 the disease was only known to the western United States where over the past decade it has been involved in several large scale die-offs of walnut, particularly black walnut, "Juglans nigra". However, in late July 2010 a well-established outbreak of the disease was found in the Knoxville, Tennessee area. This new finding is the first locating it within the native range of its susceptible host, black walnut.

The foamy bark canker is a disease affecting oak trees in California caused by the fungus "Geosmithia pallida" and spread by the Western oak bark beetle ("Pseudopityopthorus pubipennis"). This disease is only seen through the symbiosis of the bark beetles and the fungal pathogen. The bark beetles target oak trees and bore holes through the peridermal tissues, making tunnels within the phloem. The fungal spores are brought into these tunnels by the beetles and begin to colonize the damaged cells inside the tunnels. Symptoms of the developing fungus include wet discoloration seeping from the beetle entry holes as the fungus begins to consume phloem and likely other tissues. If bark is removed, necrosis of the phloem can be observed surrounding the entry hole(s). As the disease progresses, a reddish sap and foamy liquid oozes from entry holes, thus giving the disease the name Foamy bark canker. Eventually after the disease has progressed, the tree dies. This disease is important because of its detrimental effects on oak trees and its ability to spread to several new Californian counties in just a couple years.

Black pod disease is caused by many different "Phytophthora spp." pathogens all expressing the same symptoms in cocoa trees ("Theobroma cacao"). This pathogen if left untreated can destroy all yields; annually the pathogen can cause a yield loss of up to 1/3 and up to 10% of total trees can be lost completely. With the value of the cocoa industry throughout the world being so large there are much research and control efforts that go into these "Phytophthora spp." pathogens.

This pathogen can be located anywhere on the cocoa trees but is most noted for the black mummified look it will give to the fruit of the cocoa tree. Staying ahead of the pathogen is the best means of control, the pathogen can be greatly reduced if leaf litter is not allowed to stay on the ground and if the pathogen gets out of hand chemical control can be used. This pathogen is mostly found in tropical areas where the cocoa trees are located and need rainfall in order to spread its spores.

Sudden Death Syndrome (SDS) in Soybean plants quickly spread across the southern United States in the 1970s, eventually reaching most agricultural areas of the US. SDS is caused by a Fusarium fungi, more specifically the soil borne root pathogen "Fusarium virguliforme," formerly known as "Fusarium solani" f. sp. "glycines"."." Losses could exceed hundreds of millions of dollars in US soybean markets alone making it one of the most important diseases found in Soybeans across the US

Grapevine trunk diseases (GTD) are the most destructive diseases of vineyards worldwide. Fungicides (such as sodium arsenite or 8-hydroxyquinoline, used to fight esca) with the potential to control GTD have been banned in Europe and there are no highly effective treatments available. Action to develop new strategies to fight these diseases are needed.

The following fungal species are responsible for grapevine trunk diseases:

- "Botryosphaeria dothidea" and other "Botryosphaeria" species, such as , "B. obtusa", "B. parva" and "B. australis",

- "Cylindrocarpon" spp., "Ilyonectria" spp., "Dactylonectria" spp. and "Campylocarpon" spp.(cause of black foot disease)

- "Diplodia seriata" (cause of bot canker)

- "Diplodia mutila" (cause of Botryosphaeria dieback)

- "Dothiorella iberica"

- "Dothiorella viticola"

- "Eutypa lata" (cause of Eutypa dieback)

- "Fomitiporia mediterranea" (cause of esca)

- "Lasiodiplodia theobromae" (cause of Botryosphaeria dieback)

- "Neofusicoccum australe"

- "Neofusicoccum luteum"

- "Neofusicoccom parvum"

- "Phaeoacremonium minimum" (cause of esca and Petri disease) and other "Phaeoacremonium" species

- "Phaeomoniella chlamydospora" (cause of esca and Petri disease)

Hosts associated with "Geosmithia pallida" include a number of tree species, including oak and other hardwoods, pine and spruce trees, depending on the beetle vector. In this case, the western oak bark beetles target live oak trees of western United States. Beetles tend to attack stressed trees that are already weakened from drought or injury. Symptoms causing branch dieback and tree death also include a cinnamon-colored gum seeping from multiple beetle entry holes on the bole, followed by a prolific, cream-colored foamy liquid. These symptoms, as well as signs (entry holes, larvae, beetles) of bark beetles, are key factors in diagnosis. Necrosis of xylem and phloem tissues underneath bark can be observed.

Common Symptoms:

- Wet discoloration on bark

- Phloem necrosis

- Beetle entry holes

- Reddish sap oozing from entry holes

- Foamy liquid from entry holes

Most of the SDS symptoms can be confused with other factors like nutrient deficiencies and some other diseases like brown stem rot and stem canker. Usually the first symptom seen is interveinal chlorosis, which is the yellowing of the plant material between the leaf veins. When leaves begin to die, puckering and mottling can also be observed along with the chlorosis. As severity increases, necrosis (death of cells) occurs and eventually these leaves will fall off, leaving only petioles left on the stem. If the conditions are right (cool and wet), these symptoms can appear suddenly, causing large yield reductions. Normally, this is seen in mid or late July around the time of flowering and pod production.

In addition to foliar symptoms, the stem of the soybean plant can show symptoms as well. If a soybean stem with SDS is split, the pith will be visibly white while the cortical tissue around the pith will be tan to light brown in color. If the pith is brown in color (or if the whole stem looks brown on the inside), it is likely that the plant has brown stem rot, rather than SDS

Along with the above ground foliar and stem symptoms, the roots usually show some kind of rotting and decrease in vigor compared to other healthy soybean roots. If soil conditions are moist, roots are also likely to show blue masses of spores (macroconidia) around the taproot just below the soil surface. Blue fungal masses, found along with the foliar and stem symptoms, are strong diagnostic indicators for SDS

The hosts for Leucostoma canker include stone fruits such as cultivated peach, plum, prune, cherry ("Prunus spp".), or other wild "Prunus" spp. It can also be found on apple ("Malus domestica"). Stone fruits are referred to as drupe, which are fruits containing a seed encased by a hard endocarp, surrounded by a fleshy outer portion.

Leucostoma canker symptoms differ depending on where on the tree infection takes place. Discoloration occurs in sunken patches on infected twigs. Light and dark concentric circles of narcotic tissue characterize this symptom, occurring near buds killed by cold or on leaf scars. Infections on the nodes are seen 2–4 weeks after bud break. As time passes, darkening occurs within diseased tissues, and eventually, amber gum ooze may seep from infected tissue. Nodal infections are particularly vulnerable in one-year-old shoots that develop within the center of the tree. If fungal growth persists without treatment, scaffold limbs and large branches will likely become invaded within a short time frame. Cankers occurring on branches that are the product of such infections will contain dead twigs or twig stubs at the canker’s center.

The most striking symptom of infection includes cankers located on the main trunk, branch crotches, scaffold limbs, and older branches. A symptom called “flagging” can be found on necrotic scaffold limbs. The cankers are parallel to the long axis of the stem and take on an oval shape. Normally, large-scale production of amber colored gum marks the first external symptom of such cankers. While gum production is the typical plant response to irritation, the gum secretion of Leucostoma occurs in bulk amounts. This gum darkens as time passes, gradually leading to the drying and cracking of bark; thus exposing the blackened tissue below.

As the tree continues to mature in the early growing season, the tree resists additional fungal penetration through the formation of callus rings surrounding the canker. However, the Leucostoma generally reinvades the tissue late in the growing season while the tree switches into dormancy. Due to the alteration of callus production and canker formation, cankers with circular callus rings are usually observed.

Foliar symptoms might develop from branch or twig infections. Symptoms include chlorosis, wilting, and necrosis. Signs include small black structures on dead bark which contain pycnidia.

Verticillium wilt is a wilt disease of over 350 species of eudicot plants caused by six species of Verticillium genus, "V. dahliae", "V. albo-atrum", "V. longisporum", V. nubilum, V. theobromae and

V. tricorpus. (See, for example, Barbara, D.J. & Clewes, E. (2003). "Plant pathogenic Verticillium species: how many of them are there?" Molecular Plant Pathology 4(4).297-305. Blackwell Publishing.) Many economically important plants are susceptible including cotton, tomatoes, potatoes, oilseed rape, eggplants, peppers and ornamentals, as well as others in natural vegetation communities. Many eudicot species and cultivars are resistant to the disease and all monocots, gymnosperms and ferns are immune.

Symptoms are superficially similar to "Fusarium" wilts. There is no chemical control for the disease but crop rotation, the use of resistant varieties and deep plowing may be useful in reducing the spread and impact of the disease.

"Verticillium" spp. attack a very large host range including more than 350 species of vegetables, fruit trees, flowers, field crops, and shade or forest trees. Most vegetable species have some susceptibility, so it has a very wide host range. A list of known hosts is at the bottom of this page.

The symptoms are similar to most wilts with a few specifics to "Verticillium". Wilt itself is the most common symptom, with wilting of the stem and leaves occurring due to the blockage of the xylem vascular tissues and therefore reduced water and nutrient flow. In small plants and seedlings, "Verticillium" can quickly kill the plant while in larger, more developed plants the severity can vary. Some times only one side of the plant will appear infected because once in the vascular tissues, the disease migrates mostly upward and not as much radially in the stem. Other symptoms include stunting, chlorosis or yellowing of the leaves, necrosis or tissue death, and defoliation. Internal vascular tissue discoloration might be visible when the stem is cut.

In "Verticillium", the symptoms and effects will often only be on the lower or outer parts of plants or will be localized to only a few branches of a tree. In older plants, the infection can cause death, but often, especially with trees, the plant will be able to recover, or at least continue living with the infection. The severity of the infection plays a large role in how severe the symptoms are and how quickly they develop.

In the past few years, the bacterial pathogen "Pseudomonas syringae pv. aesculi" has emerged as a new and virulent agent for this disease in Western Europe. Specific to horse chestnut trees, this pathogen infects the bark (cambium) around the trunk and main branches. As it spreads, it cuts off the water supply to the crown; and when it completely encircles the trunk, the tree will die.

This particular infective agent emerged in the past few years, and has now spread rapidly to infect many trees in Western Europe.

Initially the outbreak was attributed to "Phytophthora", until DNA tests suggested that a pathovar of "Pseudomonas syringae" was responsible; and this hypothesis was confirmed in 2007 with tests satisfying Koch's postulates.

The disease has risen markedly in the UK since 2003, and now approximately one half of all horse chestnuts in Great Britain are affected and showing symptoms to some degree.

The disease is spreading at an alarming rate in the Netherlands,

where one third of all horse chestnuts are affected to a greater or lesser extent.

A similar upsurge is reported in Belgium and France.

Aphthous stomatitis is a common condition characterized by the repeated formation of benign and non-contagious mouth ulcers (aphthae) in otherwise healthy individuals. The informal term canker sores is also used, mainly in North America, although this may also refer to any mouth ulcer.

The cause is not completely understood, but involves a T cell-mediated immune response triggered by a variety of factors. Different individuals have different triggers, which may include nutritional deficiencies, local trauma, stress, hormonal influences, allergies, or genetic predisposition.

These ulcers occur periodically and heal completely between attacks. In the majority of cases, the individual ulcers last about 7–10 days, and ulceration episodes occur 3–6 times per year. Most appear on the non-keratinizing epithelial surfaces in the mouth (i.e. anywhere except the attached gingiva, the hard palate and the dorsum of the tongue), although the more severe forms, which are less common, may also involve keratinizing epithelial surfaces. Symptoms range from a minor nuisance to interfering with eating and drinking. The severe forms may be debilitating, even causing weight loss due to malnutrition.

The condition is very common, affecting about 20% of the general population to some degree. The onset is often during childhood or adolescence, and the condition usually lasts for several years before gradually disappearing. There is no cure, and treatments aim to manage pain, reduce healing time and reduce the frequency of episodes of ulceration. The term is from meaning "mouth ulcer".

Persons with aphthous stomatitis have no detectable systemic symptoms or signs (i.e., outside the mouth). Generally, symptoms may include prodromal sensations such as burning, itching, or stinging, which may precede the appearance of any lesion by some hours; and pain, which is often out of proportion to the extent of the ulceration and is worsened by physical contact, especially with certain foods and drinks (e.g., if they are acidic). Pain is worst in the days immediately following the initial formation of the ulcer, and then recedes as healing progresses. If there are lesions on the tongue, speaking and chewing can be uncomfortable, and ulcers on the soft palate, back of the throat, or esophagus can cause painful swallowing. Signs are limited to the lesions themselves.

Ulceration episodes usually occur about 3–6 times per year. However, severe disease is characterized by virtually constant ulceration (new lesions developing before old ones have healed) and may cause debilitating chronic pain and interfere with comfortable eating. In severe cases, this prevents adequate nutrient intake leading to malnutrition and weight loss.

Aphthous ulcers typically begin as erythematous macules (reddened, flat area of mucosa) which develop into ulcers that are covered with a yellow-grey fibrinous membrane that can be scraped away. A reddish "halo" surrounds the ulcer. The size, number, location, healing time, and periodicity between episodes of ulcer formation are all dependent upon the subtype of aphthous stomatitis.

The symptom of black pod disease is the necrotic lesion on the cocoa pod with brown or black color, which eventually enlarged to cover the whole pod. White mycelia growth on lesions that appeared several days after infection is the sign for the causal pathogen of black pod disease, which is "Phytophthora spp".

Black pod disease starts when the infected pod shows some little yellow spots, which eventually turn brown and enlarge to a dark brown or black lesion within five days. The lesion is fast growing and covers the entire pod after eighth day of infection. The infection does not only occur on the pod surface, but also invades inside the pod affecting the beans. The growth of white mycelia on black pod is visible after 11 days and the sporulation is initiated. The dispersal of sporangia or zoospores through water, ants and other insects occurs at this stage and will infect other healthy pods nearby. Direct contact of a black pod with healthy pods also leads to the spread of disease. In addition, the infected flower cushion and mummified pods are the locations for "P. palmivora" survival during dry season, where the pathogen will grow and continue to infect other developing pods

The infection occurs on any stage of pod development, where it causes wilting and dying of young pods and destroyed the beans of mature pods. The fully infected pods (the mummified pod), which then become dehydrated, are capable of providing the inoculum of "P. palmivora" for at least 3 years. "P. megakarya" causes the same symptom as "P. palmivora", but the occurrence is faster and generally produces greater amount of spores. Both "P. palmivora" and "P. megakarya" also caused canker on bark, flower cushion and chupons, and cankers on the base could extend to the main roots. Cankers were identified as one of inoculum sources for black pod disease. Furthermore, the pattern of infection caused by "P. megakarya" starts from the ground and moves up to the canopy, however there is no distinct pattern of disease infection caused by "P. palmivora" was reported. This pattern of infection could be due to "P. megakarya" and "P. palmivora" that were found to survive in soil and "P. megakarya" could be surviving in the roots of a few species of shade trees found in cocoa plantation.

Oral and maxillofacial pathology (also termed oral pathology, stomatognathic disease, dental disease, or mouth disease) refers to the diseases of the mouth ("oral cavity" or "stoma"), jaws ("maxillae" or "gnath") and related structures such as salivary glands, temporomandibular joints, facial muscles and perioral skin (the skin around the mouth). The mouth is an important organ with many different functions. It is also prone to a variety of medical and dental disorders.

The specialty oral and maxillofacial pathology is concerned with diagnosis and study of the causes and effects of diseases affecting the oral and maxillofacial region. It is sometimes considered to be a specialty of dentistry and pathology. Sometimes the term head and neck pathology is used instead, but this might imply that the pathologist deals with otorhinolaryngologic disorders (i.e. ear, nose and throat) in addition to maxillofacial disorders. In this role there is some overlap between the expertise of head and neck pathologists and that of endocrine pathologists.

A great many diseases involve the mouth, jaws and orofacial skin. Some example pathologies which can involve the oral and maxillofacial region are listed. Some are more common than others, and this list is by no means complete. The examples are considered according to a surgical sieve.

Aphthous stomatitis (also termed recurrent aphthous stomatits, RAS, and commonly called "canker sores") is a very common cause of oral ulceration. 10–25% of the general population suffer from this non-contagious condition. The appearance of aphthous stomatitis varies as there are 3 types, namely minor aphthous ulceration, major aphthous ulceration and herpetiform ulceration. Minor aphthous ulceration is the most common type, presenting with 1–6 small (2-4mm diameter), round/oval ulcers with a yellow-grey color and an erythematous (red) "halo". These ulcers heal with no permanent scarring in about 7–10 days. Ulcers recur at intervals of about 1–4 months. Major aphthous ulceration is less common than the minor type, but produces more severe lesions and symptoms. Major aphthous ulceration presents with larger (>1 cm diameter) ulcers that take much longer to heal (10–40 days) and may leave scarring. The minor and major subtypes of aphthous stomatitis usually produce lesions on the non-keratinized oral mucosa (i.e. the inside of the cheeks, lips, underneath the tongue and the floor of mouth), but less commonly major aphthous ulcers may occur in other parts of the mouth on keratinized mucosal surfaces. The least common type is herpetiform ulceration, so named because the condition resembles primary herpetic gingivostomatitis. Herpetiform ulcers begin as small blisters (vesicles) which break down into 2-3mm sized ulcers. Herpetiform ulcers appear in "crops" sometimes hundreds in number, which can coalesce to form larger areas of ulceration. This subtype may cause extreme pain, heals with scarring and may recur frequently.

The exact cause of aphthous stomatitis is unknown, but there may be a genetic predisposition in some people. Other possible causes include hematinic deficiency (folate, vitamin B, iron), stopping smoking, stress, menstruation, trauma, food allergies or hypersensitivity to sodium lauryl sulphate (found in many brands of toothpaste). Aphthous stomatitis has no clinically detectable signs or symptoms outside the mouth, but the recurrent ulceration can cause much discomfort to sufferers. Treatment is aimed at reducing the pain and swelling and speeding healing, and may involve systemic or topical steroids, analgesics (pain killers), antiseptics, anti-inflammatories or barrier pastes to protect the raw area(s).

As a result of radiotherapy to the mouth, radiation-induced stomatitis may develop, which can be associated with mucosal erosions and ulceration. If the salivary glands are irradiated, there may also be xerostomia (dry mouth), making the oral mucosa more vulnerable to frictional damage as the lubricating function of saliva is lost, and mucosal atrophy (thinning), which makes a breach of the epithelium more likely. Radiation to the bones of the jaws causes damage to osteocytes and impairs the blood supply. The affected hard tissues become hypovascular (reduced number of blood vessels), hypocellular (reduced number of cells), and hypoxic (low levels of oxygen). Osteoradionecrosis is the term for when such an area of irradiated bone does not heal from this damage. This usually occurs in the mandible, and causes chronic pain and surface ulceration, sometimes resulting in non-healing bone being exposed through a soft tissue defect. Prevention of osteradionecrosis is part of the reason why all teeth of questionable prognosis are removed before the start of a course of radiotherapy.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.