Differentiation between this and SCC would be based on a history of recent trauma or dental treatment in the area.

Immunohistochemistry may aid the diagnosis. If the lesion is NS, there will be focal to absent immunoreactivity for p53, low immunoreactivity for MIB1 (Ki-67), and the presence of 4A4/p63- and calponin-positive myoepithelial cells.

Healing is prolonged, and usually takes 6–10 weeks. The ulcer heals by secondary intention.

While recent case series (n=9-80) studies have found a mortality rate of 20-40%, a large (n=1641) 2009 study reported a mortality rate of 7.5%.

Acute esophageal necrosis can only be diagnosed by an upper gastrointestinal endoscopy.

Diagnosis is made by clinical observation and the following tests.

(1) Gram stain of the fluid from pustules or bullae, and tissue swab.

(2) Blood culture

(3) Urine culture

(4) Skin biopsy

(5) Tissue culture

Magnetic resonance imaging can be done in case of ecthyma gangrenosum of plantar foot to differentiate from necrotizing fasciitis.

Fournier gangrene is usually diagnosed clinically, but laboratory tests and imaging studies are used to confirm diagnosis, determine severity and predict outcomes. X-rays and ultrasounds may show the presence of gas below the surface of the skin. A CT scan can be useful in determining the site of origin and extent of spread.

Early diagnosis is difficult as the disease often looks early on like a simple superficial skin infection. While a number of laboratory and imaging modalities can raise the suspicion for necrotizing fasciitis, the gold standard for diagnosis is a surgical exploration in the setting of high suspicion. When in doubt, a small "keyhole" incision can be made into the affected tissue, and if a finger easily separates the tissue along the fascial plane, the diagnosis is confirmed and an extensive debridement should be performed.

Computed tomography (CT scan) is able to detect approximately 80% of cases while MRI may pick up slightly more.

Currently, there is no direct treatment for AEN. Only treatment is for the underlying main diseases or conditions. Appropriate hydration is set. Antacids are also added for further recovery support. Common support drugs of antacids are either H receptor antagonists, and/or a proton pump inhibitor. Sucralfate was used as an option. Parenteral nutrition greatly increased chance of recovery. An esophagectomy can be issued if the disorder is severe enough.

Chronic ulcerative stomatitis is a recently discovered condition with specific immunopathologic features. It is characterized by erosions and ulcerations which relapse and remit. Lesions are located on the buccal mucosa (inside of the cheeks) or on the gingiva (gums). The condition resembles Oral lichen planus when biopsied.

The diagnosis is made with Immunofluorescence techniques, which shows circulating and tissue-bound autoantibodies (particulate stratified squamous-epithelium-specific antinuclear antibody) to DeltaNp63alpha protein, a normal component of the epithelium. Treatment is with hydroxychloroquine.

Cerebral angiography and magnetic resonance imaging, family medical history, symptoms, a complete physical examination, and ultimately biopsy of the brain, are often required for the diagnosis. Also, many lab tests must be done for the diagnosis; tests may reveal anemia (a shortage of red blood cells), a high white blood cell count, a high platelet count, allergic reactions, immune complexes, antibodies (tools the body uses to fight off threats) and elevation of inflammatory markers. Another crucial part in the diagnosis of cerebral vasculitis is the use of imaging techniques. Techniques such as conventional digital subtraction angiography (DSA) and magnetic resonance imaging (MRI) are used to find and monitor cerebral involvement.

The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score can be utilized to risk stratify people having signs of cellulitis to determine the likelihood of necrotizing fasciitis being present. It uses six serologic measures: C-reactive protein, total white blood cell count, hemoglobin, sodium, creatinine and glucose. A score greater than or equal to 6 indicates that necrotizing fasciitis should be seriously considered. The scoring criteria are as follows:

- CRP (mg/L) ≥150: 4 points

- WBC count (×10/mm)

- <15: 0 points

- 15–25: 1 point

- >25: 2 points

- Hemoglobin (g/dL)

- >13.5: 0 points

- 11–13.5: 1 point

- <11: 2 points

- Sodium (mmol/L) <135: 2 points

- Creatinine (umol/L) >141: 2 points

- Glucose (mmol/L) >10: 1 point

As per the derivation study of the LRINEC score, a score of ≥6 is a reasonable cut-off to rule in necrotizing fasciitis, but a LRINEC <6 does not completely rule out the diagnosis. Diagnoses of severe cellulitis or abscess should also be considered due to similar presentations. 10% of patients with necrotizing fasciitis in the original study still had a LRINEC score <6. But a validation study showed that patients with a LRINEC score ≥6 have a higher rate of both mortality and amputation.

The main organism associated with ecthyma gangrenosum is "Pseudomonas aeruginosa". However, multi-bacterial cases are reported as well. Prevention measures include practicing proper hygiene, educating the immunocompromised patients for awareness to avoid possible conditions and seek timely medical treatment.

The white lesion cannot be wiped away, unlike some other common oral white lesions, e.g. pseudomembranous candidiasis, and this may aid in the diagnosis. Diagnosis of OHL is mainly clinical, but can be supported by proof of EBV in the lesion (achieved by in situ hybridization, polymerase chain reaction, immunohistochemistry, Southern blotting, or electron microscopy) and HIV serotesting. When clinical appearance alone is used to diagnose OHL, there is a false positive rate of 17% compared to more objective methods. The appearance of OHL in a person who is known to be infected with HIV does not usually require further diagnostic tests as the association is well known. OHL in persons with no known cause of immunocompromise usually triggers investigations to look for an underlying cause. If tissue biopsy is carried out, the histopathologic appearance is of hyperlastic and parakeratinized epithelium, with "balloon cells" (lightly staining cells) in the upper stratum spinosum and "nuclear beading" in the superficial layers (scattered cells with peripheral margination of chromatin and clear nuclei, created by displacement of chromatin to the peripheral nucleus by EBV replication). Candida usually is seen growing in the parakeratin layer, but there are no normal inflammatory reactions to this in the tissues. There is no dysplasia (OHL is not a premalignant lesion).

The diagnostic testing for vasculitis should be guided by the patient's history and physical exam. The clinician should ask about the duration, onset, and presence any associated symptoms such as weight loss or fatigue (that would indicate a systemic cause). It is important to distinguish between IgA and non-IgA vasculitis. IgA vasculitis is more likely to present with abdominal pain, bloody urine, and joint pain. In the case that the cause is not obvious, a reasonable initial workup would include a complete blood count, urinalysis, basic metabolic panel, fecal occult blood testing, erythrocyte sedimentation rate (ESR), and C-reactive protein level. Small vessel cutaneous vasculitis is a diagnosis of exclusion and requires ruling out systemic causes of the skin findings. Skin biopsy (punch or excisional) is the most definitive diagnostic test and should be performed with 48 hours of appearance of the vasculitis. A skin biopsy will be able to determine if the clinical findings are truly due to a vasculitis or due to some other cause.

Treatment is first with many different high-dose steroids, namely glucocorticoids. Then, if symptoms do not improve additional immunosuppression such as cyclophosphamide are added to decrease the immune system's attack on the body's own tissues. Cerebral vasculitis is a very rare condition that is difficult to diagnose, and as a result there are significant variations in the way it is diagnosed and treated.

Diagnosis is usually clinical. Smear for fusospirochaetal bacteria and leukocytes; blood picture occasionally. The important differentiation is with acute leukaemia or herpetic stomatitis.

Other than identifying and treating any underlying conditions in secondary livedo, idiopathic livedo reticularis may improve with warming the area.

As of tissue or discharge are generally unreliable, the diagnosis of mucormycosis tends to be established with a biopsy specimen of the involved tissue.

A detailed history is important to elicit any recent medications, any risk of hepatitis infection, or any recent diagnosis with a connective tissue disorder such as systemic lupus erythematosus (SLE). A thorough physical exam is needed as usual.

- Lab tests. Basic lab tests may include a CBC, chem-7 (look for creatinine), muscle enzyme, liver function tests, ESR, hepatitis seroloties, urinalysis, CXR, and EKG. Additional, more specific tests include:

- Antinuclear antibody (ANA) test can detect an underlying connective tissue disorder, especially SLE

- Complement levels that are low can suggest mixed cryoglobulinemia, hepatitis C infection, and SLE, but not most other vasculitides.

- Antineutrophil cytoplasmic antibody (ANCA) may highly suggest granulomatosis with polyangiitis, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis, or drug-induced vasculitis, but is not diagnostic.

- Electromyography. It is useful if a systemic vasculitis is suspected and neuromuscular symptoms are present.

- Arteriography. Arteriograms are helpful in vasculitis affecting the large and medium vessels but not helpful in small vessel vasculitis. Angiograms of mesenteri or renal arteries in polyarteritis nodosa may show aneurysms, occlusions, and vascular wall abnormalities. Arteriography are not diagnostic in itself if other accessible areas for biopsy are present. However, in Takayasu's arteritis, where the aorta may be involved, it is unlikely a biopsy will be successful and angiography can be diagnostic.

- Tissue biopsy. This is the gold standard of diagnosis when biopsy is taken from the most involved area.

Diagnosis of mouth ulcers usually consists of a medical history followed by an oral examination as well as examination of any other involved area. The following details may be pertinent: The duration that the lesion has been present, the location, the number of ulcers, the size, the color and whether it is hard to touch, bleeds or has a rolled edge. As a general rule, a mouth ulcer that does not heal within 2 or 3 weeks should be examined by a health care professional who is able to rule out oral cancer (e.g. a dentist, oral physician, oral surgeon, or maxillofacial surgeon). If there have been previous ulcers which have healed, then this again makes cancer unlikely.

An ulcer that keeps forming on the same site and then healing may be caused by a nearby sharp surface, and ulcers that heal and then recur at different sites are likely to be RAS. Malignant ulcers are likely to be single in number, and conversely, multiple ulcers are very unlikely to be oral cancer. The size of the ulcers may be helpful in distinguishing the types of RAS, as can the location (minor RAS mainly occurs on non-keratinizing mucosa, major RAS occurs anywhere in the mouth or oropharynx). Induration, contact bleeding and rolled margins are features of a malignant ulcer. There may be nearby causative factor, e.g. a broken tooth with a sharp edge that is traumatizing the tissues. Otherwise, the person may be asked about problems elsewhere, e.g. ulceration of the genital mucous membranes, eye lesions or digestive problems, swollen glands in neck (lymphadenopathy) or a general unwell feeling.

The diagnosis comes mostly from the history and examination, but the following special investigations may be involved: blood tests (vitamin deficiency, anemia, leukemia, Epstein-Barr virus, HIV infection, diabetes) microbiological swabs (infection), or urinalysis (diabetes). A biopsy (minor procedure to cut out a small sample of the ulcer to look at under a microscope) with or without immunofluorescence may be required, to rule out cancer, but also if a systemic disease is suspected. Ulcers caused by local trauma are painful to touch and sore. They usually have an irregular border with erythematous margins and the base is yellow. As healing progresses, a keratotic (thickened, white mucosa) halo may occur.

The oral lesion itself is benign and self-limiting, however this may not necessarily be the case for the underlying cause of immunocompromise. For instance, OHL with HIV/AIDS is a predictor of bad prognosis, (i.e. severe immunosuppression and advanced disease).

Dry socket typically causes pain on the second to fourth day following a dental extraction. Other causes of post extraction pain usually occur immediately after the anesthesia/analgesia has worn off, (e.g., normal pain from surgical trauma or mandibular fracture) or has a more delayed onset (e.g., osteomyelitis, which typically causes pain several weeks following an extraction). Examination typically involves gentle irrigation with warm saline and probing of the socket to establish the diagnosis. Sometimes part of the root of the tooth or a piece of bone fractures off and is retained in the socket. This can be another cause of pain in a socket, and causes delayed healing. A dental radiograph (x-ray) may be indicated to demonstrate such a suspected fragment.

A systematic review reported that there is some evidence that rinsing with chlorhexidine (0.12% or 0.2%) or placing chlorhexidine gel (0.2%) in the sockets of extracted teeth reduces the frequency of dry socket. Another systematic review concluded that there is evidence that prophylactic antibiotics reduce the risk of dry socket (and infection and pain) following third molar extractions of wisdom teeth, however their use is associated with an increase in mild and transient adverse effects. The authors questioned whether treating 12 patients with antibiotics to prevent one infection would do more harm overall than good, in view of the potential side effects and also of antibiotic resistance. Nevertheless, there is evidence that in individuals who are at clear risk may benefit from antibiotics. There is also evidence that antifibrinolytic agents applied to the socket after the extraction may reduce the risk of dry socket.

Some dentists and oral surgeons routinely debride the bony walls of the socket to encourage hemorrhage (bleeding) in the belief that this reduces the incidence of dry socket, but there is no evidence to support this practice. It has been suggested that dental extractions in females taking oral contraceptives be scheduled on days without estrogen supplementation (typically days 23–28 of the menstrual cycle). It has also been suggested that teeth to be extracted be scaled prior to the procedure.

Prevention of alveolar osteitis can be exacted by following post-operative instructions, including:

1. Taking any recommended medications

2. Avoiding intake of hot fluids for one to two days. Hot fluids raise the local blood flow and thus interfere with organization of the clot. Therefore, cold fluids and foods are encouraged, which facilitate clot formation and prevent its disintegration.

3. Avoiding smoking. It reduces the blood supply, leading to tissue ischemia, reduced tissue perfusion and eventually higher incidence of painful socket.

4. Avoiding drinking through a straw or spitting forcefully as this creates a negative pressure within the oral cavity leading to an increased chance of blood clot instability.

Treatment includes irrigation and debridement of necrotic areas (areas of dead and/or dying gum tissue), oral hygiene instruction and the uses of mouth rinses and pain medication. If there is systemic involvement, then oral antibiotics may be given, such as metronidazole. As these diseases are often associated with systemic medical issues, proper management of the systemic disorders is appropriate.

Because many "Candida" species are part of the human microbiota, their presence in the mouth, the vagina, sputum, urine, stool, or skin is not definitive evidence for invasive candidiasis.

Positive culture of "Candida" species from normally sterile sites, such as blood, cerebrospinal fluid, pericardium, pericardial fluid, or biopsied tissue, is definitive evidence of invasive candidiasis. Diagnosis by culturing allows subsequent susceptibility testing of causitive species. Sensitivity of blood culture is far from ideal, with a sensitivity reported to be between 21 and 71%. Additionally, whereas blood culture can establish a diagnosis during fungemia, the blood may test negative for deep-seated infections because candida may have been successfully cleared from the blood.

Diagnosis of invasive candidiasis is supported by histopathologic evidence (for example, yeast cells or hyphae) observed in specimens of affected tissues.

Additionally, elevated serum β-glucan can demonstrate invasive candidiasis while a negative test suggests a low likelihood of systemic infection.

The emergence of multidrug-resistant "C. auris" as a cause of invasive candidiasis has necessitated additional testing in some settings. "C. auris"-caused invasive candidiasis is associated with high mortality. Many "C. auris" isolates have been found to be resistant to one or more of the three major antifungal classes (azoles, echinocandins, and polyenes) with some resistant to all three classes - severely limiting treatment options. Biochemical-based tests currently used in many laboratories to identify fungi, including API 20C AUX and VITEK-2, cannot differentiate "C. auris" from related species (for example, "C. auris" can be identified as "C. haemulonii"). Therefore, the Centers for Disease Control and Prevention recommends using a diagnostic method based on matrix-assisted laser desorption/ionization-time of flight mass spectrometry or a molecular method based on sequencing the D1-D2 region of the 28s rDNA to identify "C. auris" in settings were it may be present.