Last update August 14, 1998
Ed Friedlander, M.D., Chairman, Department of Pathology
University of Health Sciences, Kansas City MO -- Jan. 24, 1996
QUIZBANK Disk 9: Bone & joint #'s 57-106
Most patients with arthritis do not know which type they have (Mo. Med. 87: 145, 1990), and, appropriately, most cases of joint disease never get examined by a pathologist. Yet joint problems are the #1 recognized cause of occupational disability, and cause suffering comparable in prevalence and severity (though not in kind) to alcoholism and major mental illness.
This unit includes a major systemic disease (rheumatoid arthritis) and several important single-organ problems. You have completed the learning objectives when you know the handout at recall level, and have examined the photos in Big Robbins or your own favorite pathology text.
"Joint diseases" involve the diarthrodial (hinge, synovial) joints. (Rule: Disease does not affect non-moving joints like skull sutures or the pubic symphysis). Don't forget the major autoimmune diseases and fibromyaligia syndrome in evaluating musculoskeletal or joint pain.
-- joint capsule (pain-sensitive) lined by synovium (vascular tissue with an inner layer of synovial cells) which out-pouches to form bursae.
You remember that type A synovial lining cells are phagocytes, while type B synovial lining cells add hyaluronic acid to extracellular fluid to make the slimy synovial fluid.
-- articular cartilage (shock absorber, heals poorly)
-- synovial fluid (lubrication and nourishment for cartilage)
Many major systemic diseases affect joints. These include amyloidosis, gout, lupus, Lyme disease, hemochromatosis, hemophilia, inflammatory bowel disease (most forms and also post-ileal-bypass), ochronosis ("alkaptonuria"), rheumatic fever, sarcoid, scleroderma, sickle cell disease, syphilis, and various viremias. {49499} ochronosis ("alkaptonuria"), femoral head. Also remember the various causes of clubbing ("hypertrophic osteoarthropathy") and neuropathic joint disease ("Charcot's joints"). Ankylosis of a joint is scarring which is sufficient to prevent movement in that joint.
"OSTEOARTHRITIS" ("osteoarthrosis", "degenerative joint disease";Br. Med. J. 299: 1476, 1989; NEJM 320: 1322, 1989)
A very common, slowly progressive, noninflammatory disorder of unknown cause, occurring later in life. Most osteoarthritis fortunately never becomes symptomatic. When it does, victims experience the slow onset of stiffness, pain, minor deformity, limitation of motion without heat or effusion. Most often involved are the great weight-bearing joints of spine, hips, knees. Especially troublesome is lipping in the cervical and lumbar spine ("osteophytes"), which can impinge on nerve roots of the spinal foramina. For some reason, the phalangeal-metacarpal joint of the thumb, distal interphalangeal joints (spurs here are called "Heberden's nodes"), and TMJ are also common involved. (So much for the idea that "heavy weight-bearing" is the overriding cause of osteoarthritis....)
* Medical history buffs: This is the same Dr. Heberden who distinguished chickenpox from smallpox, described angina pectoris, and described night blindness. The wrists, elbows and shoulders are generally spared.
Primary osteoarthritis is the common "arthritis" which affects most older people. This is supposedly due to "wear-and-tear" (it's commoner (sic) in big people, especially in the overweight; see J. Rheumatol. 17: 283, 1990) and/or metabolic changes in cartilage (the bewildering array in Big Robbins is only the beginning, but they cannot all be primary.)
Secondary osteoarthritis has an identifiable congenital or acquired predisposing factor (i.e., football knee, dancers, power drill operators, congenital hip malformation, hemochromatosis, ochronosis, deposits, * defective type II collagen gene J. Clin. Inv. 87: 357, 1991, * other poorly understood autosomal dominant syndromes, see J. Rheum. 18(S27): 7, 1991.)
Athletes probably do not have more osteoarthritis than others (for example, Am. J. Med. 88: 452, 1990), but there are many variables.
* Kashin-Beck disease is an endemic arthritis seen in Siberia, Mongolia, Tibet, and the remote areas of Red China ("the people's paradise"). The cause is almost certainly selenium deficiency coupled with fulvic acid (from rotting organic material; it poisons procollagen type II processing Eur. J. Biochem. 202: 1141, 1991) in the drinking water (J. Tox. 35: 79, 1992; Am. J. Clin. Nut. 57(S2): 259S, 1993; Bio. Trace El. Res. 31: 1, 1991). Animal model: Biochem. J. 289: 829, 1993.
Histopathology Virch. Arch. A. 423: 483, 1993.
Regardless of whether osteoarthritis is "primary" or "secondary", the pathologist sees characteristic changes:
-- cartilage "fibrillation" (collagen fibers within the cartilage become visible because they have lost their carbohydrate)
-- erosion and flaking of articular cartilage
-- subchondral sclerosis ("eburnation", ivory) and cyst formation
-- osteophyte formation ("spurring", "lipping" -- outward growth of bone and cartilage at the margins of articular surfaces)
-- joint mice (sometimes; detached bits of cartilage and bone, resulting in pain or recurrent locking) {10946} spurred spine {24637} spur, histology {24638} eburnation {24639} "cyst" formation in articular bone {24640} joint mouse {40180} femoral head, eroded cartilage {45612} x-ray, showing narrowed joint spaces
RHEUMATOID ARTHRITIS ("RA"; poem NEJM 320: 674, 1989)
A common, usually chronic, systemic, dread inflammatory disease (* probably a group of diseases) of unknown etiology. Its outstanding feature is progressive, symmetrical synovitis, with pain and morning stiffness, and which may lead to deformity and destruction of the joints.
Up to 3% of women and 1% of men worldwide will be affected; most cases arise in young or middle-aged adults. Why women get more rheumatoid arthritis is mysterious; no doubt it has something to do with women's immune system being more powerful than men's.
Going on the oral contraceptive pill has been said to help RA, and estrogen actually relieves some animal models (Br. J. Rheumatol. 28(S1): 54, 1989.) {25016} rheumatoid arthritis, ulnar deviation {25017} rheumatoid arthritis, ulnar deviation {38225} rheumatoid arthritis, hand {45602} rheumatoid arthritis, x-ray {45648} rheumatoid arthritis, foot
* HLA-DR4 is weakly associated with the disease in the U.S. and elsewhere, but the antigen is extremely common. In other populations, rheumatoid arthritis associates with HLA-DR1 instead; it now appears that, whatever number is assigned the actual high-risk tissue-type, they have a common epitope (Postgrad. Med. J. 67: 114, 1991),
Cases with positive rheumatoid factor ("seropositive") cases show a soft familial tendency, but the identical twin of a RA patient has only about a 30% chance of getting the disease. Cases with negative rheumatoid factor ("seronegative") usually do not fun in families.
An acute ("exudative", and destructive) and chronic (considered the underlying problem) inflammatory synovitis leads to proliferation of a vascular connective tissue in the synovium, which later fills with polys, T-cells, and plasma cells ("pannus"; for histology see Ann. Rheum. Dis. 44: 549, 1985; Arthr. Rheum. 31: 956, 1988). This spreads over and erodes the articular cartilage and even bone leading to fibrosis of the joint. {49503} pannus, gross {49504} pannus, gross {46391} pannus, gross, up close {24636} pannus, micro, eroding bone {10313} pannus, micro, eroding bone {19415} pannus, showing lymphocytes {19418} pannus, showing lymphocytes
The etiology is obscure, but surely involves an immune system abnormality. (* See Lancet 1: 832, 1985 for a novel treatment.) Most people presently think that some foreign agent -- EB virus? parvovirus? mycoplasma? dietary factor? something nasty from the gut (J. Rheumatol. 16: 1017 & 1061, 1990)? bacterial shock proteins (Arthr. Rheum. 32: 1497, 1989; Arthr. Rheum. 34: 486, 1991) -- initiates an inappropriate immune response (Am. J. Med. 80(4B): 4, 1986).
Mediators of inflammation that seem strongly involved in rheumatoid arthritis are macrophage-derived: IL-1, IL-6 (Br. J. Rheum. 34: 321, 1995), interleukin-8 (J. Lab. Cln. Med. 123: 183, 1994), leukotriene B4, complement components, and à-TNF (it abounds in rheumatoid fluids; Arthr. Rheum. 31: 1041, 1988).
These summon the polys and cause other harmful things to happen. The factors produced primarily in lymphocytes do not seem to be involved.
Interleukin 1 (and more recently, à-TNF) have been shown stimulate production of collagenase and prostaglandin E2 in rheumatoid joints. These wreck havoc.
Omega-3s (fish oil) have recently been demonstrated as useful in controlling symptoms of rheumatoid arthritis (Ann. Int. Med. 106: 497, 1987; Artthr. Rheum. 37: 824, 1994). We think they block production of leukotriene B4 and interleukin 1.
There is also considerable interest in substance P, released from nerve terminals in joints. This is in keeping with observations that emotional stress triggers flare-ups, and that joints paralyzed by strokes are spared the effects of rheumatoid arthritis. See J. Rheumatol. 13: 651, 1986; Science 235: 893, 1987; Science 239: 258, 1988; Arthr. Rheum. 33: 87, 1990. Relate all this to the mouse model of scrambled neural circuitry, and the atypical depression of rheumatoid arthritis patients: JAMA 267: 910, 1992.
Rheumatoid factor, present in most RA patients, is antibody against the Fc portion of IgG. It may contribute to pathogenesis, * perhaps by activating NK cells (Arthr. Rheum. 34: 423, 1991). More on this later in your clinical years.
Food hypersensitivity is related anecdotally to some cases of rheumatoid arthritis, and some of the evidence is impressive. On the usefulness of elimination diets in this disease, see Ann. Rheum. Dis. 44: 549, 1985; the value of a vegetarian diet (at least try it for a year) is now accepted: Br. J. Rheum. 33: 638 & 569, 1994.
One of the best experimental models involves sensitizing the T-cells of various animals to type II collagen. The HLA sequence that permits this to happen (at least in mice) has just been identified (Proc. Nat. Acad. Sci. 86: 8475, 1990), and an epitope which suppresses the autoimmunity in some species (J. Exp. Med. 170: 1999, 1989). Definitely stay tuned.
New evidence suggests that a clone of autoreactive T4 cells, accumulating in the joints, is responsible (Science 253: 325. July 19, 1991).
* Synthetic protease inhibitors suppress inflammation in some experimental models (Am. J. Path. 136: 909, 1990) -- this is hardly surprising, but may lead to new treatments someday.
* Current thinking about the pathogenesis of rheumatoid arthritis: Am. J. Med. 85(4-A): 12, Oct. 14, 1988; NEJM 322: 1277, 1990; J. Rheumatol. 17: 127, 1990. Making the diagnosis still requires pattern recognition by clinicians: Am. J. Med. 85(4-A): 2, Oct. 14, 1988.
Small joints are most often affected, especially the proximal interphalangeal joints (swan-neck deformity, boutonniere deformity, sometimes ankylosis, more often subluxation), metacarpophalangeal joints (ulnar deviation), wrists, knees, ankles. {24635} rheumatoid arthritis, damaged joint {24633} rheumatoid arthritis, mutilated joints {46392} rheumatoid arthritis, x-ray showing erosions {24634} destruction of finger joints in rheumatoid arthritis
* Rheumatoid joints really are stiffer in wet weather (Scand. J. Rheum. 15: 27, 1986). Or maybe we're just seeing faces in the clouds (Proc. Nat. Acad. Sci. 93: 2895, 1996).
Rheumatoid subluxation of the cervical spine is a surgical emergency when the spinal cord is compressed (Ann. Rheum. Dis. 44: 867, 1985; J. Rhematol. 17: 285, 1990; J. Nat. Med. Assoc. 82: 297, 1990). {30286} rheumatoid disease of axis {30288} rheumatoid disease of axis
The rheumatoid arthritis patient has a systemic disease and many other problems:
Patients may develop splenomegaly (when this causes neutropenia, this is the ominous Felty's syndrome, see Medicine 69: 69. 1990), anemia of chronic disease, generalized lymphadenopathy (J. Clin. Path. 43: 106, 1990), and/or myopathy. Mild fever and severe malaise are common. Amyloidosis occurs in around 15%. Most of these bad effects are probably due to interleukin 1 (IL-1) production.
Rheumatoid lung -- fibrosis of the alveolar septa, which make them impermeable to oxygen and decreases lung compliance -- occurs in around a quarter of these patients. RA patients must stop smoking. Fibrous tissue may also selectively obliterate the bronchioles and small vessels. Rheumatoid nodules occur in maybe 20% of patients with rheumatoid arthritis (and many patients with rheumatic fever, or with neither). These consist of an acellular center of eosinophilic material ("fibrinoid", as before a mix of plasma proteins) surrounded by palisaded histiocytes and other cells, maybe with a rim of granulation tissue. They may occur nearly anywhere; most often about extensor surfaces, sometimes the pericardium, aortic valve, lung parenchyma (coal miners -- that's Caplan's syndrome, part of the "black lung" mess.) {12473} rheumatoid nodule, patient { 9000} rheumatoid nodule, histology { 8999} rheumatoid nodule, histology Osteoporosis of disuse develops around affected joints.
Rheumatoid vasculitis (type III immune injury, no surprise in a disease in which antibodies can be directed against themselves) can and do cause MI, stroke, gangrene, finger and leg ulcers, Raynaud's, etc. Check these patients for cryoglobulins. Sj"gren's syndrome can develop (* 15%).
Pleurisy (painful inflammation of the pleural surfaces) can develop and produce effusions that compress the lungs. Pericarditis is less common. Treatment centers around aspirin or non-steroidal anti-inflammatory drugs, muscle-strengthening, and rest. (Nice review: Hosp. Pract. 23(1): 57, Jan. 15, 1988). The next line of attack is gold. Manipulation fails for rheumatoid arthritis: J. Musculoskel. Med., June 1990.
Immunosuppression is reserved for resistant cases, but there is no shortage of such patients. Methods include glucocorticoids, antimetabolites such as azathioprine, methotrexate (Ann. Int. Med. 107: 418, 1987; Arthr. Rheum. 31: 305, 1988; Ann. Int. Med. 110: 581, 1989; J. Rheum. 18: 334, 1991; Arth. Rheum. 37: 193, 1994), cyclophosphamide, others, also cyclosporine (Arth. Rheum. 30: 11, 1987; Lancet 335: 1051, 1990, JAMA 261: 1864, 1989; J. Rheum. 18: 19, 1991), total lymphoid radiation (Arth. Rheum. 30: 1, 1987), gamma interferon (NEJM 317: 940, 1987; J. Rheumatol. 15: 570, 1988 -- seems to help), anti-CD4 monoclonal antibody (Arthr. Rheum. 34: 129, 1991). Review of all "big guns" for RA: JAMA 259: 2446, 1988. Strong medicine -- but worth trying before your RA patient commits suicide. The most bizarre new therapy is oral administration of altered type II collagen to "tolerize" the T-cells (however that works, and it seems to): Science 261: 1727, 1993. * The prototype of a promising new line of drugs is the simple carbohydrate amiprilose (Ann. Int. Med. 111: 455, 1989).
In evaluating any therapeutic claim you may hear for rheumatoid arthritis, remember that it is a disease of exacerbations and remissions, many cases just go away, and only a minority lead to profound deformity and disability ("arthritis mutilans"). Flagrant arthritis quackery is a *$3 billion-a-year business in the U.S. alone (see also Med. J. Aust. 143: 516, 1985.) Folk cures are less disturbing (Arthr. Rheum. 32: 1604, 1989).
JUVENILE RHEUMATOID ARTHRITIS ("Still's disease")
Apparent rheumatoid arthritis in one or more joints beginning under age 16 (peak incidence 1-3 years). A febrile prodrome for weeks or months, big lymph nodes and liver, pleuritis, pericarditis, iridocyclitis, and/or skin rash may appear. Rheumatoid factor is usually absent. Don't worry about the subtypes now. Many cases remit. * A surprising new Rx: Br. Med. J. 296: 1362, 1988. Despite the obvious differences between Still's disease and classical rheumatoid arthritis, the joint changes appear to be the same. * The most exciting new fact (if confirmed) is that cases with high titers against influenza A are suppressed by the innocuous anti-influenza drug amantadine (Br. J. Rheum. 28: 521, 1989). Autoimmune disease in children: Ped. Clin. N.A. 33(5): Oct, 1986.
"THE REACTIVE ENTHESOPATHIES" (seronegative spondyloarthropathies, HLA-B27 family; these are not "variants of rheumatoid arthritis")
This is a curious family of common, overlapping illnesses which include ankylosing spondylitis (Marie-Strumpell disease, "bamboo spine", "poker-back"), Reiter's syndrome, enteropathic arthropathy (shigella, salmonella, campylobacter, yersinia; the tendency is to lump these with Reiter's as "reactive arthritis": see Clin. Exp. Rheum. 11S8: S29, 1993), ulcerative colitis / Crohn's, psoriasis (big review Postgrad. Med. 97(4): 97, April 1995), and Beh‡et's syndrome. All are more common and more severe in men. More on spondylitis. {46390} ankylosing spondylitis {49505} ankylosing spondylitis {49506} ankylosing spondylitis
An "enthesis" is the point at which a ligament attaches to bone. The axial entheses are involved. Joints do not erode, but ankylose (fuse solid).
Remember they are all strongly associated with HLA-B27, especially in whites. Rheumatoid factor is not present and synovial membranes are usually not inflamed.
* For interesting evidence about strains of Klebsiella that mimic HLA-B27, see Ann. Rheum. Dis. 44: 169, 1985; Arthr. Rheum. 32: 437, 1989.
The pathology mostly involves ligamentous attachments. Concurrent inflammation of the urethra, conjunctiva, iris, and aortic valve ring are common.
Reiter's syndrome is arthritis, eye problems, and a horny rash on the glans, trunk, and especially palms and soles, all following an episode of urethritis in B27 men (* "Can't see, can't pee, can't go out with me!"). Chlamydial antigens abound in the pannus: Arthr. Rheum. 31: 937, 1988. The symptoms come and go, and generally vanish for good after a few months. This disease is not rare. {12289} Reiter's, scaly rash {12290} Reiter's, scaly rash
Spondylitis patients tend to get better by themselves, especially after the spine is no longer mobile. * Holist Norman Cousins got relief from his ankylosing spondylitis by watching Marx Brothers' and Three Stooges movies. (Is this possible?? I think so....)
Nice reviews: Med. Clin. N.A. 70: 325, 1986, Disease-a-Month 31(1): Jan. 1985. * Maybe one gorilla in four is crippled by ankylosing spondylitis (Arthr. Rheum. 31: 934, 1988).
LOW BACK PAIN (remember there's also "neck pain"). Review Br. Med. J. 310: 929, 1995.
This ubiquitous clinical problem has baffled the scientific medical profession until recently:
(1) Imaginary etiologies (notably "muscle spasm") are routinely invoked to explain it, resulting in a whole class of drugs ("muscle relaxants") which are used very questionably. (I hope you enjoy reading "The Myth of Skeletal Muscle Spasm", Am. J. Phys. Med. Rehab. 68: 1, 1989, as much as I did.)
(2) Bulges and protrusions (but not extrusions) seen on MRI scans were considered etiologic, until it turned out that folks without back pain have indistinguishable "pathology" (NEJM 331: 69, 1994).
(3) Anecdotal evidence of better results from treatment through "systems of alternative medicine" (osteopathy, chiropractic), which treat back pain using empirical techniques. See West. J. Med. 150: 351, 1989. This has found recent support in a pretty good controlled study: Br. Med. J. 300: 1431, 1990; Lancet, July 28, 1990, p. 220, others.
(4) Recent discovery by the medical profession of such common-sense processes as facet syndrome (Hosp. Pract. 23: 41, Oct. 30, 1988), which is probably the most common cause of back pain without sciatica.
Risk factors for low back pain are tall stature, overweight, large breast size, slouching, lack of physical conditioning, cigaret smoking (Lancet 1: 1305, 1989), and drunkenness.
Truck drivers and nurses have more than their share of back troubles.
Mechanical problems that give rise to low back pain are only now being elucidated.
It has been known for centuries that the nucleus pulposus has dried up and the annulus has cracked in most discs by age 60. See Dr. J. Wallach's Pig Arthritis Formula . These cause a variety of problems (Hosp. Pract. 24: 135, Sept. 1989). When a nucleus pulposus herniates through the annulus and impinges on a nerve root, the pain can be severe. (You'll learn about the "straight leg raising test" and other techniques in clinic).
In "facet syndrome", we think that the posterior interlaminar facet joints sublux as a result of disc space narrowing. Patients typically report sudden onset on bending or twisting, have negative straight leg raising tests, and have relief when a local anesthetic is injected into the joint.
Another plausible-sounding theory of the origin of this kind of pain is herniation of a bit of synovium into the space around the nerve -- it's easy to see how manipulation could relieve this problem immediately. Stay tuned.
Magnetic resonance imaging is elucidating the more subtle mechanical problems which have previously eluded radiologists: South. Med. J. 81: 1487, 1988.
Please remember that there are many non-mechanical causes of low back pain. These patient may have rupturing aortic aneurysms, metastatic cancer, epidural abscesses, Pott's disease (i.e. TB of the spine), etc., etc. {11449} Pott's disease
"Science is self-correcting". Just as mechanical explanations are finally being figured out, mechanical therapies are finally being appreciated by scientific physicians. Flaws in previous studies, pro and con: Br. Med. J. 303: 1298, 1991. However, no less a figure that the chief of Harvard's pain clinic teaches physicians (M.D.'s, that is) to perform manipulations Hosp. Pract. 24: 89, March 1989.
* We learn with hope of the formation of the National Association for Chiropractic Medicine (P.O. Box 794, Middleton WI 53562; phone 608-233-8991), dedicated to upgrading the profession's scientific and ethical standards. This is welcome news, but these reformers continue to meet much resistance from ideologues and charlatans.
For example:
"We must not alter or modify our philosophy to fit today's facts. Instead, we must wait for the emergence of new information that supports and proves philosophical truth." --"The Chiropractic Journal", Dec. 1992
(Claiming AIDS is not a viral illness)
Can you imagine even a communist talking like that nowadays? For more on the current divisions in chiropractic, see Consumer Reports, June 1994, cover story.
Terms: "radiculopathy", "lumbago" and "sciatica" indicate nerve root involvement, typically with radiating pain. The most common cause, of course, is a bad disc. "Cauda equina syndrome", from compression of the cauda equina by a midline herniated nucleus pulposus, tumor or abscess is a surgical emergency. Practical management of low back pain for generalists: Prim. Care 15: 827, 1988. Remember there's still malingerers out there.
* Ignore Big Robbins both on "muscle strain" and on "design" (p. 1346) -- the imperfections of nature tell the real story.
SUPPURATIVE ARTHRITIS (i.e., bacterial infection in a joint)
The most common agents are gonococcus, gram positive cocci (Staph, Strep), and gram negative rods (E. coli, H. 'flu, Pseudomonas; Salmonella in sickle cell disease). These organisms arrive by hematogenous spread.
Suppurative arthritis is uncommon in children (think of H. 'flu or spread from contiguous osteomyelitis).
Bacterial arthritis is usually monarticular and involves large joints. (Gonococcal arthritis often involves a series of joints.) The cartilage is quickly ruined by hydrolytic enzymes from polys. In bad cases, the joint may be ankylosed.
Tuberculous arthritis follows primary pulmonary infection. It is likely to be bad and chronic, with pannus and ankylosis.
CALCIUM CRYSTAL DEPOSITION DISEASE:
Pseudogout involves deposition of calcium phosphates, usually in the knees. The process is poorly understood. {14258} pseudogout (or so they tell me...) {14261} pseudogout (ditto)
SYNOVIAL SARCOMA
Biphasic (usually, spindle cell and epithelial-like "synovioblast") sarcoma that usually arises in or about Hunter's canal in young adults. (These tumors usually does not arise in synovium.) It metastasizes either by blood or lymphatics. (The latter fact is unusual for sarcomas.) Prognosis is fair, with 50% ten-year survival.
Pigmented villinodular synovitis is a quasi-neoplastic, destructive lesion within a single joint (usually the knee). { 9655} pigmented villinodular synovitis, gross
FIBROUS HISTIOCYTOMAS
Dermatofibroma ("sclerosing hemangioma"): skin and elsewhere This is a solitary, hard nodule. The phagocytes contain lipid, making them yellow on cross-section. They also contain hemosiderin, imparting a brown color, and this also causes melanocytic pigmentation of the overlying skin, particularly around the edges, so these appear as brown bumps. {25592} dermatofibroma, gross {12203} dermatofibroma, darkly pigmented {12774} dermatofibroma, gross {12775} dermatofibroma, gross; this one was quite vascular {12777} dermatofibroma, gross {39954} dermatofibroma, section {24260} dermatofibroma, histology (good spindle- cell histiocytes) Giant cell tumor of tendon sheath ("fingeroma", "xanthofibroma"): quasi-neoplastic benign yellow mass Malignant fibrous histiocytoma: the commonest sarcoma, develops deep in limbs or in retroperitoneum. The cell of origin is the "macrophage acting as a fibroblast". Don't worry about such arcane stuff; leave that to pathologists. {21145} malignant fibrous histiocytoma, buttock; you need only recognize this is a deep soft-tissue cancer (i.e., probably a sarcoma) { 9019} malignant fibrous histiocytoma, histology; you need only recognize this is a spindle-cell malignancy { 9021} malignant fibrous histiocytoma; you need only recognize this is a malignancy; the cells do remind me of those in a granuloma
Tenosynovitis and bursitis result from injury (usually mild and repeated). Syndromes includes housemaid's knee (* an occupational hazard of certain monastics as well) and tennis elbow. {12025} bursitis
Carpal tunnel syndrome: annular fibrosis of the flexor retinaculum, impinging on the median nerve. Very common. Most cases are idiopathic, but remember amyloidosis.
Ganglion cyst: a blob on wrist or fingers, formed by myxoid degeneration of connective tissue. It is neither a "ganglion" nor a "cyst", and it does not communicate with the joint. The home remedy -- smash it with a holy book -- is about as successful as surgery.
Dupuytren's contracture: fibrosis of the palmar aponeurosis.
The relationships to alcoholism and diabetes are probably overstated. A similar lesion can involve the plantar aponeurosis.
* Ronald Reagan had a "Dupuytren's" removed while president. {49523} Dupuytren's contracture
Osgood-Schlatter's disease is a banal but uncomfortable, very common, locally-destructive process involving the anterior tubial tuberosity of athletically-active, rapidly growing teens. The cause is probably repeated, tiny avulsions of the periosteum from the pull of the quadriceps tendon. See Am. Fam. Phys. 41: 173, 1990.
Famous arthritics (Clin. Rheum. 8: 442, 1989): John Madison (rheumatoid arthritis); Renoir (rheumatoid arthrititis); Rubens (rheumatoid arthritis); Columbus (Reiter's; also Arch. Int. Med. 152: 274, 1992)