The smear layer is a layer of microcrystalline and organic particle debris that is found spread on root canal walls after root canal instrumentation. It was first described in 1975 and much research has been performed since then to evaluate its importance in assisting or preventing the penetration of bacteria into the dentinal tubules. More broadly, it is the organic layer found over all hard tooth surfaces.

Clark-Holke et al. (2003) focused on determining the effect of the smear layer on the magnitude of bacterial penetration through the apical foramen around obturating materials. Thirty extracted teeth were classified into two test groups; the first group had the smear layer removed by rinsing with 17% EDTA while in the second group the smear layer was left intact. Canal preparation and obturation using lateral condensation, gutta-percha, and AH 26 sealer was performed on all of the teeth. The model systems consisted of an upper chamber attached to the cemento-enamel junction and a lower chamber at the apices of the teeth. Standardized bacterial suspensions containing "Fusobacterium nucleatum", "Campylobacter rectus" and "Peptostreptococcus micros" were inoculated into the upper chambers. Models were incubated anaerobically at 37 degrees C. Leakage results were as follows: In the first group 6 teeth showed bacterial leakage, the second group and third groups showed no bacterial leakage. This study indicated that removal of the smear layer reduced the leakage of bacteria through the root canal system.

Kokkas et al. (2004) examined the effect of the smear layer on the penetration depth of three different sealers (AH Plus, Apexit, and a Grossman type-Roth 811) into the dentinal tubules. Sixty four extracted human single-rooted teeth were used and divided into two groups. The smear layer remained intact in all the roots of group A. Complete removal of the smear layer in group B was achieved after irrigation with 3 ml of 17% EDTA for 3 min, followed by 3 ml of 1% NaOCl solution. Ten roots from each group were obturated with AH Plus and laterally condensed gutta-percha points. The same process was repeated for the remaining roots by using sealers Apexit and Roth 811 correspondingly. After complete setting, the maximum penetration depth of the sealers into the dentinal tubules was examined in upper, middle, and lower levels. The smear layer prevented all the sealers from penetrating dentinal tubules. In contrast, in smear layer–free root canals, all the sealers penetrated dentinal tubules, although the depth of penetration varied between the sealers. Furthermore smear layer adversely affected the coronal and apical sealing ability of sealers.

Çobankara et al. (2004) determined the effect of the smear layer on apical and coronal leakage in root canals obturated with AH26 or RoekoSeal sealers. A total of 160 maxillary anterior teeth were used. Eight groups were created by all possible combinations of three factors: smear layer (present/absent), leakage assessment (apical/coronal), and sealer used (AH26/Roeko-Seal). All teeth were obturated using lateral condensation technique of gutta-percha. A fluid filtration method was used to test apical or coronal leakage. According to the results of this study, the smear (+) groups displayed higher apical and coronal leakage than those smear (-) groups for both root canal sealers. Apical leakage was significantly higher than coronal leakage for both root canal sealers used in this study. It was determined that that removal of the smear layer has a positive effect in reducing apical and coronal leakage for both AH26 and RoekoSeal root canal sealers.

However Bertacci et al. (2007) evaluated the ability of a warm gutta-percha obturation system Thermafil to fill lateral channels in the presence or absence of the smear layer. Forty single-rooted extracted human teeth were randomly divided into two groups one of which had the smear layer removed by 5 ml of 5% NaOCl followed by 2.5 ml of 17% EDTA. Obturation was performed using AH Plus sealer and Thermafil. Specimens were cleared in methyl salicylate and analyzed under a stereomicroscope to evaluate the number, length, and diameter of lateral channels. All lateral channels were found to be filled in both groups. No statistically significant differences regarding number, length, and diameter were observed between the two groups. It was concluded that the smear layer did not prevent the sealing of lateral channels.

Yildirim et al. (2008) investigated the effect of the smear layer on apical microleakage in teeth obturated with MTA. Fifty single-rooted central maxillary teeth were used in this study. The selected teeth were instrumented and randomly divided into 2 groups. In the first group (smear [+]), the teeth were irrigated with only 5.25% NaOCl. In the second group (smear [-]), the teeth were irrigated with EDTA (17%) and NaOCl (5.25%) to remove the smear layer. The teeth were then filled with MTA. The computerized fluid filtration method was used for evaluation of apical microleakage. The quantitative apical leakage of each tooth was measured after 2, 30, and 180 days. It was found that there was no difference between the groups after 2 days but removal of the smear layer caused significantly more apical microleakage than when the smear layer was left intact after 30 and 180 days. It was concluded that the apical microleakage of MTA is less when the smear layer is present than when it is absent.

Saleh et al. (2008) studied the effect of the smear layer on the penetration of bacteria along different root canal filling materials. A total of 110 human root segments were instrumented to size 80 under irrigation with 1% sodium hypochlorite. Half of the roots were irrigated with a 5-mL rinse of 17% EDTA to remove the smear layer. Roots were filled with gutta-percha (GP) and AH Plus sealer (AH), GP and Apexit sealer (AP), or RealSeal cones and sealer (RS). Following storage in humid conditions at 37 degrees C for 7 days, the specimens were mounted into a bacterial leakage test model for 135 days. Survival analyses were performed to calculate the median time of leakage and log-rank test was used for pairwise comparisons of groups. Selected specimens were longitudinally sectioned and inspected by scanning electron microscopy for the presence of bacteria at the interfaces. In the presence of the smear layer, RS and AP leaked significantly more slowly than in its absence. In the absence of the smear layer, AH leaked significantly more slowly than RS. It was concluded that removal of the smear layer did not impair bacterial penetration along root canal fillings. A comparison of the sealers revealed no difference except that AH performed better than RS in the absence of the smear layer.

Fachin et al.(2009) evaluated whether smear layer removal has any influence on the filling of the root canal system, by examining the obturation of lateral canals, secondary canals and apical deltas. Eighty canines were randomly divided into two groups, according to their irrigation regimen. Both groups were irrigated with 1% NaOCl during canal shaping, but only the teeth in Group II received a final irrigation with 17% EDTA for smear layer removal. The root canals were obturated with lateral condensation of gutta-percha and the specimens were cleared, allowing for observation under the microscope. The results showed that In Groups I and II, 42.5% and 37.5% of the teeth, respectively, presented at least one filled canal ramification. In conclusion, smear layer removal under the conditions tested in this study did not affect the obturation of root canal ramifications when lateral condensation of gutta-percha was the technique used for root canal filling.

Dentin hypersensitivity is a relatively common condition. Due to differences in populations studied and methods of detection, the reported incidence ranges from 4-74%. Dentists may under-report dentin hypersensitivity due to difficulty in diagnosing and managing the condition. When questionnaires are used, the reported incidence is usually higher than when clinical examination is used. Overall, it is estimated to affect about 15% of the general population to some degree.

It can affect people of any age, although those aged 20–50 years are more likely to be affected. Females are slightly more likely to develop dentin hypersensitivity compared to males. The condition is most commonly associated with the maxillary and mandibular canine and bicuspid teeth on the facial (buccal) aspect, especially in areas of periodontal attachment loss.

Dentin hypersensitivity may affect individuals' quality of life. Over time, the dentin-pulp complex may adapt to the decreased insulation by laying down tertiary dentin, thereby increasing the thickness between the pulp and the exposed dentin surface and lessening the symptoms of hypersensitivity. Similar process such as formation of a smear layer (e.g. from toothbrushing) and dentin sclerosis. These physiologic repair mechanisms are likely to occur with or without any form of treatment, but they take time.

Tobacco smoking or chewing is the most common causative factor, with more than 80% of persons with leukoplakia having a positive smoking history. Smokers are much more likely to suffer from leukoplakia than non-smokers. The size and number of leukoplakia lesions in an individual is also correlated with the level of smoking and how long the habit has lasted for. Other sources argue that there is no evidence for a direct causative link between smoking and oral leukoplakia. Cigarette smoking may produce a diffuse leukoplakia of the buccal mucosa, lips, tongue and rarely the floor of mouth. Reverse smoking, where the lit end of the cigarette is held in the mouth is also associated with mucosal changes. Tobacco chewing, e.g. betel leaf and areca nut, called paan, tends to produce a distinctive white patch in a buccal sulcus termed "tobacco pouch keratosis". In the majority of persons, cessation triggers shrinkage or disappearance of the lesion, usually within the first year after stopping.

Although the synergistic effect of alcohol with smoking in the development of oral cancer is beyond doubt, there is no clear evidence that alcohol is involved in the development of leukoplakia, but it does appear to have some influence. Excessive use of a high alcohol containing mouth wash (> 25%) may cause a grey plaque to form on the buccal mucosa, but these lesions are not considered true leukoplakia.

A 2003 survey of diseases of the foot in 16 European countries found onychomycosis to be the most frequent fungal foot infection and estimates its prevalence at 27%. Prevalence was observed to increase with age. In Canada, the prevalence was estimated to be 6.48%. Onychomycosis affects approximately one-third of diabetics and is 56% more frequent in people suffering from psoriasis.

Following effective treatment recurrence is common (10–50%).

Nail fungus can be painful and cause permanent damage to nails. It may lead to other serious infections if the immune system is suppressed due to medication, diabetes or other conditions. The risk is most serious for people with diabetes and with immune systems weakened by leukemia or AIDS, or medication after organ transplant. Diabetics have vascular and nerve impairment, and are at risk of cellulitis, a potentially serious bacterial infection; any relatively minor injury to feet, including a nail fungal infection, can lead to more serious complications. Infection of the bone is another rare complication.

The exact cause of Majocchi's granuloma is not well established however a dysfunctinoal immune system may be a causative factor. The first form of MG, the superficial perifollicular form occurs predominately on the legs of otherwise healthy young women who repeatedly shave their legs and develop hair follicle occlusions that directly or indirectly disrupt the follicle and allow for passive introduction of the organism into the dermis. Hence, the physical barrier of the skin is important because it prevents the penetration of microorganisms. Physical factors that play a major role in inhibiting dermal invasion include the interaction among keratin production, the rate of epidermal turnover, the degree of hydration and lipid composition of the stratum corneum, CO levels, and the presence or absence of hair. Keratin and/or necrotic material can also be introduced into the dermis with an infectious organism to further enhance the problem. In immunocompromised individuals, the use of topical corticosteroids may lead to a dermatophyte infection due to local immunosuppression.

"Follicular hyperkeratosis" dass (also called "phrynoderma") is a skin condition characterized by excessive development of keratin in hair follicles, resulting in rough, cone-shaped, elevated papules. The openings are often closed with a white plug of encrusted sebum.

This condition has been shown in several small-scale studies to respond well to supplementation with vitamins and fats rich in essential fatty acids. Deficiencies of vitamin E, vitamin A, and B complex vitamins have been implicated in causing the condition.

Sarcoma botryoides normally is found in children under 8 years of age. Onset of symptoms occurs at age 3 years (38.3 months) on average. Cases of older women with this condition have also been reported.

Hyperkeratosis is thickening of the stratum corneum (the outermost layer of the epidermis), often associated with the presence of an abnormal quantity of keratin, and also usually accompanied by an increase in the granular layer. As the corneum layer normally varies greatly in thickness in different sites, some experience is needed to assess minor degrees of hyperkeratosis.

It can be caused by vitamin A deficiency or chronic exposure to arsenic.

Hyperkeratosis can also be caused by B-Raf inhibitor drugs such as Vemurafenib and Dabrafenib.

It can be treated with urea-containing creams, which dissolve the intercellular matrix of the cells of the stratum corneum, promoting desquamation of scaly skin, eventually resulting in softening of hyperkeratotic areas.

Fungicidal agents such as azadirachtin and phytoallexin have been used against some muscardine pathogens. Silkworm breeders dust their cages with slaked lime to discourage fungal growth. In India a dust of chaff soaked in formalin is applied to the larvae.

Muscardine is a disease of insects. It is caused by many species of entomopathogenic fungus. Many muscardines are known for affecting silkworms. Muscardine may also be called calcino.

While studying muscardine in silkworms in the 19th century, Agostino Bassi found that the causal agent was a fungus. This was the first demonstration of the germ theory of disease, the first time a microorganism was recognized as an animal pathogen.

There are many types of muscardine. They are often named for the color of the conidial layer each fungus leaves on its host.

This condition is an autosomal recessive genetic disorder, which means the defective gene is located on an autosome, and both parents must carry one copy of the defective gene in order to have a child born with the disorder. Carriers of a recessive gene usually do not show any signs or symptoms of the disorder.

One form of ichthyosis lamellaris (LI1) is associated with a deficiency of the enzyme keratinocyte transglutaminase.

Genes involved include:

Cervical ectropion is a normal phenomenon, especially in the ovulatory phase in younger women, during pregnancy, and in women taking the oral contraceptive pill, which increases the total estrogen level in the body. It also may be a congenital problem by persistence of the squamocolumnar junction which is normally present prior to birth.

Mucopurulent cervicitis may increase the size of the cervical ectropion.

"Cervical ectropion" (or cervical eversion) is a condition in which the cells from the ‘inside’ of the cervical canal known as glandular cells (or columnar epithelium), are present on the ‘outside’ of the vaginal portion of the cervix. The cells on the ‘outside’ of the cervix are called squamous epithelial cells. Where the two cells meet is called the transformation zone also known as the stratified squamous epithelium. Although having this condition is not an abnormality, it is indistinguishable from early cervical cancer. When at a routine check up, it can be seen by the nurse when a cervical screening test (or smear test) is done. The area may look red because the glandular cells are red. While many women are born with cervical ectropion, it can be caused by a number of reasons, such as:

- Hormonal changes, so meaning it can be common in young women.

- Taking “the pill” to protect from pregnancy

- Pregnancy

The appearance is often described as a shiny film looking like a layer of vaseline. The eyelids and mouth may have the appearance of being forced open due to the tightness of the skin. There can be associated eversion of the eyelids (ectropion).

Collodion baby can have severe medical consequences, mainly because the baby can lose heat and fluid through the abnormal skin. This can lead to hypothermia and dehydration. Strategies to prevent these problems are the use of emollients or nursing the baby in a humidified . There is also an increased risk of skin infection and mechanical compression, leading to problems like limb ischemia. There is also a risk of intoxication by cutaneous absorption of topical products, for example salicylate intoxication (similar to aspirin overdose) due to keratolytics.

The condition is not thought to be painful or in itself distressing to the child. Nursing usually takes place in a neonatal intensive care unit, and good intensive care seems to have improved the prognosis markedly. The collodion membrane should peel off or "shed" 2 to 4 weeks after birth, revealing the underlying skin disorder.

The condition can resemble but is different from harlequin type ichthyosis.

Given that episodes tend to occur on awakening and managed by use of good 'wetting agents', approaches to be taken to help prevent episodes include:

- Environmental:

- ensuring that the air is humidified rather than dry, not overheated and without excessive airflow over the face. Also avoiding irritants such as cigarette smoke.

- use of protective glasses especially when gardening or playing with children.

- General personal measures:

- maintaining general hydration levels with adequate fluid intake.

- not sleeping-in late as the cornea tends to dry out the longer the eyelids are closed.

- Pre-bed routine:

- routine use of long-lasting eye ointments applied before going to bed.

- occasional use of the anti-inflammatory eyedrop FML (prescribed by an ophthalmologist or optometrist) before going to bed if the affected eye feels inflamed, dry or gritty

- use of a hyperosmotic (hypertonic) ointment before bed reduces the amount of water in the epithelium, strengthening its structure

- use the pressure patch as mentioned above.

- use surgical tape to keep the eye closed (if Nocturnal Lagophthalmos is a factor)

- Waking options:

- learn to wake with eyes closed and still and keeping artificial tear drops within reach so that they may be squirted under the inner corner of the eyelids if the eyes feel uncomfortable upon waking.

- It has also been suggested that the eyelids should be rubbed gently, or pulled slowly open with your fingers, before trying to open them, or keeping the affected eye closed while "looking" left and right to help spread lubricating tears. If the patient's eyelids feel stuck to the cornea on waking and no intense pain is present, use a fingertip to press firmly on the eyelid to push the eye's natural lubricants onto the affected area. This procedure frees the eyelid from the cornea and prevents tearing of the cornea.

The disease used to be uniformly fatal, with a 5-year survival rate between 10 and 35%. As a result, treatment was radical surgery. New multidrug chemotherapy regimens with or without radiation therapy are now used in combination with less radical surgery with good results, although outcome data are not yet available.

Historically, there have been many types of dermatophytes that were known to cause Majocchi's granuloma. Trichophyton violaceum used to be one of the most common species of dermatophytes to cause this disease. Today, however, Trichophyton rubrum proves to be the main culprit is most cases. These fungi are keratinophilic and colonize or infect the superficial keratinized tissues (the skin, nails, and hair) of humans and animals. The organisms are usually restricted to the non-living cornified layer of the epidermis and do not invade beyond the epidermis. The fungi are usually unable to penetrate into viable tissues in a immunocompetent host and therefore many times the infection incidence is higher in immune compromised individuals. There are two forms of MG: (i) the small, perifollicular papular form, which is a localized dermal infection that usually occurs in healthy individuals and (ii) the form featuring deep subcutaneous plaques or nodular lesions that occur in immunosuppressed hosts. Tinea corporis is the name of the subset of this disease that only remains restricted to the stratum corneum. Otherwise, the atypical deeper involvement is known as Majocchi's granuloma. Because keratinophilic dermatophytes digest keratin, the introduction of keratin into the dermis may also act as a medium for continued growth of the organism.

Black pigment gallstones can form in Rokitansky–Aschoff sinuses of the gallbladder after the fourth to fifth decades of life in absence of the typical risk factors for bilirubin suprasaturation of bile. Hence, they are associated with gallstones (cholelithiasis). Cases of gall bladder cancer have also been reported to arise from Rokitansky–Aschoff sinuses.

A cutaneous condition is any medical condition that affects the integumentary system—the organ system that encloses the body and includes skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment.

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 causes 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), cause (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). The 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. The introduction of cutaneous ultrasound has allowed the detection of cutaneous tumors, inflammatory processes, nail disorders and hair diseases.

Diseases of the skin include skin infections and skin neoplasms (including skin cancer).

Neutrophil-specific granule deficiency (SGD, previously known as lactoferrin deficiency) is a rare congenital immunodeficiency characterized by an increased risk for pyogenic infections due to defective production of specific granules and gelatinase granules in patient neutrophils.