Fibrous ankylosis is a fibrous connective tissue process which results in decreased range of motion. Symptoms present as bony ankylosis, in which osseous tissue fuses two bones together reducing mobility, which is why fibrous ankylosis is also known as false ankylosis.

Pathology may be the result of trauma, disease, chronic inflammation, or surgery.

Some research suggests fibrous ankylosis may precede the development of bony ankylosis

DISH can present with spinal stiffness on forward flexion/back extension, or with mild back pain. It is symptomatic for thoracic spinal pain in approximately 80% of patients. Back pain or stiffness is worse in the morning in almost two-thirds of patients. It may also be asymptomatic and discovered as an incidental radiological abnormality. Dysphagia from cervical spine osteophyte impingement of esophagus is reported in some cases. Similar calcification and ossification may be seen at peripheral entheseal sites, including the shoulder, iliac crest, ischial tuberosity, trochanters of the hip, tibial tuberosities, patellae, and bones of the hands and/or feet.

Ankylosis or anchylosis (from Greek ἀγκύλος, bent, crooked) is a stiffness of a joint due to abnormal adhesion and rigidity of the bones of the joint, which may be the result of injury or disease. The rigidity may be complete or partial and may be due to inflammation of the tendinous or muscular structures outside the joint or of the tissues of the joint itself.

When the structures outside the joint are affected, the term "false ankylosis" has been used in contradistinction to "true ankylosis", in which the disease is within the joint. When inflammation has caused the joint-ends of the bones to be fused together, the ankylosis is termed "osseous" or complete and is an instance of synostosis. Excision of a completely ankylosed shoulder or elbow may restore free mobility and usefulness to the limb. "Ankylosis" is also used as an anatomical term, bones being said to ankylose (or anchylose) when, from being originally distinct, they coalesce, or become so joined together that no motion can take place between them.

In 2014, there was a rare case of Ankylosis, wherein a six-year old girl was able to open her mouth only a couple millimeters after one of her jaw joints got fused. Liliana Cernecca was the patient's name. She underwent a surgery at King's College Hospital in London, during which her jaw was operated on and unlocked.She was said to be one of the youngest patients to have undergone this surgery.

By far, the two most common symptoms described are pain and the feeling that teeth no longer correctly meet (traumatic malocclusion, or disocclusion). The teeth are very sensitive to pressure (proprioception), so even a small change in the location of the teeth will generate this sensation. People will also be very sensitive to touching the area of the jaw that is broken, or in the case of condylar fracture the area just in front of the tragus of the ear.

Other symptoms may include loose teeth (teeth on either side of the fracture will feel loose because the fracture is mobile), numbness (because the inferior alveolar nerve runs along the jaw and can be compressed by a fracture) and trismus (difficulty opening the mouth).

Outside the mouth, signs of swelling, bruising and deformity can all be seen. Condylar fractures are deep, so it is rare to see significant swelling although, the trauma can cause fracture of the bone on the anterior aspect of the external auditory meatus so bruising or bleeding can sometimes be seen in the ear canal. Mouth opening can be diminished (less than 3 cm). There can be numbness or altered sensation (anesthesia/paraesthesia in the chin and lower lip (the distribution of the mental nerve).

Intraorally, if the fracture occurs in the tooth bearing area, a step may seen between the teeth on either side of the fracture or a space can be seen (often mistaken for a lost tooth) and bleeding from the gingiva in the area. There can be an open bite where the lower teeth, no longer meet the upper teeth. In the case of a unilateral condylar fracture the back teeth on the side of the fracture will meet and the open bite will get progressively greater towards the other side of the mouth.

Sometimes bruising will develop in the floor of the mouth (sublingual eccymosis) and the fracture can be moved by moving either side of the fracture segment up and down. For fractures that occur in the non-tooth bearing area (condyle, ramus, and sometimes the angle) an open bite is an important clinical feature since little else, other than swelling, may be apparent.

This type of fractured mandible can involve one condyle (unilateral) or both (bilateral). Unilateral condylar fracture may cause restricted and painful jaw movement. There may be swelling over the temporomandibular joint region and bleeding from the ear because of lacerations to the external auditory meatus. The hematoma may spread downwards and backwards behind the ear, which may be confused with Battle's sign (a sign of a base of skull fracture), although this is an uncommon finding so if present, intra-cranial injury must be ruled out. If the bones fracture and overlie each other there may be shortening of the height of the ramus. This results in gagging of the teeth on the fractured side (the teeth meet too soon on the fractured side, and not on the non fractured side, i.e. "open bite" that becomes progressively worse to the unaffected side). When the mouth is opened, there may be deviation of the mandible towards the fractured side. Bilateral condylar fractures may cause the above signs and symptoms, but on both sides. Malocclusion and restricted jaw movement are usually more severe. Bilateral body or parasymphysis fractures are sometimes termed "flail mandible", and can cause involuntary posterior movement of the tongue with subsequent obstruction of the upper airway. Displacement of the condyle through the roof of glenoid fossa and into the middle cranial fossa is rare. Bilateral condylar fractures combined with a symphyseal fracture is sometimes termed a guardsman's fracture. The name comes from this injury occurring in soldiers who faint on parade grounds and strike the floor with their chin.

Diffuse idiopathic skeletal hyperostosis (DISH) is a non-inflammatory spondyloarthropathy which predominantly affects the spine. It is characterized by ankylosis and enthesopathy (ossification of the ligaments and entheses). It most commonly affects the thoracic and thoraco-lumbar spine, but involvement is variable and can include the entire spine.

Synostosis (plural: synostoses) is fusion of two bones. It can be normal in puberty, fusion of the epiphysis, or abnormal. When synostosis is abnormal it is a type of dysostosis.

Examples of synostoses include:

- craniosynostosis – an abnormal fusion of two or more cranial bones;

- radioulnar synostosis – the abnormal fusion of the radius and ulna bones of the forearm;

- tarsal coalition – a failure to separately form all seven bones of the tarsus (the hind part of the foot) resulting in an amalgamation of two bones; and

- syndactyly – the abnormal fusion of neighboring digits.

Synostosis within joints can cause ankylosis.

Evidence for ankylosis found in the fossil record is studied by paleopathologists, specialists in ancient disease and injury. Ankylosis has been reported in dinosaur fossils from several species, including "Allosaurus fragilis", "Becklespinax altispinax", "Poekilopleuron bucklandii", and "Tyrannosaurus rex" (including the Stan specimen).

Radioulnar synostosis is one of the more common failures of separation of parts of the upper limb. There are two general types: one is characterized by fusion of the radius and ulna at their proximal borders and the other is fused distal to the proximal radial epiphysis. Most cases are sporadic, congenital (due to a defect in longitudinal segmentation at the 7th week of development) and less often post-traumatic, bilateral in 60%, and more common in males. Familial cases in association with autosomal dominant transmission appear to be concentrated in certain geographic regions, such as Sicily.

The condition frequently is not noted until late childhood, as function may be normal, especially in unilateral cases. Increased wrist motion may compensate for the absent forearm motion. It has been suggested that individuals whose forearms are fixed in greater amounts of pronation (over 60 degrees) face more problems with function than those with around 20 degrees of fixation. Pain is generally not a problem, unless radial head dislocation should occur.

Most examples of radioulnar synostosis are isolated (non-syndromic). Syndromes that may be accompanied by radioulnar synostosis include X chromosome polyploidy (e.g., XXXY) and other chromosome disorders (e.g., 4p- syndrome, Williams syndrome), acrofacial dysostosis, Antley–Bixler syndrome, genitopatellar syndrome, Greig cephalopolysyndactyly syndrome, hereditary multiple osteochondromas (hereditary multiple exostoses), limb-body wall complex, and Nievergelt syndrome.

Craniosynostosis (from cranio, cranium; + syn, together; + ostosis relating to bone) is a condition in which one or more of the fibrous sutures in an infant skull prematurely fuses by turning into bone (ossification). Craniosynostosis has following kinds: scaphocephaly, trigonocephaly, plagiocephaly, anterior plagiocephaly, posterior plagiocephaly, brachycephaly, oxycephaly, pansynostosis.

Tooth ankylosis refers to a fusion (ankylosis) of teeth to bone. The condition is diagnosed with radiographs (X-rays), which show loss of the periodontal ligament space and blending of the root with the bone. Clinically the tooth sounds solid when percussed (tapped) compared to the dull, cushioned sound from normal teeth. Ankylosis of teeth is uncommon, more so in deciduous teeth than permanent teeth.

Generally, degenerative joint changes are associated with greater pain.

Signs and symptoms of temporomandibular joint disorder vary in their presentation. The symptoms will usually involve more than one of the various components of the masticatory system, muscles, nerves, tendons, ligaments, bones, connective tissue, or the teeth.

The three classically described, cardinal signs and symptoms of TMD are:

- Pain and tenderness on palpation in the muscles of mastication, or of the joint itself (preauricular pain – pain felt just in front of the ear). Pain is the defining feature of TMD and is usually aggravated by manipulation or function, such as when chewing, clenching, or yawning, and is often worse upon waking. The character of the pain is usually dull or aching, poorly localized, and intermittent, although it can sometimes be constant. The pain is more usually unilateral (located on one side) rather than bilateral. It is rarely severe.

- Limited range of mandibular movement, which may cause difficulty eating or even talking. There may be locking of the jaw, or stiffness in the jaw muscles and the joints, especially present upon waking. There may also be incoordination, asymmetry or deviation of mandibular movement.

- Noises from the joint during mandibular movement, which may be intermittent. Joint noises may be described as clicking, popping, or crepitus (grating).

Other signs and symptoms have also been described, although these are less common and less significant than the cardinal signs and symptoms listed above. Examples include:

- Headache (possibly), e.g. pain in the occipital region (the back of the head), or the forehead; or other types of facial pain including migraine, tension headache. or myofascial pain.

- Pain elsewhere, such as the teeth or neck.

- Diminished auditory acuity (hearing loss).

- Tinnitus (occasionally).

- Dizziness.

- Sensation of malocclusion (feeling that the teeth do not meet together properly).

Ankylosis of deciduous teeth ("submerged teeth") may rarely occur. The most commonly affected tooth is the mandibular (lower) second deciduous molar. Partial root resorption first occurs and then the tooth fuses to the bone. This prevents normal exfoliation of the deciduous tooth and typically causes impaction of the permanent successor tooth. As growth of the alveolar bone continues and the adjacent permanent teeth erupt, the ankylosed deciduous tooth appears to submerge into the bone, although in reality it has not changed position. Treatment is by extraction of the involved tooth, to prevent malocclusion, periodontal disturbance or dental caries.

This type of failure of eruption takes place when the affected tooth is ankylosed to the bone around it. This is different than primary failure of eruption where the affected tooth/teeth were not ankylosed. In mechanical failure of eruption, affected tooth has partial or complete loss of PDL in a panoramic radiograph and teeth distal to affected tooth do not have this condition. On a percussion test, a tooth with mechanical failure of eruption will have a dull metallic sound.

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.

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.

The term primary failure of eruption was named by Dr. William Proffit and Dr. Katherine Vig in 1981. This type of failure of eruption has a genetic or familial background precursor as a cause. The prevalence is of PFE is about 0.06% in population. In this type of failure, teeth that are non-ankylosed fail to erupt in the mouth. These teeth do not have a precursor tooth that is blocking their path. These teeth tend to erupt partially but then fail to erupt as the time goes on. Profitt stated that only the posterior teeth are the ones to be affected and all the teeth which are distal to the affected tooth are also affected. Both permanent and primary teeth may equally be affected. This often results in posterior open bite in patients mouth who have primary failure of eruption. This phenomenon can occur in any quadrant of the mouth.

There are two types of primary failure of eruption. Type I involves failure of eruption of teeth distal to the most mesial affected tooth to be all same. Type II involves a greater eruption pattern, not complete, among the teeth distal to the most mesial affected tooth. It is difficult to diagnose between these two types of failure of eruption because 2nd molar does not erupt until a patient is 15 years of age. Plenty of times, patient's receive orthodontic care much before they turn 15 years old. Therefore, to properly diagnose between two types, a patient needs to be over 15 and a definitive proof of uneruption of 2nd molar is required.

Dental avulsion is the complete displacement of a tooth from its socket in alveolar bone owing to trauma.

The treatment for permanent teeth consists of replantation, immediately if possible. Deciduous teeth should not be replanted due to the risk of damaging the permanent tooth germ. Immediate replantation ensures the best possible prognosis but is not always possible since more serious injuries may be present. Studies have shown that teeth that are protected in a physiologically ideal media can be replanted within 15 minutes to one hour after the accident with good prognosis. The success of delayed replantation depends on the vitality of the cells remaining on the root surface. In normal conditions, a tooth is connected to the socket by means of the periodontal ligament. When a tooth is knocked out, that ligament stretches and splits in half. Maintaining the vitality of the cells that remain attached to the root surface is the key to success following replantation. Years ago, it was thought that the key to maintaining root cell vitality was keeping the knocked-out tooth wet, thus giving rise to storage media recommendations such as water, the mouth and milk. Recent research has shown that one of the key elements for maintaining vitality is storing the tooth in an environment that closely resembles the original socket environment. This environment is one that has the proper osmolality (cell pressure), pH, nutritional metabolites and glucose. There are scientifically designed storage media that provide this environment. These storage media are now available in retail products. Use of devices that incorporate the ideal storage media and protective apparatuses have increased the success rate of replanted knocked-out teeth to over 90% when used within sixty minutes of the accident.

The long-term prognosis of replanted knocked out teeth is very variable. The treatment for knocked-out teeth has progressed from a success rate of 10% to over 90%.

However, this success rate can only be achieved with the institution of optimum care within fifteen minutes to an hour of the accident. In the case of knocked-out teeth, being prepared and knowing what to do can mean the difference between a person retaining or losing replanted knocked-out teeth for life. Teeth that have been knocked out when they are fully matured, that is, when the root has completely formed, have a much better prognosis than those teeth that are immature and not fully formed. This is due to the fragility of the root. When teeth have not fully formed, the walls of the root are thinner and thus more fragile. Another complication for the prognosis is the length of time that the tooth has been out of its socket. Teeth that are replanted within fifteen minutes of the accident have an excellent prognosis. Teeth that have been extra-oral and dry stored for more than one hour have a poor prognosis. Teeth that have been placed in an optimal storage medium within one hour of the accident also have an excellent prognosis. All teeth that have been knocked out should be replanted but watched carefully for the development of root resorption. Teeth that do not have root canal treatment within two weeks of replantation also have a poor prognosis.

The symptoms of Felty's syndrome are similar to those of rheumatoid arthritis. Patients suffer from painful, stiff, and swollen joints, most commonly in the joints of the hands, feet, and arms. In some affected individuals, Felty's syndrome may develop during a period when the symptoms and physical findings associated with rheumatoid arthritis have subsided or are not present; in this case, Felty's syndrome may remain undiagnosed. In more rare instances, the development of Felty's syndrome may precede the development of the symptoms and physical findings associated with rheumatoid arthritis.

Felty's syndrome is also characterized by an abnormally enlarged spleen (splenomegaly) and abnormally low levels of certain white blood cells (neutropenia). As a result of neutropenia, affected individuals are increasingly susceptible to certain infections. Keratoconjunctivitis sicca may occur due to secondary Sjorgen's syndrome. Individuals with Felty's syndrome may also experience fever, weight loss, and/or fatigue. In some cases, affected individuals may have discoloration (abnormal brown pigmentation) of the skin, particularly of the leg, sores (ulcers) on the lower leg, and/or an abnormally large liver (hepatomegaly). In addition, affected individuals may have abnormally low levels of circulating red blood cells (anemia), a decrease in circulating blood platelets that assist in blood clotting functions (thrombocytopenia), abnormal liver function tests and/or inflammation of the blood vessels (vasculitis).

Felty's syndrome, also called Felty syndrome, (FS) is rare autoimmune disease characterized by the triad of rheumatoid arthritis, splenomegaly and neutropenia. The condition is more common in those aged 50–70 years, specifically more prevalent in females than males, and more so in Caucasians than those of African descent. It is a deforming disease that causes many complications for the individual.

Hearing loss is sensory, but may have accompanying symptoms:

- pain or pressure in the ears

- a blocked feeling

There may also be accompanying secondary symptoms:

- hyperacusis, heightened sensitivity to certain volumes and frequencies of sound, sometimes resulting from "recruitment"

- tinnitus, ringing, buzzing, hissing or other sounds in the ear when no external sound is present

- vertigo and disequilibrium

- tympanophonia, abnormal hearing of one's own voice and respiratory sounds, usually as a result of a patulous eustachian tube or dehiscent superior semicircular canals

- disturbances of facial movement (indicating possible tumour or stroke)

Human hearing extends in frequency from 20-20,000 Hz, and in amplitude from 0 dB to 130 dB or more. 0 dB does not represent absence of sound, but rather the softest sound an average unimpaired human ear can hear; some people can hear down to -5 or even -10 dB. 130 dB represents the threshold of pain. But the ear doesn't hear all frequencies equally well; hearing sensitivity peaks around 3000 Hz. There are many qualities of human hearing besides frequency range and amplitude that can't easily be measured quantitatively. But for many practical purposes, normative hearing is defined by a frequency versus amplitude graph, or audiogram, charting sensitivity thresholds of hearing at defined frequencies. Because of the cumulative impact of age and exposure to noise and other acoustic insults, 'typical' hearing may not be normative.

In malignant-type smallpox (also called flat smallpox) the lesions remained almost flush with the skin at the time when raised vesicles form in the ordinary type. It is unknown why some people developed this type. Historically, it accounted for 5–10 percent of cases, and the majority (72 percent) were children. Malignant smallpox was accompanied by a severe prodromal phase that lasted 3–4 days, prolonged high fever, and severe symptoms of toxemia. The rash on the tongue and palate was extensive. Skin lesions matured slowly and by the seventh or eighth day they were flat and appeared to be buried in the skin. Unlike ordinary-type smallpox, the vesicles contained little fluid, were soft and velvety to the touch, and may have contained hemorrhages. Malignant smallpox was nearly always fatal.

Complications of smallpox arise most commonly in the respiratory system and range from simple bronchitis to fatal pneumonia. Respiratory complications tend to develop on about the eighth day of the illness and can be either viral or bacterial in origin. Secondary bacterial infection of the skin is a relatively uncommon complication of smallpox. When this occurs, the fever usually remains elevated.

Other complications include encephalitis (1 in 500 patients), which is more common in adults and may cause temporary disability; permanent pitted scars, most notably on the face; and complications involving the eyes (2 percent of all cases). Pustules can form on the eyelid, conjunctiva, and cornea, leading to complications such as conjunctivitis, keratitis, corneal ulcer, iritis, iridocyclitis, and optic atrophy. Blindness results in approximately 35 percent to 40 percent of eyes affected with keratitis and corneal ulcer. Hemorrhagic smallpox can cause subconjunctival and retinal hemorrhages. In 2 to 5 percent of young children with smallpox, virions reach the joints and bone, causing "osteomyelitis variolosa". Lesions are symmetrical, most common in the elbows, tibia, and fibula, and characteristically cause separation of an epiphysis and marked periosteal reactions. Swollen joints limit movement, and arthritis may lead to limb deformities, ankylosis, malformed bones, flail joints, and stubby fingers.