The disorder is more common in older adults. The disease is often occult until crystal deposits are coincidentally detected and diagnosed by a pathologist in various orthopedic specimens. It may be asymptomatic, or it can be associated with osteoarthritis, or it can present as an acute or chronic inflammatory arthritis that causes pain in one or more joints. The white blood cell count is often raised.

The arthritis is usually polyarticular (i.e., it leads to an inflammation of several joints in the body), although it may begin as monoarticular (i.e., confined to just one joint). CPPD crystals tend to form within articular tissues. In theory, any joint may be affected, but statistics show that the knees are the most commonly affected joints, as well as wrists and hips.

In many instances, patients may also have signs of carpal tunnel syndrome. This condition can also be associated with Milwaukee shoulder syndrome.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, also known as pseudogout and pyrophosphate arthropathy is a rheumatologic disorder with varied symptoms and signs arising from the resultant accumulation of crystals of calcium pyrophosphate dihydrate in the connective tissues. The alternative names emphasize particular aspects of the clinical or radiographic findings. The knee joint is the most commonly affected.

Pain, which can vary in severity, is a common symptom in virtually all types of arthritis. Other symptoms include swelling, joint stiffness and aching around the joint(s). Arthritic disorders like lupus and rheumatoid arthritis can affect other organs in the body, leading to a variety of symptoms. Symptoms may include:

- Inability to use the hand or walk

- Stiffness, which may be worse in the morning, or after use

- Malaise and fatigue

- Weight loss

- Poor sleep

- Muscle aches and pains

- Tenderness

- Difficulty moving the joint

It is common in advanced arthritis for significant secondary changes to occur. For example, arthritic symptoms might make it difficult for a person to move around and/or exercise, which can lead to secondary effects, such as:

- Muscle weakness

- Loss of flexibility

- Decreased aerobic fitness

These changes, in addition to the primary symptoms, can have a huge impact on quality of life.

Osteoarthritis is the most common form of arthritis. It can affect both the larger and the smaller joints of the body, including the hands, wrists, feet, back, hip, and knee. The disease is essentially one acquired from daily wear and tear of the joint; however, osteoarthritis can also occur as a result of injury. In recent years, some joint or limb deformities, such as knock-knee or acetabular overcoverage or dysplasia, have also been considered as a predisposing factor for knee or hip osteoarthritis. Osteoarthritis begins in the cartilage and eventually causes the two opposing bones to erode into each other. The condition starts with minor pain during physical activity, but soon the pain can be continuous and even occur while in a state of rest. The pain can be debilitating and prevent one from doing some activities. Osteoarthritis typically affects the weight-bearing joints, such as the back, knee and hip. Unlike rheumatoid arthritis, osteoarthritis is most commonly a disease of the elderly. More than 30 percent of women have some degree of osteoarthritis by age 65. Risk factors for osteoarthritis include prior joint trauma, obesity, and a sedentary lifestyle.

When monoarthritis is caused by "pseudogout" (calcium pyrophosphate deposition disease, CPPD), the inflammation usually lasts days to weeks, and involves the knees in half of all attacks. Like gout, attacks can occur spontaneously or with physical trauma or metabolic stress. Patients may feel well in between pseudogout attacks, and 5% present with pseudo-rheumatoid symptoms.

Monoarthritis is inflammation ("arthritis") of one joint at a time. It is usually caused by trauma, infection, or crystalline arthritis.

Arthropathy may also include joint conditions caused by physical trauma to joints, but is traditionally used to describe the following conditions:

- "Reactive arthropathy" (M02-M03) is caused by an infection, but not a direct infection of the synovial space. (See also Reactive arthritis)

- "Enteropathic arthropathy" (M07) is caused by colitis and related conditions.

- "Crystal arthropathy" (also known as "crystal arthritis") (M10-M11) involves the deposition of crystals in the joint.

- In gout, the crystal is uric acid.

- In pseudogout/chondrocalcinosis/calcium pyrophosphate deposition disease, the crystal is calcium pyrophosphate.

- "Diabetic arthropathy" (M14.2, E10-E14) is caused by diabetes.

- "Neuropathic arthropathy" (M14.6) is associated with a loss of .

An arthropathy is a disease of a joint. Arthritis is a form of arthropathy that involves inflammation of one or more joints, while the term arthropathy may be used regardless of whether there is inflammation or not.

Spondylarthropathy is any form of arthropathy of the vertebral column.

A common cause of chondrocalcinosis is calcium pyrophosphate dihydrate crystal deposition disease (CPPD).

Excessive calcium (due to hypomagnesemia) has a potential relationship with chondrocalcinosis, and magnesium supplementation may reduce or alleviate symptoms. In some cases, arthritis from injury can cause chondrocalcinosis.

Other causes of chondrocalcinosis include:

- Hypercalcaemia, especially when caused by hyperparathyroidism

- Arthritis

- Gout

- Wilson disease

- Hemochromatosis

- Ochronosis

- Hypothyroidism

- Hyperoxalemia

- Acromegaly

- osteoarthritis

Chondrocalcinosis can be visualized on projectional radiography, CT scan, MRI, US, and nuclear medicine. CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule), however radiography is more successful. At ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage. As with most conditions, chondrocalcinosis can present with similarity to other diseases such as ankylosing spondylitis and gout.

The presentation of amyloidosis is broad and depends on the site of amyloid accumulation. The kidney and heart are the most common organs involved.

Amyloid deposition in the kidneys can cause nephrotic syndrome, which results from a reduction in the kidney's ability to filter and hold on to proteins. The nephrotic syndrome occurs with or without elevations in creatinine and blood urea concentration, two biochemical markers of kidney injury. In AA amyloidosis, the kidneys are involved in 91–96% of people, symptoms ranging from protein in the urine to nephrotic syndrome and rarely renal insufficiency.

Amyloid deposition in the heart can cause both diastolic and systolic heart failure. EKG changes may be present, showing low voltage and conduction abnormalities like atrioventricular block or sinus node dysfunction. On echocardiography, the heart shows a restrictive filling pattern, with normal to mildly reduced systolic function. AA amyloidosis usually spares the heart.

People with amyloidosis do not get central nervous system involvement but can develop sensory and autonomic neuropathies. Sensory neuropathy develops in a symmetrical pattern and progresses in a distal to proximal manner. Autonomic neuropathy can present as orthostatic hypotension but may manifest more gradually with nonspecific gastrointestinal symptoms like constipation, nausea, or early satiety.

Accumulation of amyloids in the liver can lead to elevations in serum aminotransferases and alkaline phosphatase, two biomarkers of liver injury, which is seen in about one third of people. Liver enlargement is common. In contrast, spleen enlargement is rare, occurring in 5% of people. Splenic dysfunction, leading to the presence of Howell-Jolly bodies on blood smear, occurs in 24% of people with amyloidosis. Malabsorption is seen in 8.5% of AL amyloidosis and 2.4% of AA amyloidosis. One suggested mechanism for the observed malabsorption is that amyloid deposits in the tips of intestinal villi (fingerlike projections that increase the intestinal area available for absorption of food), begin to erode the functionality of the villi, presenting a sprue-like picture.

A rare development is a susceptibility to bleeding with bruising around the eyes, termed "raccoon-eyes," caused by amyloid deposition in the blood vessels and a reduced activity of thrombin and factor X, two clotting proteins that lose their function after binding with amyloid.

Amyloid deposits in tissue and causes enlargement of structures. Twenty percent of people with AL amyloidosis have an enlarged tongue, that can lead to obstructive sleep apnea, difficulty swallowing, and altered taste. Tongue enlargement does not occur in ATTR or AA amyloidosis. Enlarged shoulders, "shoulder pad sign," results from amyloid deposition in synovial space. Deposition of amyloid in the throat can cause hoarseness. Aβ2MG amyloidosis (Hemodialysis associated amyloidosis) likes to deposit in synovial tissue, causing chronic synovitis, which can lead to repeated carpal tunnel syndrome.

Both the thyroid and adrenal gland can be infiltrated. It is estimated that 10–20% of individuals with amyloidosis have hypothyroidism. Adrenal infiltration may be harder to appreciate given that its symptoms of orthostatic hypotension and low blood sodium concentration may be attributed to autonomic neuropathy and heart failure.

"Amyloid deposits occur in the pancreas of patients with diabetes mellitus, although it is not known if this is functionally important. The major component of pancreatic amyloid is a 37-amino acid residue peptide known as islet amyloid polypeptide or 'amylin.' This is stored with insulin in secretory granules in B cells and is co secreted with insulin." (Rang and Dale's Pharmacology, 2015.)

An older clinical method of classification refers to amyloidoses as systemic or localised

- Systemic amyloidoses affect more than one body organ or system. Examples are AL, AA and Aβ2m.

- Localised amyloidoses affect only one body organ or tissue type. Examples are Aβ, IAPP, Atrial natriuretic factor (in isolated atrial amyloidosis), and Calcitonin (in medullary carcinoma of the thyroid)

Another classification is primary or secondary.

- Primary amyloidoses arise from a disease with disordered immune cell function, such as multiple myeloma or other immunocyte dyscrasias.

- Secondary (reactive) amyloidoses occur as a complication of some other chronic inflammatory or tissue-destroying disease. Examples are reactive systemic amyloidosis and secondary cutaneous amyloidosis.

Additionally, based on the tissues in which it is deposited, it is divided into mesenchymal (organs derived from mesoderm) or parenchymal (organs derived from ectoderm or endoderm).

Tumoral calcinosis is a rare condition in which there is calcium deposition in the soft tissue in periarticular location i.e. around joints. The accumulations are outside the joint capsule. They are frequently seen in patients undergoing renal dialysis. It is also considered by some to have a hereditary predisposition. The name indicates calcinosis (calcium deposition) which resembles tumor (like a new growth). They are not true neoplasms - they don't have dividing cells. They are just deposition of inorganic calcium with serum exudate.

Children and adolescents (6 to 25 years) are the most commonly affected. The symptom that the accumulations cause is not pain but swelling around joints. They have propensity to enlarge progressively and ulcerate the overlying skin and extrude. They are most common around shoulders, hips and elbows. Laboratory evaluation reveal normal serum calcium levels and hyperphosphatemia. Rarely ALP (alkaline phosphatase - an enzyme active at sites of bone formation) may be elevated. Treatment is normalization of serum phosphate levels and resection of lesion. Surgical removal should be complete and if part of it is left, there is inevitable recurrence. Cutting through the excised calcium deposition reveals semifluid calcium suspension in albumin encapsulated by fibrous tissue.

Most individuals diagnosed with LECT2 amyloidosis in the United States (88%) are of Mexican descent and reside in Southwest region of the United States (New Mexico, Arizona, far Western Texas). Other groups with higher incidence rates of the disorder include First Nation Peoples in Canada, Punjabis, South Asians, Sudanese, Native Americans, and Egyptians. In Egyptians, for example, LECT2 is second most common cause of renal amyloidosis, accounting for nearly 31% of all cases.

ALECT2 amyloidosis is generally diagnosed in individuals between the ages 40 and 90, with a mean age of 67 years old. The disorder commonly presents with renal disease that in general is advanced or at an end stage. Associated signs and symptoms of their renal disease may include fatigue, dehydration, blood in urine, and/or other evidence for the presence of the nephrotic syndrome or renal failure. Further studies may find that these individuals have histological or other evidence of LECT2 amyloid deposition in the liver, lung, spleen, kidney, and/or adrenal glands but nonetheless they rarely show any symptoms or signs attributable to dysfunction in these organs. Unlike many other forms of systemic amyloidosis, LECT2 deposition has not been reported to be deposited in the myocardium or brain of affected individuals. Thus, LECT2 amyloidosis, while classified as a form of systemic amyloidosis, almost exclusively manifests clinically as renal amyloidosis. No familial link has been found in the disorder although there have been several cases described among siblings.

LECT2 Amyloidosis is a form of amyloidosis caused by the LECT2 protein. It was found to be the third most common (~3% of total) cause of amyloidosis in a set of more than 4,000 individuals studied at the Mayo Clinic; the first and second most common forms the disorder were AL amyloidosis and AA amyloidosis, respectively. Amyloidosis is a disorder in which the abnormal deposition of a protein in organs and/or tissues gradually leads to organ failure and/or tissue injury.

Although more than 30 different proteins can cause amyloidosis, the disorder caused by LECT2 is distinctive in three ways. First, it has an unusually high incidence in certain ethnic populations. Second, it is a systemic form of amyloidosis (i.e. amyloid deposited in multiple organs), as opposed to a localized form (amyloid deposits limited to a single organ) but nonetheless injures the kidney without or rarely injuring the other organs in which it is deposited. Third, LECT2 amyloidosis is diagnosed almost exclusively in elderly individuals.

Given its relatively recent discovery, exceptionally strong ethnic bias, limitation to causing kidney disease, and restriction to elderly individuals, LECT2 amyloidosis appears at present to be an under-recognized cause of chronic kidney disease particularly in the ethnic groups that exhibit a high incidence of the disorer.

Septic arthritis most commonly causes pain, swelling, and warmth at the affected joint. Therefore, those affected by septic arthritis will often refuse to use the extremity and prefer to hold the joint rigidly. Fever is also a symptom; however, it is less likely in older patients.

The most common joint affected is the knee. Hip, shoulder, wrist, or elbow joints are less commonly affected. Spine, sternoclavicular, and sacroiliac joints can also be involved; however, the most common cause of arthritis in these joints is intravenous drug use.

Usually only one joint is effected. More than one joint can be involved if bacteria are seeded through the bloodstream.

Osteoarthritis knee pain usually occurs while the joint is bearing weight, so the pain typically subsides with rest; some patients suffer severe pain, while others report no discomfort. Even if one knee is much larger than the other, pain is not guaranteed.

Signs and symptoms of water on the knee depend on the cause of excess synovial fluid build-up in the knee joint. These may include:

Jaccoud arthropathy (JA), Jaccoud deformity or Jaccoud's arthopathy is a chronic non-erosive reversible joint disorder that may occur after repeated bouts of arthritis. It is caused by inflammation of the joint capsule and subsequent fibrotic retraction, causing ulnar deviation of the fingers, through metacarpophalangeal joint (MCP) subluxation, primarily of the ring and little-finger. Joints in the feet, knees and shoulders may also get affected. It is commonly associated with systemic lupus erythematosus (SLE), and occurs in roughly 5% of all cases.

When associated with rheumatic fever it is also called chronic post–RF arthropathy.

Originally thought to be associated only with rheumatic fever, it has since been shown to occur also in SLE, Sjögren syndrome, scleroderma, dermatomyositis, psoriatic arthritis, vasculitis, ankylosing spondylitis, mixed connective tissue disease, and pyrophosphate deposition disease. It is distinct from bone erosion which is commonly associated with rheumatic arthritis, and also distinct from mild deforming arthropathy which is associated with SLE. There have also been cases of non-rheumatic JA associated with Lyme disease, HIV-infection and a number of other conditions.

Treatment focuses toward alleviating pain and in maintaining functionality of the affected joints through use of nonsteroidal anti-inflammatory drugs, corticosteroids, antimalarial drugs and physiotherapy. Surgery is also a possibility, with osteotomy or stabilization with Kirschner intramedullary wire. Tendon relocation, however, has been shown to only work in 30% of cases. The condition is named after the French 19th century physician Sigismond Jaccoud.

Diffuse scleroderma can cause musculoskeletal, pulmonary, gastrointestinal, renal and other complications. Patients with greater cutaneous involvement are more likely to have involvement of the internal tissues and organs. Most patients (over 80%) have vascular symptoms and Raynaud's phenomenon, which leads to attacks of discoloration of the hands and feet in response to cold. Raynaud's normally affects the fingers and toes. Systemic scleroderma and Raynaud's can cause painful ulcers on the fingers or toes which are known as digital ulcers. Calcinosis (deposition of calcium in lumps under the skin) is also common in systemic scleroderma, and is often seen near the elbows, knees or other joints.

- Musculoskeletal

The first joint symptoms that patients with scleroderma have are typically non specific joint pains, which can lead to arthritis, or cause discomfort in tendons or muscles. Joint mobility, especially of the small joints of the hand, may be restricted by calcinosis or skin thickening. Patients may develop muscle weakness, or myopathy, either from the disease or its treatments.

- Lungs

Some impairment in lung function is almost universally seen in patients with diffuse scleroderma on pulmonary function testing; however, it does not necessarily cause symptoms, such as shortness of breath. Some patients can develop pulmonary hypertension, or elevation in the pressures of the pulmonary arteries. This can be progressive, and can lead to right-sided heart failure. The earliest manifestation of this may be a decreased diffusion capacity on pulmonary function testing.

Other pulmonary complications in more advanced disease include aspiration pneumonia, pulmonary hemorrhage and pneumothorax.

- Digestive tract

Diffuse scleroderma can affect any part of the gastrointestinal tract. The most common manifestation in the esophagus is reflux esophagitis, which may be complicated by peptic stricturing, or benign narrowing of the esophagus. This is best initially treated with proton pump inhibitors for acid suppression, but may require bougie dilatation in the case of stricture.

Scleroderma can decrease motility anywhere in the gastrointestinal tract. The most common source of decreased motility is the esophagus and the lower esophageal sphincter, leading to dysphagia and chest pain. As scleroderma progresses, esophageal involvement from abnormalities in decreased motility may worsen due to progressive fibrosis (scarring). If this is left untreated, acid from the stomach can back up into the esophagus, causing esophagitis and GERD. Further scarring from acid damage to the lower esophagus many times leads to the development of fibrotic narrowing, also known as strictures which can be treated by dilatation, and Barrett's esophagus.

Duodenum: In patients with neuromuscular disorders, particularly progressive systemic sclerosis and visceral myopathy, the duodenum is frequently involved. There may be dilatation, which is often more pronounced in the second, third and fourth parts. The dilated duodenum may be slow to empty and the grossly dilated, atonic organ may produce a sump effect.

The small intestine can also become involved, leading to bacterial overgrowth and malabsorption of bile salts, fats, carbohydrates, proteins, and vitamins. The colon can be involved, and can cause pseudo-obstruction or ischemic colitis.

Rarer complications include pneumatosis cystoides intestinalis, or gas pockets in the bowel wall, wide mouthed diverticula in the colon and esophagus, and liver fibrosis. Patients with severe gastrointestinal involvement can become profoundly malnourished.

Scleroderma may also be associated with gastric antral vascular ectasia (GAVE), also known as "watermelon stomach". This is a condition where atypical blood vessels proliferate usually in a radially symmetric pattern around the pylorus of the stomach. GAVE can be a cause of upper gastrointestinal bleeding or iron deficiency anemia in patients with scleroderma.

- Kidneys

Renal involvement, in scleroderma, is considered a poor prognostic factor and frequently a cause of death.

The most important clinical complication of scleroderma involving the kidney is "scleroderma renal crisis". Symptoms of scleroderma renal crisis are malignant hypertension (high blood pressure with evidence of acute organ damage), hyperreninemia (high renin levels), azotemia (kidney failure with accumulation of waste products in the blood) and microangiopathic hemolytic anemia (destruction of red blood cells). Apart from the high blood pressure, hematuria (blood in the urine) and proteinuria (protein loss in the urine) may be indicative.

In the past scleroderma renal crisis was almost uniformily fatal. While outcomes have improved significantly with the use of ACE inhibitors the prognosis is often guarded, as a significant number of patients are refractory to treatment and develop renal failure. Approximately 5–10% of all diffuse cutaneous scleroderma patients develop renal crisis at some point in the course of their disease. Patients that have rapid skin involvement have the highest risk of renal complications. It is most common in diffuse cutaneous scleroderma, and is often associated with antibodies against RNA polymerase (in 59% of cases). Many proceed to dialysis, although this can be stopped within three years in about a third of cases. Higher age and (paradoxically) a lower blood pressure at presentation make it more likely that dialysis is needed.

Treatments for scleroderma renal crisis include ACE inhibitors. Prophylactic use of ACE inhibitors is currently not recommended, as recent data suggest a poorer prognosis in patient treated with these drugs prior to the development of renal crisis. Transplanted kidneys are known to be affected by scleroderma and patients with early onset renal disease (within one year of the scleroderma diagnosis) are thought to have the highest risk for recurrence.

In the skin, systemic sclerosis causes hardening and scarring. The skin may appear tight, reddish, or scaly. Blood vessels may also be more visible. Where large areas are affected, fat and muscle wastage may weaken limbs and affect appearance. Patients report severe and recurrent itching of large skin areas. The severity of these symptoms varies greatly among patients: Some having scleroderma of only a limited area of the skin (such as the fingers) and little involvement of the underlying tissue, while others have progressive skin involvement. Digital ulcers — open wounds on especially on fingertips and less commonly the knuckles — are not uncommon.

Mild or early cases of Pagets are asymptomatic, and so most people are diagnosed with Paget's disease incidentally during medical evaluation for another problem. Approximately 35% of patients with Paget's have symptoms related to the disease when they are first diagnosed. Overall, the most common symptom is bone pain. When symptoms do occur, they may be confused with those of arthritis or other disorders, and so diagnosis may be delayed.

Paget's may first be noticed as an increasing deformity of a person's bones.

Paget's disease affecting the skull may lead to loss of hearing in one or both ears due to compression of the nerves in the inner ear. Rarely, skull involvement may lead to compression of the nerves that supply the eye, leading to vision loss.

Potential signs and symptoms include:

- Cardiovascular: Raynaud's phenomenon (is the presenting symptom in 30% of affected persons, occurs in 95% of affected individuals at some time during their illness); healed pitting ulcers on the fingertips; skin and mucousal telangiectasis; palpitations, irregular heart rate and fainting due to conduction abnormalities, hypertension and congestive heart failure.

- Digestive: gastroesophageal reflux disease, bloating, indigestion, loss of appetite, diarrhoea alternating with constipation, sicca syndrome and its complications, loosening of teeth and hoarseness (due to acid reflux).

- Pulmonary: progressive worsening of shortness of breath, chest pain (due to pulmonary artery hypertension) and dry, persistent cough due to interstitial lung disease.

- Musculoskeletal: joint, muscle aches, loss of joint range of motion, carpal tunnel syndrome and muscle weakness.

- Genitourinary: erectile dysfunction, dyspareunia, scleroderma renal crises and kidney failure.

- Other: facial pain due to trigeminal neuralgia, hand paresthesias, headache, stroke, fatigue, calcinosis and weight loss.

Thesebacteriaaccount for over 80% of septic arthritis cases and are usuallystaphyloccoci or streptococci. It is commonly spread through the blood from an infection site elsewhere, but can be introduced directly into the joint or from surrounding tissue.

The kidney is the organ most frequently affected. Proteinuria, loss of protein in the urine, is characteristic. More than 90% of people with LCDD develop kidney failure, often with rapid progression of disease.

Light chains may be deposited in many other organs and may or may not result in any symptoms. Other than the kidneys, liver and heart are the most commonly involved organs. Deposition of light chains in the liver may lead to hepatomegaly, an enlarged liver, or rarely portal hypertension or liver failure. The heart is affected in up to 80% of patients with LCDD, and may cause arrythmias and congestive heart failure.