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.

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.

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.

IgG4-related ophthalmic disease (IgG4-ROD) is the recommended term to describe orbital (eye socket) manifestations of the systemic condition IgG4-related disease, which is characterised by infiltration of lymphocytes and plasma cells and subsequent fibrosis in involved structures. It can involve one or more of the orbital structures.

Frequently involved structures include the lacrimal glands, extraocular muscles, infraorbital nerve, supraorbital nerve and eyelids. It has also been speculated that ligneous conjunctivitis may be a manifestation of IgG4-related disease (IgG4-RD).

As is the case with other manifestations of IgG4-related disease, a prompt response to steroid therapy is a characteristic feature of IgG4-ROD in most cases, unless significant fibrosis has already occurred.

Patients usually present with otorrhea, conductive hearing loss, and otalgia, while bleeding and a sensation of a mass are much less common.

Although imaging is not required to yield a diagnosis, it may be obtained to exclude other disorders, such as a concurrent cholesteatoma.

Symptoms of scleritis include:

- Redness of the sclera and conjunctiva, sometimes changing to a purple hue

- Severe ocular pain, which may radiate to the temple or jaw. The pain is often described as deep or boring.

- Photophobia and tearing

- Decrease in visual acuity, possibly leading to blindness

The pain of episcleritis is less severe than in scleritis. In hyperemia, there is a visible increase in the blood flow to the sclera (hyperaemia), which accounts for the redness of the eye. Unlike in conjunctivitis, this redness will not move with gentle pressure to the conjunctiva.

The symptoms depend on the specific location of the tumour, which can be anywhere in the body.

Secondary keratitis or uveitis may occur with scleritis. The most severe complications are associated with necrotizing scleritis.

Patients with trochleitis typically experience a dull fluctuating aching over the trochlear region developing over a few days. Some may also feel occasional sharp pains punctuating the ache. In patients with migraines, trochleitis may occur simultaneously with headache. Presentation is usually unilateral with palpable swelling over the affected area supranasal to the eye. The trochlear region is extremely tender to touch. Pain is exacerbated by eye movements looking down and inwards, and especially in supraduction (looking up) and looking outwards, which stretches the superior oblique muscle tendon. Notably, there is no restriction of extraocular movements, no diplopia, and often no apparent ocular signs such as proptosis. However, occasionally mild ptosis is found. The absence of generalized signs of orbital involvement is helpful in eliminating other more common causes of periorbital pain.

Necrotizing granulomas can develop in patients with rheumatoid arthritis, typically manifesting as bumps in the soft tissues around the joints (so-called rheumatoid nodules) or in the lungs.

Symptoms are usually limited to one side of the head, and in most cases the individual affected will experience intense, sharp pain and paralysis of muscles around the eye. Symptoms may subside without medical intervention, yet recur without a noticeable pattern.

In addition, affected individuals may experience paralysis of various facial nerves and drooping of the upper eyelid (ptosis). Other signs include double vision, fever, chronic fatigue, vertigo or arthralgia. Occasionally the patient may present with a feeling of protrusion of one or both eyeballs (exophthalmos).

A foreign-body granuloma occurs when a foreign body (such as a wood splinter, piece of metal, glass etc.) penetrates the body's soft tissue followed by acute inflammation and formation of a granuloma. In some cases the foreign body can be found and removed even years after the precipitating event.

Some discrepancy exists as to whether acute zonal occult outer retinopathy (AZOOR) is actually considered a white dot syndrome. However, AZOOR may definitely be related to other diseases included in the white dot syndrome group. AZOOR occurs in young to middle age adults and may eventually progress to retinal cell death. Symptoms include acute visual field loss and photopsias. Suspected causes for AZOOR include autoimmune, viral, and fungal.

Multifocal Choroiditis (MPC) occurs mainly in myopic females. The fundus presents with yellow or gray lesions (white dots) at the level of the choroid and RPE. The size of the white dots are between 50 and 500 micrometres and localized in the macula. MPC is characterized by vitritis and anterior chamber inflammation. Decreased vision due to vitreous inflammation may occur. Unlike MEWDS, MPC is a chronic disorder and macular scarring contributes to severe visual loss. Theories regarding the cause include an exogenous pathogen sensitizing an individual to antigens within photoreceptors, RPE, or choroid.

Inflammatory myofibroblastic tumours are diagnosed based on their appearance under the microscope, by pathologists. Medical imaging findings are non-specific.

Necrobiosis lipoidica is a necrotising skin condition that usually occurs in patients with diabetes mellitus but can also be associated with rheumatoid arthritis. In the former case it may be called necrobiosis lipoidica diabeticorum (NLD). NLD occurs in approximately 0.3% of the diabetic population, with the majority of sufferers being women (approximately 3:1 females to males affected).

The severity or control of diabetes in an individual does not affect who will or will not get NLD. Better maintenance of diabetes after being diagnosed with NLD will not change how quickly the NLD will resolve.

The cause of trochleitis is often unknown (idiopathic trochleitis), but it has been known to occur in patients with rheumatological diseases such as systemic lupus erythematosus, rheumatoid arthritis, enteropathic arthropathy, and psoriasis. In his study, Tychsen and his group evaluated trochleitis patients with echography and CT scan to demonstrate swelling and inflammation. Imaging studies showed inflammation of superior oblique tendon/ trochlear pulley. It was unclear whether the inflammation involved the trochlea itself, or the tissues surrounding the trochlea.

Tolosa–Hunt syndrome (THS) is a rare disorder characterized by severe and unilateral headaches with orbital pain, along with weakness and paralysis (ophthalmoplegia) of certain eye muscles (extraocular palsies).

In 2004, the International Headache Society provided a definition of the diagnostic criteria which included granuloma.

Plasma cell granuloma is a lesional pattern of inflammatory pseudotumour, different from the "inflammatory myofibroblastic tumor" pattern.

It is linked to IgG4-related disease.

Peripheral giant-cell granuloma (PGCG) is an oral pathologic condition that appears in the mouth as an overgrowth of tissue due to irritation or trauma. Because of its overwhelming incidence on the gingiva, the condition is associated with two other diseases, though not because they occur together. Instead, the three are associated with each other because they appear frequently on gingiva: pyogenic granuloma and peripheral ossifying fibroma. Because of its similar microscopic appearance to the bony lesions called central giant-cell granulomas, peripheral giant-cell granulomas are considered by some researchers to be a soft tissue equivalent.

The appearance of peripheral giant-cell granulomas is similar to pyogenic granulomas. The color ranges from red to bluish-purple, but is usually more blue in comparison to pyogenic granulomas. It can be sessile or pedunculated with the size usually being less than 2 cm.

There is a gender difference with 60% of the disease occurring in females. The prevalence of peripheral giant-cell granulomas is highest around 50 - 60 years of age. It appears only on the gingiva or on an edentulous (without teeth) alveolar ridge. It is more often found in the mandible rather than the maxilla but can be found in either anterior or posterior areas. The underlying alveolar bone can be destroyed, leaving a unique appearance referred to as "cupping resorption" or "saucerization".

NL/NLD most frequently appears on the patient's shins, often on both legs, although it may also occur on forearms, hands, trunk, and, rarely, nipple, penis, and surgical sites. The lesions are often asymptomatic but may become tender and ulcerate when injured. The first symptom of NL is often a "bruised" appearance (erythema) that is not necessarily associated with a known injury. The extent to which NL is inherited is unknown.

NLD appears as a hardened, raised area of the skin. The center of the affected area usually has a yellowish tint while the area surrounding it is a dark pink. It is possible for the affected area to spread or turn into an open sore. When this happens the patient is at greater risk of developing ulcers. If an injury to the skin occurs on the affected area, it may not heal properly or it will leave a dark scar.

Peripheral giant-cell granulomas appear microscopically as a large number of multinucleated giant cells, which can have up to dozens of nuclei. Additionally, there are mesenchymal cells that are ovoid and spindle-shaped. Near the borders of the lesion, deposits of hemosiderin and hemorrhage is often found. In 50% of cases, ulcerations are present.

Tuberculous lymphadenitis (or tuberculous adenitis) is a chronic specific granulomatous inflammation of the lymph node with caseation necrosis, caused by infection with "Mycobacterium tuberculosis" or "Mycobacterium bovis".

The characteristic morphological element is the tuberculous granuloma (caseating tubercule). This consists of giant multinucleated cells and (Langhans cells), surrounded by epithelioid cells aggregates, T cell lymphocytes and fibroblasts. Granulomatous tubercules eventually develop central caseous necrosis and tend to become confluent, replacing the lymphoid tissue.

Stages of tubercular lymphadenitis:

1. Lymphadenitis

2. Periadenitis

3. Cold abscess

4. 'Collar stud' abscess

5. Sinus

Tuberculous lymphadenitis is popularly known as collar stud abscess, due to its proximity to the collar bone and superficial resemblance to a collar stud, although this is just one of the five stages of the disease. The characteristic morphological element is the tuberculous granuloma (caseating tubercule): giant multinucleated cells (Langhans cells), surrounded by epithelioid cells aggregates, T cell lymphocytes and few fibroblasts. Granulomatous tubercules evolve to central caseous necrosis and tend to become confluent, replacing the lymphoid tissue.