Although the origin of the disease is unknown, there is speculation that it is an aggressive healing response to small tears in the plantar fascia, almost as if the fascia over-repairs itself following an injury. There is also some evidence that it might be genetic.

In the early stages, when the nodule is single and/or smaller, it is recommended to avoid direct pressure to the nodule(s). Soft inner soles on footwear and padding may be helpful.

MRI and sonogram (diagnostic ultrasound) are effective in showing the extent of the lesion, but cannot reveal the tissue composition. Even then, recognition of the imaging characteristics of plantar fibromatoses can help in the clinical diagnosis.

Surgery of Ledderhose's disease is difficult because tendons, nerves, and muscles are located very closely to each other. Additionally, feet have to carry heavy load, and surgery might have unpleasant side effects. If surgery is performed, the biopsy is predominantly cellular and frequently misdiagnosed as fibrosarcoma. Since the diseased area (lesion) is not encapsulated, clinical margins are difficult to define. As such, portions of the diseased tissue may be left in the foot after surgery. Inadequate excision is the leading cause of recurrence.

Radiotherapy has been shown to reduce the size of the nodules and reduce the pain associated with them. It is approximately 80% effective, with minimal side-effects.

Post-surgical radiation treatment may decrease recurrence. There has also been variable success in preventing recurrence by administering gadolinium. Skin grafts have been shown to control recurrence of the disease.

In few cases shock waves also have been reported to at least reduce pain and enable walking again. Currently in the process of FDA approval is the injection of collagenase. Recently successful treatment of Ledderhose with cryosurgery (also called cryotherapy) has been reported.

Cortisone injections, such as Triamcinolone, and clobetasol ointments have been shown to stall the progression of the disease temporarily, although the results are subjective and large-scale studies far from complete. Injections of superoxide dismutase have proven to be unsuccessful in curing the disease while radiotherapy has been used successfully on Ledderhose nodules.

Soft tissue disorders are medical conditions affecting soft tissue.

Often soft tissue injuries are some of the most chronically painful and difficult to treat because it is very difficult to see what is going on under the skin with the soft connective tissues, fascia, joints, muscles and tendons.

Musculoskeletal specialists, manual therapists and neuromuscular physiologists and neurologists specialize in treating injuries and ailments in the soft tissue areas of the body. These specialized clinicians often develop innovative ways to manipulate the soft tissue to speed natural healing and relieve the mysterious pain that often accompanies soft tissue injuries. This area of expertise has become known as soft tissue therapy and is rapidly expanding as the technology continues to improve the ability of these specialists to identify problem areas more quickly.

A promising new method of treating wounds and soft tissue injuries is via platelet growth factor (PGF).

There is a close overlap between the term "soft tissue disorder" and rheumatism. Sometimes the term "soft tissue rheumatic disorders" is used to describe these conditions.

The radiological features of myositis ossificans are ‘faint soft tissue calcification within 2–6 weeks, (may have well-defined

bony margins by 8 weeks) separated from periosteum by lucent zone and on CT, the characteristic feature is peripheral ossification’.

Diagnosis can be made solely on the basis of history and physical examination in people who present with only facial asymmetry. For those who report neurological symptoms such as migraine or seizures, MRI scan of the brain is the imaging modality of choice. A diagnostic lumbar puncture and serum test for autoantibodies may also be indicated in people who present with a seizure disorder of recent onset.

No treatment is required, but neoplastic processes (metastatic maliganancy to the submandibular lymph nodes and/or salivary gland tumours) should be ruled out. This is usually done with clinical exam and imaging. Very rarely, since the defect contains salivary gland tissue, salivary gland tumors can occur within an established defect but there is likely no difference in the risk of neoplasia in salivary gland tissue at other sites.

The diagnosis is made clinically, and usually this is clear cut if the lesion is associated with the flange of a denture. Tissue biopsy is not usually indicated before removal of the lesion, since the excises surgical specimen is usually sent for histopathologic examination and the diagnosis is confirmed retrospectively. Rarely, incisional biopsy may be indicated to rule out neoplasia, e.g. in the presence of suspicious ulceration. The appearance may also be confused with pyogenic granuloma.

The excessive tissue is composed of cellular, inflamed fibrous connective tissue. The appearance of an epulis fissuratum microscopically is an overgrowth of cells from the fibrous connective tissue. The epithelial cells are usually hyperkeratotic and irregular, hyperplastic rete ridges are often seen.

Most infants with infantile cortical hyperostosis are diagnosed by physical examination. X-rays can confirm the presence of bone changes and soft tissue swelling. Biopsy of the affected areas can confirm the presence of typical histopathological changes. No specific blood tests exist, but tests such as erythrocyte sedimentation rate (ESR) and alkaline phosphatase levels are often elevated. A complete blood count may show anemia (low red blood cell count) and leukocytosis (high white blood cell count). Other tests may be done to help exclude other diagnoses. Ultrasound imaging can help diagnose prenatal cases.

Calcification is typically depicted 2 weeks earlier by ultrasound (US) when compared to radiographs. The lesion develops in two distinct stages with different presentations at US. In the early stage, termed immature, it is depicts a non-specific soft tissue mass that ranges from a hypoechoic area with an outer sheet-like hyperechoic peripheral rim to a highly echogenic area with variable shadowing. In the late stage, termed mature, myositis ossificans is depicted as an elongated calcific deposit that is aligned with the long-axis of the muscle, exhibits acoustic shadowing, and has no soft tissue mass associated. US may suggest the diagnosis at early stage, but imaging features need to evolve with successive maturation of the lesion and formation of the characteristic late stage changes before they become pathognomonic.

The differential diagnosis includes many tumoral and nontumoral pathologies. A main concern is to differentiate early myositis ossificans from malignant soft-tissue tumors, and the latter is suggested by a fast-growing process. If clinical or sonographic findings are dubious and extraosseous sarcoma is suspected, biopsy should be performed. At histology, detection of the typical zonal phenomenon is diagnostic of myositis ossificans, though microscopic findings may be misleading during the early stage.

CREST syndrome can be noted in up to 10% of patients with primary biliary cirrhosis.

A urologist may be able to diagnose the disease and suggest treatment. An ultrasound can provide conclusive evidence of Peyronie's disease, ruling out congenital curvature or other disorders.

Osteomyelitis (bone infection), which is much more common than infantile cortical hyperostosis, must be excluded, since it requires urgent treatment. Other diagnoses that can mimic this disorder and need to be excluded include physical trauma, child abuse, Vitamin A excess, hyperphosphatemia, prostaglandin E1 and E2 administration, scurvy, infections (including syphilis), Ewing sarcoma, and metastatic neuroblastoma.

CREST is not easily diagnosed as it closely mimics symptoms of other connective tissue and autoimmune diseases. Diagnoses are usually given when a patient presents three or more of the five major clinical symptoms. Additionally, blood exams can be given to test for a positive ANAs and ACAs or skin biopsies can be given to help confirm a diagnosis.

A non-vital tooth is necessary for the diagnosis of a periapical cyst, meaning the nerve has been removed by root canal therapy. Oral examination of the surrounding intraoral anatomical structures should be palpated to identify the presence of bone expansion or displacement of tooth roots as well as crepitus noises during examination, indicating extensive bone damage. Bulging of the buccal or lingual cortical plates may be present. Age of occurrence in the patient, the location of the cyst, the edges of cystic contours, and the impact that the cyst has on adjacent structures must all be considered for proper diagnosis.

Several lesions can appear similarly in radiographic appearance. Intraoral X-rays or a 3-D cone beam scan of the affected area can be used to obtain radiological images and confirm diagnosis of cysts in the periapical area. Circular or ovoid radiolucency surrounding the root tip of approximately 1-1.5 cm in diameter is indicative of the presence of a periapical cyst. The border of the cyst is seen as a narrow opaque margin contiguous with the lamina dura. In cysts that are actively enlarging, peripheral areas of the margin may not be present. Periapical cysts have a characteristic unilocular shape on radiographs. There is also a severe border of cortication between the cyst and surrounding bone. Pseudocysts, on the other hand, have a fluid filled cavity but are not lined by epithelium, therefore they have a less severe and more blurred border between the fluid and bony surroundings.

Resorption of the roots of affected teeth may also be observed as the absence of portions of normal root structures.

Infected cysts will produce a positive percussion test on the affected tooth as well as a negative response to the pulp test. There may also be visible swelling in the overlying soft tissues. The affected tooth may also exhibit discoloration.

The histological and ultrastructural features of Ledderhose and Dupuytren's disease are the same, which supports the hypothesis that they have a common cause and pathogenesis. As with Dupuytren's disease, the root cause(s) of Ledderhose's disease are not yet understood. It has been noted that it is an inherited disease and of variable occurrence within families, i.e. the genes necessary for it may remain dormant for a generation or more and then surface in an individual, or be present in multiple individuals in the same generation with varying degree.

There are certain identified risk factors. The disease is more commonly associated with -

- A family history of the disease

- Higher incidence in males

- Palmar fibromatosis 10-65% of the time.

- Peyronie's disease

- Epilepsy patients

- Patients of diabetes mellitus

There is also a suspected, although unproven, link between incidence and alcoholism, smoking, liver diseases, thyroid problems, and stressful work involving the feet.

Stafne's defect is usually discovered by chance during routine dental radiography. Radiographically, it is a well-circumscribed, monolocular, round, radiolucent defect, 1–3 cm in size, usually between the inferior alveolar nerve (IAN) and the inferior border of the posterior mandible between the molars and the angle of the jaw. It is one of the few radiolucent lesions that can occur below the IAN. The border is well corticated and it will have no effect on the surrounding structures. Computed tomography (CT) will show a shallow defect through the medial cortex of the mandible with a corticated rim and no soft tissue abnormalities, with the exception of a portion of the submandibular gland. Neoplasms, such as metastatic squamous cell carcinoma to the submandibular lymph nodes or a salivary gland tumour, could create a similar appearance but rarely have such well defined borders and can usually be palpated in the floor of the mouth or submandibular triangle of the neck as a hard mass. CT and clinical exam is typically sufficient to distinguish between this and a Stafne defect. The Stafne defect also tends to not increase in size or change in radiographic appearance over time (hence the term "static bone cyst"), and this can be used to help confirm the diagnosis. Tissue biopsy is not usually indicated, but if carried out, the histopathologic appearance is usually normal salivary gland tissue. Sometimes attempted biopsy of Stafne defects reveals an empty cavity (possibly because the gland was displaced at the time of biopsy), or other contents such as blood vessels, fat, lymphoid or connective tissues. Defects of the anterior lingual mandible may require biopsy for correct diagnosis at this unusual location. The radiolucent defect here may be superimposed on the lower anterior teeth and be mistaken for an odontogenic lesion. Sometimes the defect may interrupt the contour of the lower border of the mandible, and may be palpable. Sialography may be sometimes used to help demonstrate the salivary gland tissue within the bone.

If severe pain persists after the first 24hours it is recommended that an individual consult with a professional who can make a diagnosis and implement a treatment plan so the patient can return to everyday activities (Flegel, 2004). These are some of the tools that a professional can use to help make a full diagnosis;

Nerve conduction studies may also be used to localize nerve dysfunction ("e.g.", carpal tunnel syndrome), assess severity, and help with prognosis.

Electrodiagnosis also helps differentiate between myopathy and neuropathy.

Ultimately, the best method of imaging soft tissue is magnetic resonance imaging (MRI), though it is cost-prohibitive and carries a high false positive rate.

There is no official diagnostic criteria for UCTD. Diagnostic testing generally aims to determine whether a patient has a "definite" or "undifferentiated" connective tissue disease.

The diagnosis is clinical. Amalgam tattoo can be distinguished from other causes of localized oral pigmentation because it does not change significantly in size or color, although it may appear to slowly enlarge for several months after the initial implantation of the metal particles. Some amalgam tattoos appear radio-opaque on radiographs (i.e. they show up on x-rays), although in many cases amalgam tattoos have no radiographic features since the responsible particle(s) of amalgam are very small even though clinically the area of discolored mucosa is much larger.

If necessary, the diagnosis can be confirmed histologically by excisional biopsy, which excludes nevi and melanomas. If a biopsy is taken, the histopathologic appearance is:

- Pigmented fragments of metal within connective tissue

- Staining of reticulin fibers with silver salts

- A scattered arrangement of large, dark, solid fragments or a fine, black or dark brown granules

- Large particles may be surrounded by chronically inflamed fibrous tissue

- Smaller particles surrounded by more significant inflammation, which may be granulomatous or a mixture of lymphocytes and plasma cells

Outbreaks may be measurable clinically by elevated levels of alkaline phosphatase and bone-specific alkaline phosphatase.

If the causative factor persists, tissue will become more fibrous over time.

Theoretically, routine use of a dental dam during dental procedures which involve amalgam should reduce the risk of amalgam tattoo.

Most patients will maintain a diagnosis of undifferentiated connective tissue disease. However, about one third of UCTD patients will differentiate to a specific autoimmune disease, like rheumatoid arthritis or systemic sclerosis. About 12 percent of patients will go into remission.

Severe vitamin D deficiency has been associated with the progression of UCTD into defined connective tissue diseases. The presence of the autoantibodies anti-dsDNA, anti-Sm, and anti-cardiolipin has been shown to correlate with the development of systemic lupus erythematosus, specifically.

The standard treatment of COC is enucleation and curettage (E&C). Recurrence following E&C is rare.

There is no diagnosis as yet for Cutis verticis gyrata (CVH), but it can generally be found out by self, when the person is applying oil to the scalp or getting the hair fully shaven. The ripples are present either in identical form, mostly in the posterior direction, sometimes horizontally also, but it looks more like the ripples of the brain.

There is no clinical diagnosis for CVG as these cases are rarely seen and is often comorbid with other conditions.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.