Acute inflammation is a short-term process, usually appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus. It involves a coordinated and systemic mobilization response locally of various immune, endocrine and neurological mediators of acute inflammation. In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and then ceases. It is characterized by five cardinal signs:

An acronym that may be used to remember the key symptoms is "PRISH", for pain, redness, immobility (loss of function), swelling and heat.

The traditional names for signs of inflammation come from Latin:

- Dolor (pain)

- Calor (heat)

- Rubor (redness)

- Tumor (swelling)

- Functio laesa (loss of function)

The first four (classical signs) were described by Celsus (ca. 30 BC–38 AD), while "loss of function" was probably added later by Galen. However, the addition of this fifth sign has also been ascribed to Thomas Sydenham and Virchow.

Redness and heat are due to increased blood flow at body core temperature to the inflamed site; swelling is caused by accumulation of fluid; pain is due to the release of chemicals such as bradykinin and histamine that stimulate nerve endings. Loss of function has multiple causes.

Acute inflammation of the lung (usually caused in response to pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings.

Inflammation (from Latin "") is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

The classical signs of inflammation are heat, pain, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body.

Inflammation can be classified as either "acute" or "chronic". "Acute inflammation" is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as "chronic inflammation", leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.

Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response — the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the body's immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix "" (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word "urethritis" strictly means only "urethral inflammation", but clinical health care providers usually discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis.

It is useful to differentiate inflammation and infection as there are many pathological situations where inflammation is not driven by microbial invasion – for example, atherosclerosis, type III hypersensitivity, trauma, ischaemia. There are also pathological situations where microbial invasion does not result in classic inflammatory response—for example, parasitosis, eosinophilia.

Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. In the central nervous system (CNS), including the brain and spinal cord, microglia are the resident innate immune cells that are activated in response to these cues. The CNS is typically an immunologically privileged site because peripheral immune cells are generally blocked by the blood–brain barrier (BBB), a specialized structure composed of astrocytes and endothelial cells. However, circulating peripheral immune cells may surpass a compromised BBB and encounter neurons and glial cells expressing major histocompatibility complex molecules, perpetuating the immune response. Although the response is initiated to protect the central nervous system from the infectious agent, the effect may be toxic and widespread inflammation as well as further migration of leukocytes through the blood–brain barrier.

The "DSM-IV" specifies that ASD must be accompanied by the presence of dissociative symptoms, which largely differentiates it from PTSD.

Dissociative symptoms include a sense of numbing or detachment from emotional reactions, a sense of physical detachment, such as seeing oneself from another perspective, decreased awareness of one’s surroundings, the perception that one’s environment is unreal or dreamlike, and the inability to recall critical aspects of the traumatic event (dissociative amnesia).

In addition to the characteristic dissociative symptoms, ASD shares many of the symptoms with PTSD, including:

- the experience or witnessing of a threatening event that resulted in intense fear or horror

- the re-experiencing of the event by means of flashbacks, recurrent thoughts or dreams, and distress when reminded of the event

- the avoidance of stimuli that serve as reminders of the event, such as feelings, thoughts, places, individuals, and activities

- anxiety, including restlessness, difficulty sleeping and concentrating, and hypervigilance

- a significant disruption in normal social or work functioning

Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. However, pulpitis can also occur without any pain.

Acute stress reaction (also called acute stress disorder, psychological shock, mental shock, or simply shock) is a psychological condition arising in response to a terrifying or traumatic event, or witnessing a traumatic event that induces a strong emotional response within the individual. It should not be confused with the unrelated circulatory condition of shock/hypoperfusion. Acute stress reaction (ASR) may develop into delayed stress reaction (better known as PTSD) if stress is not correctly managed. ASR is characterized by re-living and avoiding reminders of an aversive event, as well as generalized hypervigilance after initial exposure to a traumatic event. ASD is differentiated from PTSD as a disorder that precedes it, and if symptoms last for more than one month, it will develop into PTSD. It can thus be thought of as the acute phase of PTSD.

Symptoms range in severity from mild to disabling.

Symptoms are common, but vague and non-specific for the condition. The most common are feeling tired, "brain fog" (short-term memory problems, difficulty concentrating), gastrointestinal problems, headaches, and muscle pain.

A partial list of other symptoms patients have attributed to MCS include: difficulty breathing, pains in the throat, chest, or abdominal region, skin irritation, headaches, neurological symptoms (nerve pain, pins and needles feelings, weakness, trembling, restless leg syndrome), tendonitis, seizures, visual disturbances (blurring, halo effect, inability to focus), anxiety, panic and/or anger, sleep disturbance, suppression of immune system, digestive difficulties, nausea, indigestion/heartburn, vomiting, diarrhea, joint pains, vertigo/dizziness, abnormally acute sense of smell (hyperosmia), sensitivity to natural plant fragrance or natural pine terpenes, dry mouth, dry eyes, and an overactive bladder.

Pulpitis is inflammation of dental pulp tissue. The pulp contains the blood vessels the nerves and connective tissue inside a tooth and provides the tooth’s blood and nutrients. Pulpitis is mainly caused by bacteria infection which itself is a secondary development of caries (tooth decay). It manifests itself in the form of a toothache.

There are seven sub-categories of physical urticaria:

- delayed pressure urticaria (DPU)

- cholinergic urticaria (ChU)

- cold urticaria (CU)

- solar urticaria (SU)

- Acute pressure urticaria (AU)

- chronic idiopathic urticaria (CIU)

- symptomatic dermatographism urticaria (SDU) (most common)

Kimura's disease is a benign rare chronic inflammatory disorder. Its primary symptoms are subdermal lesions in the head or neck or painless unilateral inflammation of cervical lymph nodes.

EE is rarely symptomatic and is considered a subclinical condition. However, adults may have mild symptoms or malabsorption such as altered stool consistency, increased stool frequency and weight loss.

Acute urticaria (short-term): can develop suddenly and will last "less" than 6 weeks. About 1 in 6 people will have acute hives at one point in their life.

Chronic urticaria (long-term): can develop suddenly and will persist "more" than 6 weeks. This type of urticaria is uncommon and occurs in only 0.1% of the population. 20% of people with chronic urticaria report still having problems 10 years after its onset.

Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. Chronic inflammation is the sustained activation of glial cells and recruitment of other immune cells into the brain. It is chronic inflammation that is typically associated with neurodegenerative diseases. Common causes of chronic neuroinflammation include:

- Toxic metabolites

- Autoimmunity

- Aging

- Microbes

- Viruses

- Traumatic brain injury

- Spinal cord injury

- Air pollution

- Passive smoke

Autoimmune pancreatitis (AIP) is an increasingly recognized type of chronic pancreatitis that can be difficult to distinguish from pancreatic carcinoma but which responds to treatment with corticosteroids, particularly prednisone. There are two categories of AIP: Type 1 and Type 2, each with distinct clinical profiles.

Type 1 AIP is now regarded as a manifestation of IgG4-related disease, and those affected have tended to be older and to have a high relapse rate. Type 1 is associated with pancreatitis, Sjogren syndrome, Primary sclerosing cholangitis and Inflammatory bowel disease. Patients with Type 2 AIP do not experience relapse, tend to be younger and not associated with systemic disease. AIP occurring in association with an autoimmune disorder has been referred to as "secondary" or "syndromic" AIP. AIP does not affect long-term survival.

The pain is sharp and sudden, in response to an external stimulus. The most common trigger is cold, with 75% of people with hypersensitivity reporting pain upon application of a cold stimulus. Other types of stimuli may also trigger pain in dentin hypersensitivity, including:

- Thermal – hot and cold drinks and foods, cold air, coolant water jet from a dental instrument.

- Electrical – electric pulp testers.

- Mechanical–tactile – dental probe during dental examination, periodontal scaling and root planing, toothbrushing.

- Osmotic – hypertonic solutions such as sugars.

- Evaporation – air blast from a dental instrument.

- Chemical – acids, e.g. dietary, gastric, acid etch during dental treatments.

The frequency and severity with which the pain occurs are variable.

The current gold standard diagnostic test for EE is intestinal biopsy and histological analysis. Histological changes observed include:

- Villous blunting

- Crypt hypertrophy

- Villous fusion

- Mucosal inflammation

However, this procedure is considered too invasive, complex and expensive to be implemented as standard of care. As a result, there are various research efforts underway to identify biomarkers associated with EE, which could serve as less invasive, yet representative, tools to screen for and identify EE from stool samples.

In an effort to identify simple, accurate diagnostic tests for EE, the Bill and Melinda Gates Foundation (BMGF) has established an EE biomarkers consortium as part of their Global Grand Challenges initiative (specifically, the Discover Biomarkers of Gut Function challenge).

So far, various biomarkers have been selected and studied based on the current understanding of EE pathophysiology:

- Gut permeability/barrier function

- Dual sugar permeability (lactose-to-mannitol ratio)

- Intestinal inflammation

- Alpha-1 anti-trypsin

- Neopterin

- Myeloperoxidase

- Exocrine (hormonal) markers

- Bacterial translocation markers

- Endotoxin core antibody

- Markers of systemic inflammation

- Alpha-1 glycoprotein

- C-reactive protein (CRP)

It is postulated that the limited of understanding of EE is partially due to the paucity of reliable biomarkers, making it difficult for researchers to track the epidemiology of the condition and assess the efficacy of interventions.

There is no clear consensus for the cause or causes of the symptoms of MCS. A 2007 National Institute of Environmental Health Sciences paper defined MCS as a "chronic, recurring disease caused by a person's inability to tolerate an environmental chemical or class of foreign chemicals".

In addition to extreme sensitivity to low concentrations of certain chemicals, several hypotheses have been proposed. The distinction between physiological and psychological causes is often difficult to test, and it is particularly challenging for MCS because many substances used to test for sensitivity have a strong odor. Odor cues make double blind studies of MCS patients difficult, as scents can provoke a psychosomatic response or recall expectations and prior beliefs. People with an MCS diagnosis show no differences in symptom severity, blood pressure, or heart rate when exposed to clean air or to solvents at a concentration too low to smell.

AIP is relatively uncommon and is characterized by the following features:

1. Scleral Icterus (yellow eyes), jaundice (yellow skin) which is usually painless, usually without acute attacks of pancreatitis.

2. Relatively mild symptoms, such as minimal weight loss or nausea.

3. Increased serum levels of gamma globulins, immunoglobulin G (IgG) or IgG4.

4. The presence of serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF).

5. Contrast-enhanced CT demonstrates a diffusely enlarged (sausage-shaped) pancreas.

6. Diffuse irregular narrowing of the main pancreatic duct, and stenosis of the intrapancreatic bile duct on endoscopic retrograde cholangiopancreatography (ERCP).

7. Rare pancreatic calcification or cyst formation.

8. Marked responsiveness to treatment with corticosteroids.

Two-thirds of patients present with either obstructive painless jaundice or a "mass" in the head of the pancreas mimicking carcinoma. It is mandatory to rule out carcinoma prior to making a diagnosis of AIP.

Recurrent pain is pain that arises periodically and can result in absences from school, outside activities, etc. This type of pain may be the most common.

Descriptions are:

- periodic instead of persistent

- consisting of tension and migraine headaches

- abdominal pains

- chest pain and limb pains

Fox–Fordyce disease, or apocrine miliaria, is a chronic blockage of the sweat gland ducts with a secondary, non-bacterial inflammatory response to the secretions and cellular debris in the cysts. The inflammation is often accompanied by intense itching. In general, the disease often causes skin to darken near the affected area and raised bumps or papules to appear. In addition, hair follicles can become damaged which cause hair loss.Hidradenitis is very similar, but tends to have a secondary bacterial infection so that pus-draining sinuses are formed. It is a very devastating skin disease that does not have universally curative treatments.

Autoimmunity is the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an "autoimmune disease". Prominent examples include celiac disease, diabetes mellitus type 1, sarcoidosis, systemic lupus erythematosus (SLE), Sjögren's syndrome, eosinophilic granulomatosis with polyangiitis, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, Addison's disease, rheumatoid arthritis (RA), ankylosing spondylitis, polymyositis (PM), dermatomyositis (DM) and multiple sclerosis (MS). Autoimmune diseases are very often treated with steroids.

Apical abscesses can spread to involve periodontal pockets around a tooth, and periodontal pockets cause eventual pulp necrosis via accessory canals or the apical foramen at the bottom of the tooth. Such lesions are termed periodontic-endodontic lesions, and they may be acutely painful, sharing similar signs and symptoms with a periodontal abscess, or they may cause mild pain or no pain at all if they are chronic and free-draining. Successful root canal therapy is required before periodonal treatment is attempted. Generally, the long-term prognosis of perio-endo lesions is poor.

NSAID or nonsteroidal anti-inflammatory drug hypersensitivity reactions encompasses a broad range of allergic or allergic-like symptoms that occur within minutes to hours after ingesting aspirin or other NSAID nonsteroidal anti-inflammatory drugs. Hypersensitivity drug reactions differ from drug toxicity reactions in that drug toxicity reactions result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual (see nonsteroidal anti-inflammatory drugs section on adverse reactions for NSAID-induced toxic reactions); hypersensitivity reactions are idiosyncratic reactions to a drug. Although the term NSAID was introduced to signal a comparatively low risk of adverse effects, NSAIDs do evoke a broad range of hypersensitivity syndromes. These syndromes have recently been classified by the European Academy of Allergy and Clinical Immunology Task Force on NSAIDs Hypersensitivity. The classification organizes the hypersensitivity reactions to NSAIDs into the following five categories:

- 1) NSAIDs-exacerbated respiratory disease (NERD) is an acute (immediate to several hours) exacerbation of bronchoconstriction and other symptoms of asthma (see aspirin-induced asthma) in individuals with a history of asthma and/or nasal congestion, rhinorrhea or other symptoms of rhinitis and sinusitis in individuals with a history of rhinosinusitis after ingestion of various NSAIDs, particularly those that act by inhibiting the COX-1 enzyme. NERD does not appear to be due to a true allergic reaction to NSAIDs but rather at least in part to the more direct effects of these drugs to promote the production and/or release of certain mediators of allergy. That is, inhibition of cellular COX activity deprives tissues of its anti-inflammatory product(s), particularly prostaglandin E2 while concurrently shuttling its substrate, arachidonic acid, into other metabolizing enzymes, particularly 5-lipoxygenase (ALOX5) to overproduce pro-inflammatory leukotriene and 5-Hydroxyicosatetraenoic acid metabolites and 15-lipoxygenase (ALOX15) to overproduce pro-inflammatory 15-Hydroxyicosatetraenoic acid metabolites, including eoxins; the condition is also associated with a reduction in the anti-inflammatory metabolite, lipoxin A4, and increases in certain pro-allergic chemokines such as eotaxin-2 and CCL7.

- 2) NSAIDs-exacerbated cutaneous disease (NECD) is an acute exacerbation of wheals and/or angioedema in individuals with a history of chronic urticaria. NECD also appears due to the non-allergic action of NSAIDs in inhibiting the production of COX anti-inflammatory metabolites while promoting the production 5-lipoxygenase and 15-lipoxygenase pro-inflammatory metabolites and the overproduction of certain pro-allergic chemokines, e.g. eotaxin-1, eotaxin-2, RANTES, and interleukin-5.

- 3) NSAIDs-induced urticarial disease (NEUD) is the acute development of wheals and/or angioedema in individuals with no history of chronic NSAIDs-induced urticaria or related diseases. The mechanism behind NEUD is unknown but may be due to the non-allergic action of NSAIDs in promoting the production and/or release of allergy mediators.

- 4) Single NSAID-induced urticarial/angioedema or anaphylaxis (SNIUAA) is the acute development of urticarial, angioedema, or anaphylaxis in response to a single type of NSAID and/or a single group of NSAIDs with a similar structure but not to other structurally unrelated NSAIDs in individuals with no history of underlying relevant chronic diseases. SNIUAA is due to a true IgE-mediated allergy reaction.

- 5 Single NSAID-induced delayed reactions (SNIDR) are a set of delayed onset (usually more than 24 hour) reactions to NSAIDs. SNIDR are most commonly skin reactions that may be relatively mild moderately severe such as maculopapular rash, fixed drug eruptions, photosensitivity reactions, delayed urticaria, and contact dermatitis or extremely severe such as the DRESS syndrome, acute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis (also termed Lyell's syndrome). SNIDR result from the drug-specific stimulation of CD4+ T lymphocytes and CD8+ cytotoxic T cells to elicit a delayed type hypersensitivity reaction.

Dentin hypersensitivity (abbreviated to DH, or DHS, and also termed sensitive dentin, dentin sensitivity, cervical sensitivity, and cervical hypersensitivity) is dental pain which is sharp in character and of short duration, arising from exposed dentin surfaces in response to stimuli, typically thermal, evaporative, tactile, osmotic, chemical or electrical; and which cannot be ascribed to any other dental disease.

A degree of dentin sensitivity is normal, but pain is not usually experienced in everyday activities like drinking a cooled drink. Therefore, although the terms "dentin sensitivity" and "sensitive dentin" are used interchangeably to refer to dental hypersensitivity, the latter term is the most accurate.

Signs of distress and pain are exhibited by:

- deliberate withdrawal from pain and possible guarding

- loud crying

- painful facial expressions