"Chronic nonspecific parotitis:"

This term is generally used for patients in whom no definite cause is found. Episodes may last for several days, paralleling the time course of a bacterial or viral illness. Others may experience episodes that last only a few hours from onset to resolution. Some episodes may last for several weeks. Quiescent periods between episodes last for hours, days, or even years.

"Recurrent parotitis of childhood:"

An uncommon syndrome in which recurring episodes clinically resembling mumps. Generally, episodes begin by age 5 years, and virtually all patients become asymptomatic by age 10–15 years. The duration of attacks averages 3–7 days but may last 2–3 weeks in some individuals. The spectrum varies from mild and infrequent attacks to episodes so frequent that they prevent regular school attendance.

Local heat applied to the gland, massaging the gland from back to front, and taking penicillin usually cure individual episodes. Treatment of individual infections may prevent injury to the gland parenchyma. Severe disease may be treated by parotidectomy.

"Sialadenosis (sialosis):"

In this disorder, both parotid glands may be diffusely enlarged with only modest symptoms. Patients are aged 20–60 years at onset, and the sexes are equally involved. The glands are soft and non-tender. Approximately half of the patients have endocrine disorders such as diabetes, nutritional disorders such as pellagra or kwashiorkor, or have taken drugs such as guanethidine, thioridazine, or isoprenaline.

"Sarcoidosis:"

The lungs, skin, and lymph nodes are most often affected, but the salivary glands are involved in approximately 10% of cases. Bilateral firm, smooth, and non-tender parotid enlargement is classic. Xerostomia occasionally occurs. The Heerfordt-Waldenstrom syndrome consists of sarcoidosis with parotid enlargement, fever, anterior uveitis, and facial nerve palsy.

"IgG4-related sialadenitis":

This term refers to IgG4-related disease (IgG4-RD) involving any of the major salivary glands, i.e. parotid or submandibular glands. This is often symmetrical and is usually associated with manifestations of IgG4-RD elsewhere in the body. IgG4-related sialadenitis is particularly associated with involvement of one or both of the lacrimal glands (referred to as IgG4-related dacryo-sialadenitis). "Mikulicz's disease", now considered to be a subtype of IgG4-related disease, was a term used when (i) any two of the parotid, submandibular and lacrimal glands were persistently and symmetrically enlarged and (ii) other diseases that may mimic this presentation were excluded.

"Pneumoparotitis:"

Air within the ducts of the parotid gland with or without inflammation. The duct orifice normally functions as a valve to prevent air from entering the gland from a pressurized oral cavity. Rarely, an incompetent valve allows insufflation of air into the duct system. Pneumoparotitis most commonly occurs in wind instrument players, glass blowers, and scuba divers.

Several lymph nodes reside within the parotid gland as a superficial and deep group of nodes. These nodes may be involved with any process that affects lymph nodes, including bacterial, fungal, viral, and neoplastic processes. Rarely, drugs such as iodides, phenylbutazone, thiouracil, isoproterenol, heavy metals, sulfisoxazole, and phenothiazines cause parotid swelling.

Swelling may be severe enough to put pressure on the eye and distort vision. Some patients first thought to have dacryoadenitis may turn out to have a malignancy of the lacrimal gland.

Blockage of the main parotid duct, or one of its branches, is often a primary cause of acute parotitis, with further inflammation secondary to bacterial superinfection. The blockage may be from a salivary stone, a mucous plug, or, more rarely, by a tumor, usually benign. Salivary stones (also called sialolithiasis, or salivary duct calculus) are mainly made of calcium, but do not indicate any kind of calcium disorder. Stones may be diagnosed via X-ray (with a success rate of about 80%), a computed tomography (CT) scan or Medical ultrasonography. Stones may be removed by manipulation in the doctor's office, or, in the worst cases, by surgery. Lithotripsy, also known as "shock wave" treatment, is best known for its use breaking up kidney stones. Lithotripsy can now be used on salivary stones as well. Ultrasound waves break up the stones, and the fragments flush out of the salivary duct.

About 60 percent of initial attacks of dacryocystitis will recur. Individuals with a poorly functioning immune system (immunocompromised) may develop orbital cellulitis, which may lead to optic neuritis, proptosis, motility abnormalities, or blindness.

Dacryoadenitis is inflammation of the lacrimal glands (the tear-producing glands).

Sinusitis (or rhinosinusitis) is defined as an inflammation of the mucous membrane that lines the paranasal sinuses and is classified chronologically into several categories:

- Acute rhinosinusitis – A new infection that may last up to four weeks and can be subdivided symptomatically into severe and non-severe. Some use definitions up to 12 weeks.

- Recurrent acute rhinosinusitis – Four or more full episodes of acute sinusitis that occur within one year

- Subacute rhinosinusitis – An infection that lasts between four and 12 weeks, and represents a transition between acute and chronic infection

- Chronic rhinosinusitis – When the signs and symptoms last for more than 12 weeks.

- Acute exacerbation of chronic rhinosinusitis – When the signs and symptoms of chronic rhinosinusitis exacerbate, but return to baseline after treatment

All these types of sinusitis have similar symptoms, and are thus often difficult to distinguish. Acute sinusitis is very common. Roughly ninety percent of adults have had sinusitis at some point in their life.

Headache/facial pain or pressure of a dull, constant, or aching sort over the affected sinuses is common with both acute and chronic stages of sinusitis. This pain is typically localized to the involved sinus and may worsen when the affected person bends over or when lying down. Pain often starts on one side of the head and progresses to both sides.

Acute sinusitis may be accompanied by thick nasal discharge that is usually green in color and may contain pus (purulent) and/or blood. Often a localized headache or toothache is present, and it is these symptoms that distinguish a sinus-related headache from other types of headaches, such as tension and migraine headaches. Another way to distinguish between toothache and sinusitis is that the pain in sinusitis is usually worsened by tilting the head forwards and with valsalva maneuvers.

Infection of the eye socket is possible, which may result in the loss of sight and is accompanied by fever and severe illness. Another possible complication is the infection of the bones (osteomyelitis) of the forehead and other facial bones – Pott's puffy tumor.

Sinus infections can also cause middle ear problems due to the congestion of the nasal passages. This can be demonstrated by dizziness, "a pressurized or heavy head", or vibrating sensations in the head. Post-nasal drip is also a symptom of chronic rhinosinusitis.

Halitosis (bad breath) is often stated to be a symptom of chronic rhinosinusitis; however, gold standard breath analysis techniques have not been applied. Theoretically, there are several possible mechanisms of both objective and subjective halitosis that may be involved.

A 2004 study suggested that up to 90% of "sinus headaches" are actually migraines. The confusion occurs in part because migraine involves activation of the trigeminal nerves, which innervate both the sinus region and the meninges surrounding the brain. As a result, it is difficult to accurately determine the site from which the pain originates. People with migraines do not typically have the thick nasal discharge that is a common symptom of a sinus infection.

Dacryocystitis is an infection of the lacrimal sac, secondary to obstruction of the nasolacrimal duct at the junction of lacrimal sac. The term derives from the Greek "dákryon" (tear), "cysta" (sac), and "-itis" (inflammation). It causes pain, redness, and swelling over the inner aspect of the lower eyelid and epiphora. When nasolacrimal duct obstruction is secondary to a congenital barrier it is referred to as dacrocystocele. It is most commonly caused by "Staphylococcus aureus" and "Streptococcus pneumoniae". The most common complication is corneal ulceration, frequently in association with "S. pneumoniae". The mainstays of treatment are oral antibiotics, warm compresses, and relief of nasolacrimal duct obstruction by dacryocystorhinostomy.

Affected individuals typically present with sudden painful proptosis, redness, and edema. Proptosis will vary according to the degree of inflammation, fibrosis, and mass effect. Occasionally, ptosis, chemosis, motility dysfunction (ophthalmoplegia), and optic neuropathy are seen. In the setting of extensive sclerosis there may be restriction, compression, and destruction of orbital tissue. Symptoms usually develop acutely (hours to days), but have also been seen to develop over several weeks or even months.Malaise, headaches, and nausea may accompany these symptoms. Other unusual presentations described include cystoid macular edema, temporal arteritis, and cluster headaches.

Pediatric IOI accounts for about 17% of cases idiopathic orbital inflammation. The most common sign is proptosis, but redness and pain are also experienced. Presentation varies slightly compared to adults with bilateral involvement, uveitis, disc edema and tissue eosinophilia being more common in this population. The presence of uveitis generally implies a poor outcome for pediatric IOI. Bilateral presentation may have a higher incidence of systemic disease.

Granulomatous disease, including sarcoidosis, granulomatosis with polyangiitis, and midline granuloma, may also lead to NLD obstruction.

Idiopathic orbital inflammatory (IOI) disease, or orbital pseudotumor, refers to a marginated mass-like enhancing soft tissue involving any area of the orbit. It is the most common painful orbital mass in the adult population, and is associated with proptosis, cranial nerve (Tolosa–Hunt syndrome), uveitis, and retinal detachment. Idiopathic orbital inflammatory syndrome, also known as orbital pseudotumor, was first described by Gleason in 1903 and by Busse and Hochhmein. It was then characterized as a distinct entity in 1905 by Birch-Hirschfeld. It is a benign, nongranulomatous orbital inflammatory process characterized by extraocular orbital and adnexal inflammation with no known local or systemic cause. Its diagnosis is of exclusion once neoplasm, primary infection and systemic disorders have been ruled-out. Once diagnosed, it is characterized by its chronicity, anatomic location or histologic subtype.

Idiopathic orbital inflammation has a varied clinical presentation depending on the involved tissue. It can range from a diffuse inflammatory process to a more localized inflammation of muscle, lacrimal gland or orbital fat. Its former name, orbital pseudotumor, is derived due to resemblance to a neoplasm. However, histologically it is characterized by inflammation. Although a benign condition, it may present with an aggressive clinical course with severe vision loss and oculomotor dysfunction.

Neoplasm should be considered in any patient presenting with NLD obstruction.In patients with an atypical presentation, including younger age and male gender, further workup is appropriate. Bloody punctal discharge or lacrimal sac distension above the medial canthal tendon is also highly suggestive of neoplasm.

Symptoms, if any, can be mild even in the presence of significant swelling or masses.

Lacrimal gland involvement may cause swelling of the upper eyelid, or proptosis if there is severe swelling. Other orbital masses or inflammation can result in visual disturbance (blurred vision, double vision, visual field impairment), restricted eye movements, pain or discomfort, numbness in the distribution of the supraorbital and/or infraorbital nerves, or proptosis.

IgG4-related ophthalmic disease has been estimated to account for approximately 25% of all cases of proptosis, eyelid swelling and other features of orbital swelling.

Acute pericoronitis (i.e. sudden onset and short lived, but significant, symptoms) is defined as "varying degrees of inflammatory involvement of the pericoronal flap and adjacent structures, as well as by systemic complications." Systemic complications refers to signs and symptoms occurring outside of the mouth, such as fever, malaise or swollen lymph nodes in the neck.

Pericoronitis may also be chronic or recurrent, with repeated episodes of acute pericoronitis occurring periodically. Chronic pericoronitis may cause few if any symptoms, but some signs are usually visible when the mouth is examined.

The extent of inflammation that can occur in IgG4-ROD is well demonstrated on magnetic resonance imaging (MRI).

Infraorbital nerve enlargement (IONE) is considered to be a particularly suspicious sign of IgG4-ROD, but seems to occur only when inflammation is in direct contact with the infraorbital canal. IONE is defined as the infraorbital nerve diameter being greater than the optic nerve diameter in the coronal plane.

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.

Salivary gland aplasia (also termed salivary gland agenesis) is the congenital absence of salivary glands. Usually the term relates to the absence of some or all of the major salivary glands.

It is a rare condition, and most known cases have been in association with syndromes of the ectodermal tissues, particularly the lacrimal apparatus. Example syndromes which have been reported with salivary gland aplasia include hereditary ectodermal dysplasia, mandibulofacial dysostosis and hemifacial microsomia.

The main significance of the condition is a lack of saliva, causing xerostomia (dry mouth), with accompanying susceptibility to dental caries (tooth decay), infections of the mouth, and upper respiratory tract infections (e.g., candidiasis, ascending sialadenitis, laryngitis and pharyngitis). Patients with salivary gland aplasia typically require regular application of topical fluoride to prevent tooth decay.

Inflammation is usually indicated by adding the suffix "", as shown below. However, some conditions such as asthma and pneumonia do not follow this convention. More examples are available at list of types of inflammation.

Lung disease results from clogging of the airways due to mucus build-up, decreased mucociliary clearance, and resulting inflammation. Inflammation and infection cause injury and structural changes to the lungs, leading to a variety of symptoms. In the early stages, incessant coughing, copious phlegm production, and decreased ability to exercise are common. Many of these symptoms occur when bacteria that normally inhabit the thick mucus grow out of control and cause pneumonia.

In later stages, changes in the architecture of the lung, such as pathology in the major airways (bronchiectasis), further exacerbate difficulties in breathing. Other signs include coughing up blood (hemoptysis), high blood pressure in the lung (pulmonary hypertension), heart failure, difficulties getting enough oxygen to the body (hypoxia), and respiratory failure requiring support with breathing masks, such as bilevel positive airway pressure machines or ventilators. "Staphylococcus aureus", "Haemophilus influenzae", and "Pseudomonas aeruginosa" are the three most common organisms causing lung infections in CF patients. In addition to typical bacterial infections, people with CF more commonly develop other types of lung disease. Among these is allergic bronchopulmonary aspergillosis, in which the body's response to the common fungus "Aspergillus fumigatus" causes worsening of breathing problems. Another is infection with "Mycobacterium avium" complex, a group of bacteria related to tuberculosis, which can cause lung damage and does not respond to common antibiotics.

Mucus in the paranasal sinuses is equally thick and may also cause blockage of the sinus passages, leading to infection. This may cause facial pain, fever, nasal drainage, and headaches. Individuals with CF may develop overgrowth of the nasal tissue (nasal polyps) due to inflammation from chronic sinus infections. Recurrent sinonasal polyps can occur in 10% to 25% of CF patients. These polyps can block the nasal passages and increase breathing difficulties.

Cardiorespiratory complications are the most common cause of death (about 80%) in patients at most CF centers in the United States.

Clinical examination and x rays can help diagnose the condition. For examples :

- Valsalva test (nose blowing test): Ask the patient to pinch the nostrils together and open the mouth, then blow gently through the nose. Observe if there is passage of air or bubbling of blood in the post extraction alveolus as the trapped air from closed nostrils is forced into the mouth through any oroantral communication. Gentle suction applied to the socket often produces a characteristic hollow sound.

- Perform a complete extra- and intra-oral examination using a dental mirror under good lighting, look for granulation tissue in the socket and openings into the antrum.

- Panoramic radiograph or paranasal computed tomography can help to locate the fistula, the size of it and to determine the presence of sinusitis and other foreign bodies. Other methods like radiographs (occipitomental, OPG and periapical views) can also be used to confirm the presence of any oroantral fistulas.

- To test the patency of communication the patient is asked to rinse the mouth or water is flushed in the tooth socket.

- Unilateral epistaxis is seen in case of collection of blood in the sinus cavity.

- Do not probe or irrigate the site, because it may lead to sinusitis or push foreign bodies, such as contaminated fragments, or oral flora further into the antrum. Hence, leading to the formation of a new fistula or widen an existing one.

Oroantral fistula (OAF) is an abnormal condition of the face where the maxillary sinus is exposed to the oral cavity through an epithelialised fistula. This term signifies pathology and it is not to be confused with oroantral communication (OAC). OAC if left untreated can either heal spontaneously or progress into OAF. The fistulous opening may be situated on the alveolus.

Benign lymphoepithelial lesion is most likely to occur in adults around 50 years of age. There is a predilection for gender with 60–80% being female. The gland affected has a diffuse swelling. The swelling can be asymptomatic, but mild pain can also be associated. There is a preponderance of this disease in those who suffer from HIV infection.

Most cases of benign lymphoepithelial lesions appear in conjunction with Sjögren's syndrome. When Sjögren's syndrome is present, the swelling is usually bilateral. Otherwise, the affected glands are usually only on one side of the body.

In many cases, a biopsy is needed to distinguish benign lymphoepithelial lesions from sialadenosis (sialosis).

Prior to prenatal and newborn screening, cystic fibrosis was often diagnosed when a newborn infant failed to pass feces (meconium). Meconium may completely block the intestines and cause serious illness. This condition, called meconium ileus, occurs in 5–10% of newborns with CF. In addition, protrusion of internal rectal membranes (rectal prolapse) is more common, occurring in as many as 10% of children with CF, and it is caused by increased fecal volume, malnutrition, and increased intra–abdominal pressure due to coughing.

The thick mucus seen in the lungs has a counterpart in thickened secretions from the pancreas, an organ responsible for providing digestive juices that help break down food. These secretions block the exocrine movement of the digestive enzymes into the duodenum and result in irreversible damage to the pancreas, often with painful inflammation (pancreatitis). The pancreatic ducts are totally plugged in more advanced cases, usually seen in older children or adolescents. This causes atrophy of the exocrine glands and progressive fibrosis.

The lack of digestive enzymes leads to difficulty absorbing nutrients with their subsequent excretion in the feces, a disorder known as malabsorption. Malabsorption leads to malnutrition and poor growth and development because of calorie loss. Resultant hypoproteinemia may be severe enough to cause generalized edema. Individuals with CF also have difficulties absorbing the fat-soluble vitamins A, D, E, and K.

In addition to the pancreas problems, people with cystic fibrosis experience more heartburn, intestinal blockage by intussusception, and constipation. Older individuals with CF may develop distal intestinal obstruction syndrome when thickened feces cause intestinal blockage.

Exocrine pancreatic insufficiency occurs in the majority (85% to 90%) of patients with CF. It is mainly associated with "severe" CFTR mutations, where both alleles are completely nonfunctional (e.g. ΔF508/ΔF508). It occurs in 10% to 15% of patients with one "severe" and one "mild" CFTR mutation where little CFTR activity still occurs, or where two "mild" CFTR mutations exist. In these milder cases, sufficient pancreatic exocrine function is still present so that enzyme supplementation is not required. Usually, no other GI complications occur in pancreas-sufficient phenotypes, and in general, such individuals usually have excellent growth and development. Despite this, idiopathic chronic pancreatitis can occur in a subset of pancreas-sufficient individuals with CF, and is associated with recurrent abdominal pain and life-threatening complications.

Thickened secretions also may cause liver problems in patients with CF. Bile secreted by the liver to aid in digestion may block the bile ducts, leading to liver damage. Over time, this can lead to scarring and nodularity (cirrhosis). The liver fails to rid the blood of toxins and does not make important proteins, such as those responsible for blood clotting. Liver disease is the third-most common cause of death associated with CF.

Symptoms of polyps include nasal congestion, sinusitis, loss of smell, thick nasal discharge, facial pressure, nasal speech, and mouth breathing. Recurrent sinusitis can result from polyps. Long-term, nasal polyps can cause destruction of the nasal bones and widening of the nose.

As polyps grow larger, they eventually prolapse into the nasal cavity resulting in symptoms. The most prominent symptoms of nasal polyps result blockage of the nasal passage.

People with nasal polyps due to aspirin intolerance often have symptoms known as Samter's triad, which consists of asthma worse with aspirin, a skin rash caused by aspirin, and chronic nasal polyps.