Rheumatic fever is an inflammatory disease that can affect the heart, joints, nervous system and skin following a streptococcus infection such as strep throat. It primarily affects children aged 5 to 15 years old. Rheumatoid arthritis is an autoimmune disease where the immune system attacks the body's own tissues, causing chronic inflammation of the joints and surrounding tissues. It can also affect other organs and is considered a systemic illness. Both conditions involve inflammation and can damage tissues over time.

1. RHEUMATIC DISEASES
RHEUMATIC FEVER
&
RHEUMATOID ARTHRITIS

2. RHEUMATIC FEVER

3. WHAT IS RHEUMATIC FEVER?
Rheumatic fever is a systemic
inflammatory disease that can involve
connective tissue of the heart, nervous
system, skin, and joints.
Rheumatic fever develops after
streptococcus infections plus allergic
responce.


4. Rheumatic fever can occur at any age but
primarily affects children from 5 years old to
15 years old.
Rheumatic fever develops about 20 days after
strep throat or scarlet fever.
The streptococcus infection which leads to
rheumatic fever may be asymptomatic in a
third of all cases.

5. MORPHOLOGICAL SIGNS OF
RHEUMATISM
 1. systemic progression of connective tissue deorganization (mucoid
swelling, fibrous changes, cellular reaction, sclerosis)
 2. damage of the vessels
 3. immunopathological processes: specific cellular reaction is
rheumatic granuloma(Aschoff-Talalaev’s) – in the center there is a
focus of fibrinoid necrosis with macrophages with hypertrophic
nuclei, epithelial cells located in the fan-like manner, later a crown
of lymphocytes appears.

6. Strep throat

7. Scarlet fever

8. CAUSES
 Rheumatic fever can occur after an infection of
the throat with a bacterium called Streptococcus
pyogenes, or group A streptococcus.
 Group A streptococcus infections of the throat
cause strep throat or, less commonly, scarlet
fever. Group A streptococcus infections of the
skin or other parts of the body rarely trigger
rheumatic fever.

9.  The exact link between strep infection and
rheumatic fever isn't clear, but it appears that
the bacterium "plays tricks" on the immune
system.
 The strep bacterium contains a protein similar to
one found in certain tissues of the body.
 Therefore, immune system cells that would
normally target the bacterium may treat the
body's own tissues as if they were infectious
agents — particularly tissues of the heart, joints,
skin and central nervous system.
 This immune system reaction results in
inflammation.

10. RISK FACTORS
Factors that may increase the risk of rheumatic
fever include:
 Family history. Some people may carry a gene
or genes that make them more likely to develop
rheumatic fever.
 Type of strep bacteria. Certain strains of strep
bacteria are more likely to contribute to
rheumatic fever than are other strains.
 Environmental factors. A greater risk of
rheumatic fever is associated with overcrowding,
poor sanitation and other conditions that may
easily result in the rapid transmission or
multiple exposures to strep bacteria.

12. MAIN VARIANTS OF RF
Cardio-vascular form
Polyarthritis

13. CARDIO-VASCULAR FORM
 Rheumatic perycarditis
 Rheumatic myocarditis
 Rheumatic epycarditis

14. RHEUMATIC PERICARDITIS
 More often – exudative inflammation in
perycardium
 Variants of exudates – serous, hemorragic,
fibrinous, mix. Never purulent

15. SEROUS PERICARDITIS
 Hart is increase in size (a lot) due to serous
exudate between inner and external leis of
pericard
 Serous exudate –contains a lot of water, low level
of cells and low concentration of plasmatic
proteins ( 2%-4%)
 That*s why - Cardiac failure is very extensive
but prognosis is better.

16. FIBRINOUS PERICARDITIS
 Hart is bit increase in size due to dry exudate
between inner and external leis of pericard
 Fibrinous exudate –does not contain water (dry
exudate), contains high level of cells and high
concentration of plasmatic proteins (fibrin)
 Cardiac failure is very extensive and prognosis is
very bed.
 That*s why - Fibrinous pericarditis - may be
cause of death

17. FIBRINOUS PERICARDITIS
Rough pericardium,
thick,
non-transparent

18. FIBRINOUS PERICARDITIS

19. FIBRINOUS PERICARDITIS

20. RHEUMATIC MYOCARDITIS
 3 variants –
 1.Local proliferative – with granulomas (they are
build with macrophages - Anichkov cells)
 2. Local exudative with serous exudate
 3. Diffuse exudative with serous exudate

21. LOCAL INTERSTITIAL EXUDATIVE MYOCARDITIS
 Mild form
 Local infiltration on interstitial tissue(lymphocytes, neutrophils etc.)
 Hyperemia, edema
 Outcome: reabsorption of exudate or formation of small focal
cardiosclerosis

22. NODULAR PRODUCTIVE MYOCARDITIS
 Moderate form
 Histologically can see systemic blood congestion in interstitial
tissue, infiltration(lymphocytes, histiocytes, neutrophils,
eosinophils), granulomas in stroma around vessels, moderate focal
degeneration of cardiomyocytes and protein & fat degeneration in
cardiomyocytes.
 Outcome: mild(small diffused) cardiosclerosis, restoration of
cardiomyocytes structure.

23. IMMUNOPATHOLOGICAL PROCESSES : RHEUMATIC
GRANULOMA(ASCHOFF-TALALAEV’S)

24. DIFFUSE INTERSTITIAL EXUDATIVE MYOCARDITIS
 Severe form
 Histologically can see formation of nodular granuloma surrounding
connective tissue of vessels, diffuse congestion & edema in stroma,
diffuse infiltration of histiocytes, lymphocytes, neutrophils,
eosinophils, and local degeneration of cardiomyocytes.
 Outcome: 1. acute cardiac failure
2. diffuse cardiac sclerosis

25. MYOCARDITIS

26. ASCHOFF’S BODY IN RHEUMATIC MYOCARDITIS

27. RHEUMATIC ENDOCARDITIS
 Mural variant
 Chordal variant
 Valvular variant is the most important
-mitral valve
-aortic valve
-combine pathology
_______________________________________________
In all cases – never tricuspidal
valve

28. RHEUMATIC ENDOCARDITIS
 According to A.I.Abrikosov, valvular endocarditis is
classified into:
1. diffuse or valvulitis
2. acute warty (verrucouse) endocarditis
3. fibroplastic
4. relapsing (recurrent) warty (verrucouse)
endocarditis

29. Morphological form of
endocarditis
Macroscopic Histological
1. Diffuse -normal configuration of valves. -disorganization of connective tissue in thickness
of valves (mucoid swelling, fibrinoid necrosis).
2. Acute warty -normal configuration of valves
with thrombus
-some stages of connective tissue disorganization
(mucoid swelling & fibrinoid changes), celullar
reaction, thrombosis with rough surface of
thrombus.
3. Fibroplastic -valves become irregularly thick
with rough surface
-in valves, zone of fibrosis, calcification &
vascularization, vessels are absent.
-in sclerosis, can see vascularization &
connective tissue.
4. Relapsing warty -valves become irregularly thick,
dense & whitish
-some zones involve
inconsistency of stone (in zone of
calcification) & thrombosis
-old changes: sclerosis with vascularization,
calcification & hyalinosis. Result: granuloma& specific
diffused cellular reaction, infiltration of leukocytes,
plasmaic cells, deformation of valves, & thrombus.
-new changes in new attack: zone of disorganization of
connective tissue, granuloma & unspecified diffused
cellular reaction & cellular infiltration.

30. Thin, elastic cusp
ACUTE WARTY ENDOCARDITIS IN CASE OF RHEUMATIC FEVER

31. Valvular disorders

32. RHEUMATIC DISEASE. THE
CARDIOVASCULAR FORM.
ACUTE WARTY
ENDOCARDITIS MYOCARDITIS
NEOVASCULARI
ZATION OF THE
MITRAL VALVE
MITRAL
STENOSIS
AORTAL
STENOSIS

33.  Heart failure
This is the heart of a 44 year old woman who had rheumatic fever and had
been treated for congestive heart failure for about one year. There is
extreme fibrosis of the mitral valve with fusion of commissures and
rigidity of the leaflets, leading to both stenosis and insufficiency. Note that
the cordae, which are normally like fine linen threads, look more like
ropes here. Note the enormous atrial dilation. As you would suspect, this
woman had hypertension.

34. RHEUMATISM IN VESSELS
 Morphological forms of rheumatic vasculitis:
1. destructive: prevailing in vessel wall
2. proliferative: proliferation of cells in vessels (macrophages, mast
cells)
3. mixed: small focus of degeneration, in background formation of
microthrombosis, regeneration of cells, small fossa of destruction of
brain & small hemorrhages. This form prevalently affect children.
 Rheumatic vasculitis includes fibrinoid changes of the walls. In
capilarries, there is endothelium proliferation followed by
desquamation, so called endotheliosis. Vascular permeability
increases sharply.
 Outcome: vascular sclerosis(arteriolosclerosis, arteriosclerosis,
capillarosclerosis).

35. VASCULITIS

36. VASCULITIS

37. RHEUMATOID VASCULITIS
Rheumatoid vasculitis
with skin ulceration on
the dorsum of the foot

38. RHEUMATOID
ARTHRITIS

39. RHEUMATISM IN JOINTS: POLYARTHRITIS
 Marked changes in the synovial membrane & preservation of
articular cartilage
 Histological changes:
-serous, fibrinous exudative in cavity of joint
-mucoid & fibrinous swelling of synovial membrane
-proliferation of synovial sites
-vasculitis of synovial membrane
 Clinical appearance: variety & plurality of affection of joints
 Outcome: resolution of exudate, restoration of structure of tissue
without deformation

40. WHAT IS RHEUMATOID
ARTHRITIS?
 Rheumatoid arthritis (RA) is an autoimmune
disease that causes chronic inflammation of the
joints.
 Rheumatoid arthritis can also cause
inflammation of the tissue around the joints, as
well as in other organs in the body.
 Autoimmune diseases are illnesses that occur
when the body's tissues are mistakenly attacked
by their own immune system.
 The immune system contains a complex
organization of cells and antibodies designed
normally to "seek and destroy" invaders of the
body, particularly infections.

41.  Patients with autoimmune diseases have
antibodies in their blood that target their own
body tissues, where they can be associated with
inflammation.
 Because it can affect multiple other organs of the
body, rheumatoid arthritis is referred to as a
systemic illness and is sometimes called
rheumatoid disease.
 While rheumatoid arthritis is a chronic illness,
meaning it can last for years, patients may
experience long periods without symptoms.
 However, rheumatoid arthritis is typically a
progressive illness that has the potential to cause
joint destruction and functional disability.

42. RHEUMATOID ARTHRITIS (INFECTIOUS
POLYARTHRITIS)
 Is a chronic disease with progresseive deorganization of the
connective tissue of the articular membranes and cartilages which
cause its deformation.
 Pathology: Musculoskeletal system. Rheumatoid arthritis causes a
broad spectrum of morphologic alterations, the most severe are
manifested in the joints. Intially the synovium becomes edematous,
thickened, & hyperplastic transforming its smooth contour to one
covered by delicate & bulbous fronds. A dense perivascular
inflammatory infiltrate composed of lymphoid follicles, plasma cells
& macrophages fills the synovial stroma. The vascularity is
increased with superficial hemosiderin deposits & scattered giant
cells. Aggregates of organizing fibrin cover portions of the
synovium & float in the joint space as rice bodies. Neutrophils
accumulate in the synovial fluid & cluster along the surface but
usually do not penetrate deep to the synovnocytes.

43. RHEUMATOID ARTHRITIS
Low magnification revealed
marked synovial hypertrophy.
High magnification revealed
subsynovial tissue containing a
dense lymphoid aggregate.

44. CLINICAL APPEARANCE OF RHEUMATOID ARTHRITIS
variety & plurality of affection of
joints

45. RHEUMATOID ARTHRITIS
Mild early swelling of
the metacarpal joints and
the wrist

46. RHEUMATISM IN NERVOUS SYSTEM
 The damage is connected with rheumatic vasculitis.
 Nervous cells degeneration, brain destruction & hemorrhages occur
in the brain.
 If these changes are clearly marked, they may cause chorea minor(in
children).

47. SYSYTEMIC LUPUS ERYTHEMATOSUS (LIBMAN-SACKS
DISEASE)
 Is either acute or chronic disease with involvement of connective
tissue with marked autoimmunization & damage of skin, vessels,
kidneys.
 Its incidence is the highest in young women (aged 18-23) & less
frequent in elderly women & in men.
 Etiology of Lupus Erythematosus is unknown.

48.  Pathology: Lupus Erythrematosus is characterized by different
cellular & tissue changes which can be divided into 5 groups:
1. Acute necrotic & degenerative changes of the connective tissue
(all stages of deorganization). Fibrinoid is characterized by
abundant nuclear protein arted chromatin granules.
2. Subacute interstitial inflammation of all organs including
bervous system with involvement of microcirculation(capillaritis,
arteriolitis, vasculitis)
3. Changes of sclerotic character caused by the above changes. This
group is characterized by onion-like sclerosis in the spleen.

49. 4. Changes of the immune system. Focal accumulation of leukocytes
with marked plasmatization are present in the central and peripheral
organs. Macrophage activity is increased.
5. Nuclear pathology in the cells of all organs & tissues, particularly in
lymphatic nodes. The shape of the nuclei does not change but they
gradually lose DNA & look pale after staining. After the death of the
cell, the nucleus disintegrates into granules, i.e. hematoxylin bodies,
This phenomenon characterizes lupus erythematosus. Neutrophils &
macrophages phagocytize hematoxylin bodies & form lupus cells.
Their presence in the blood is a significant sign of lupus
erythrematosus. Except for blood, they can be found in the bone
marrow, spleen, lymphatic glands & walls of the vessels.
 Visceral manifestations of lupus erythematosus: lupus endo-, myo-
& pericarditis, abacterial warty endocarditis(Libman-Sacks
endocarditis).

50. SYSTEMIC LUPUS ERYTHEMATOSUS
Butterfly skin rash

51. CLINICAL APPEARANCE OF SYSTEMIC LUPUS
ERYTHEMATOSUS

52.  Nosebleeds (epistaxis)
 Skin nodules (small, painless nodules under the skin)
 Sydenham chorea (emotional instability, muscle
weakness and quick, uncoordinated jerky movements
that mainly affect the face, feet, and hands)

53. Arthritis of the knee

54. Arthritis of the ankle

55.  Migratory Polyarthritis : usually the most
common symptom is an arthritis (joint
inflammation) that involves the larger joints of
the body, especially the knees, ankles, wrists,
and elbows, and which lasts a few days before
moving to another joint. Joint swelling; redness
or warmth

56.  Skin rash (erythema marginatum)
Skin eruption on the trunk and upper part of
the arms or legs
Eruptions that look ring-shaped or snake-like

59.  A joint is where two bones meet to allow
movement of body parts. Arthritis means joint
inflammation. The joint inflammation of
rheumatoid arthritis causes swelling, pain,
stiffness, and redness in the joints.
 The inflammation of rheumatoid disease can also
occur in tissues around the joints, such as the
tendons, ligaments, and muscles.
 In some people with rheumatoid arthritis,
chronic inflammation leads to the destruction of
the cartilage, bone, and ligaments, causing
deformity of the joints.
 Damage to the joints can occur early in the
disease and be progressive.
 Moreover, studies have shown that the
progressive damage to the joints does not
necessarily correlate with the degree of pain,
stiffness, or swelling present in the joints.

60.  Rheumatoid arthritis is a common rheumatic
disease, affecting approximately 1.3 million
people in the United States, according to current
census data. The disease is three times more
common in women as in men. It afflicts people of
all races equally. The disease can begin at any
age, but it most often starts after 40 years of age
and before 60 years of age. In some families,
multiple members can be affected, suggesting a
genetic basis for the disorder.

61. WHAT CAUSES RHEUMATOID
ARTHRITIS?
 The cause of rheumatoid arthritis is unknown. Even
though infectious agents such as viruses, bacteria,
and fungi have long been suspected, none has been
proven as the cause.
 The cause of rheumatoid arthritis is a very active
area of worldwide research.
 It is believed that the tendency to develop rheumatoid
arthritis may be genetically inherited.
 It is also suspected that certain infections or factors
in the environment might trigger the activation of the
immune system in susceptible individuals.
 This misdirected immune system then attacks the
body's own tissues.

62.  This leads to inflammation in the joints and
sometimes in various organs of the body, such as the
lungs or eyes.
 Regardless of the exact trigger, the result is an
immune system that is geared up to promote
inflammation in the joints and occasionally other
tissues of the body.
 Immune cells, called lymphocytes, are activated and
chemical messengers (cytokines, such as tumor
necrosis factor/TNF, interleukin-1/IL-1, and
interleukin-6/IL-6) are expressed in the inflamed
areas.
 Environmental factors also seem to play some role in
causing rheumatoid arthritis.
 For example, scientists have reported that smoking
tobacco increases the risk of developing rheumatoid
arthritis.

63. WHAT ARE THE SYMPTOMS AND
SIGNS OF RHEUMATOID
ARTHRITIS?
 Rheumatoid arthritis usually develops gradually, but
some patients experience sudden onset of symptoms:
one day they are perfectly healthy and the next they
are dealing with rheumatoid arthritis. Symptoms
commonly associated with rheumatoid arthritis
include:
 Joint pain, joint swelling, joint stiffness, and warmth
around the affected joint
 Morning stiffness that lasts one or more hours
 Symmetrical pattern of affected joints, meaning the
same joint on both sides of the body is affected (e.g.,
both knees)
 Small joints of the hands and feet are
characteristically involved, although any joint can be
affected

64.  Rheumatoid nodules (firm lumps under the skin),
found on elbows and hands of about one-fifth of
rheumatoid arthritis patients
 Fatigue and noticeable loss of energy
 Low grade fevers and sometimes flu-like
symptoms
 Loss of appetite, weight loss, anemia associated
with chronic diseases, depression
 Dry eyes and dry mouth associated with a
secondary condition Sjogren’s syndrome
 Joint deformity and instability from damage to
cartilage, tendons, ligaments, and bone
 Limited range of motion in affected joints

65.  Flares and remission of disease activity is
characteristic of rheumatoid arthritis
 Rheumatoid arthritis may have systemic effects
(i.e., affect the organs of the body)
 No two rheumatoid arthritis cases are exactly the
same. There is so much variety among the
symptoms that some researchers suspect
rheumatoid arthritis is not one disease but
rather several diseases with commonalities.

66. DIAGNOSING RHEUMATOID
ARTHRITIS
 Diagnosing rheumatoid arthritis (RA), in the early stages, can
be difficult. There is no single test that can clearly identify
rheumatoid arthritis. Instead, doctors diagnose rheumatoid
arthritis based on factors that are strongly associated with
this disease. The American College of Rheumatology uses this
list of criteria:
1. Morning stiffness in and around the joints for at least one
hour.
2. Swelling or fluid around three or more joints simultaneously.
3. At least one swollen area in the wrist, hand, or finger joints.
4. Arthritis involving the same joint on both sides of the body
(symmetric arthritis).
5. Rheumatoid nodules, which are firm lumps in the skin of
people with rheumatoid arthritis. These nodules are usually in
pressure points of the body, most commonly the elbows.
6. Abnormal amounts of rheumatoid factor in the blood.
7. X-ray changes in the hands and wrists typical of rheumatoid
arthritis, with destruction of bone around the involved joints.

67.  Rheumatoid arthritis is officially diagnosed if
four or more of these seven factors are present.
The first four factors must have been present for
at least six weeks.
 Several diseases can masquerade as rheumatoid
arthritis, which contributes to the difficulty in
diagnosis. These other diseases include:
1. Osteoarthritis, or "regular" arthritis
2. Gout
3. Fibromyalgia
4. Other autoimmune diseases such as systemic
lupus erythematosus (lupus)
5. Joint inflammation caused by infections

68. HOW IS RHEUMATOID ARTHRITIS
TREATED?
 The main treatment goals with rheumatoid
arthritis are to control inflammation and slow or
stop progression of RA.
 Treatment is usually a multifaceted program of
medications, occupational or physical therapy,
and regular exercise.
 Sometimes surgery is used to correct joint
damage.
 Early, aggressive treatment is key to good
results. And with today’s treatments, joint
damage can be slowed or stopped in many cases.

69.  NSAIDs
 Nonsteroidal anti-inflammatory drug (NSAID)
reduce pain and inflammation but do not slow
progression of RA.
 Therefore, people with moderate to severe RA
often require additional medications to prevent
further joint damage.
 Most people with RA require a prescription
NSAID as they offer longer lasting results and
require fewer doses throughout the day.
 All prescription NSAIDs carry a warning
regarding the increased risk of heart attack and
stroke. NSAIDs can also raise blood pressure.
 In addition, NSAIDs can cause stomach
irritation, ulcers, and bleeding.

70.  DMARDs
 Disease-modifying antirheumatic drugs
(DMARDs) help slow or stop progression of RA.
The most common DMARD used to treat
rheumatoid arthritis is methotrexate.
 In rheumatoid arthritis, an overactive immune
system targets joints and other areas of the body.
 DMARDs work to suppress the immune system.
However, they aren’t selective in their targets.
 Thus, they decrease the immune system overall
and increase the likelihood of catching infections.

71.  Biologics
 The newest and most effective treatments for
rheumatoid arthritis are biologics.
 Biologics are genetically engineered proteins.
 They are designed to inhibit specific components of
the immune system that play a pivotal role in
inflammation, a key component in rheumatoid
arthritis.
 Biologics are usually used when other medications
have failed to stop the inflammation of rheumatoid
arthritis.
 Biologics may slow or even stop RA progression.
 TNF blockers help to reduce pain and joint damage by
blocking an inflammatory protein called tumor
necrosis factor (TNF).
 There is some evidence that TNF blockers may stop
the progression of rheumatoid arthritis.
 Recent studies have shown benefits when they are
combined with methotrexate.

72. RHEUMATOID ARTHRITIS -
KNEE JOINT
 With rheumatoid arthritis, inflammation of the synovial lining
causes swelling, pain, redness, warmth, and stiffness of the
affected joint. The synovium begins to thicken and inflamed cells
release enzymes that digest bone and cartilage. Joint damage and
joint deformity may result causing limited range of motion and
decreased function of the joint.

73. A photomicrograph (magnification 200) shows the redundant folds of the
synovial lining and intense infiltration with inflammatory cells in RA.
The intimal lining layer (solid arrow) is hyperplastic, with multiple
layers of cells compared with a normal lining that is one or two cell
layers deep. The sublining region (dashed arrow) is marked by
accumulation of mononuclear cells such as CD4+ T cells, macrophages
and B cells.

74. RHEUMATOID ARTHRITIS -
HIP JOINT
 Any joint can be affected by rheumatoid arthritis. Aggressive
disease can reduce the range-of-motion of many joints. When the
weightbearing joints are affected, such as the hips, knees, and
ankles, mobility may be greatly impacted.
 Joint erosion, which is visible on x-ray, can be severe and
limiting. As the joint becomes eroded and cartilage is damaged,
bone-on-bone can be the painful end result. Severe damage to
cartilage, tendons, ligaments and bone can cause joints to become
unstable and even deformed as rheumatoid arthritis progresses.

75. RHEUMATOID ARTHRITIS
- HANDS
 Rheumatoid arthritis most commonly begins in the smaller joints
of the fingers, hands, and wrists.
 Rheumatoid arthritis can result in hand deformity, joint problems
and damage of the fingers, thumb, hand, and wrist including:
 rheumatoid nodules joint swelling joint stiffness ulnar drift/ulnar
deviation contractures wrist subluxation

77.  Juvenile rheumatoid arthritis
 Juvenile rheumatoid arthritis is arthritis that causes joint
inflammation and stiffness for more than 6 weeks in a child of 16
years of age or less.

78. RHEUMATOID ARTHRITIS -
SYSTEMIC DISEASE
 Rheumatoid arthritis not only affects the joints. Rheumatoid
arthritis is a systemic disease which may also affect other organs
of the body including the skin, lungs, heart, and kidneys.
 Rheumatoid arthritis is more prevalent in women than men.
Interestingly, rheumatoid lung disease occurs more frequently in
men who are positive for rheumatoid factor, have subcutaneous
nodules, and a long disease course.
 Rheumatoid arthritis patients also have a higher risk of coronary
heart disease than people in the general population.

79. KNEE REPLACEMENT
 Joint damage and deformity can be repaired by knee replacement
surgery, which can also reduce pain and restore function. The
knee cap is removed and the damaged portion (head) of the femur
and tibia are shaved off or resurfaced. The two-part prosthesis
(usually metal) is implanted.

80. HIP REPLACEMENT
 Hip replacement surgerycan reduce pain, restore function, and
correct joint damage and deformity. The hip is a ball (femoral head)
and socket (acetabulum) joint. A total hip prosthesis consists of an
acetabular component and femoral shaft which are surgically
implanted to replace the damaged parts of the hip.
 Joint replacements exist for other joints too, such as the shoulder,
wrist, and ankle. Knee and hip replacements are most commonly
performed. According to the National Institutes of Arthritis and
Musculoskeletal and Skin Diseases, about 435,000 Americans have a
hip or knee replaced each year.

81. RHEUMATOID NODULES
MANY PEOPLE WITH RHEUMATOID ARTHRITIS FORM
SUBCUTANEOUS NODULES. THESE ARE LUMPS THAT APPEAR ON
OR NEAR THE AFFECTED JOINT AND ARE VISIBLE JUST BENEATH
THE SKIN.

82. RHEUMATOID NEUTROPHILIC
DERMATITIS
 Sweet disease and pyoderma gangrenosum are other neutrophilic
disorders sometimes seen in association with rheumatoid
arthritis.

83. RHEUMATOID VASCULITIS
 Cutaneous vasculitis may be a complication of rheumatoid arthritis
and is characterised by dark purplish areas on the skin (purpura)
caused by bleeding into the skin from blood vessels damaged by
rheumatoid arthritis. Skin changes caused by rheumatoid vasculitis
include:
 Skin ulcers (usually leg ulcers) may be extensive and painful
 Petechiae (purplish spots) or purpura
 Nail fold or edge breakdown
 Gangrene
 In addition to skin changes, rheumatoid vasculitis can cause many
internal symptoms, including sensory or motor neuropathy (loss of
sensation), hepatomegaly (enlarged liver), splenomegaly (enlarged
spleen), bowel ulcers, and haematuria (blood in urine).

84.  Representative haematoxylin and eosin micrographs of synovium biopsies taken at osteoarthritis or
rheumatoid arthritis total knee arthroplasty. (a-c) Osteoarthritis: (a) category 1 (least inflamed), (b)
category 2, and (c) category 3 (most inflamed). I, synovium intima; L, lymphoid body; SV, small
vessel; V, villus. (d) Rheumatoid arthritis, category 3. Each biopsy was assigned to one of four
categories: 0 = normal: synovial intima less than four cells thick, sparse cellular distribution, with
few or no inflammatory cells (not shown as normal synovial fluid samples were not accompanied by
synovium biopsies); 1 = mild inflammation: synovial intima three to five cells thick, slight increase in
cellularity with few inflammatory cells; 2 = moderate inflammation: synovial intima four to six cells
thick, dense cellularity with inflammatory cells, may exhibit as small lymphoid aggregates; 3 =
severe inflammation: synovial intima five to seven or more cells thick, dense cellularity with
inflammatory cells, containing many or large perivascular lymphoid aggregates. Bar = 100 μm.

85. Histology of rheumatoid synovitis. A. The characteristic
features of rheumatoid inflammation with hyperplasia of
the lining layer (arrow) and mononuclear infiltrates in the
sublining layer (double arrow). B. A higher magnification
of the largely CD4+ T cell infiltrate around postcapillary
venules (arrow).