1. Normal joint function relies on:
    • free movement of articular surfaces
    • stability of the joint during use and stress
    • proper distribution of forces throughout the joint during stress.

    Normal function therefore depends on the shape and integrity of the articular surfaces and other important joint structures (i.e. ligaments, tendons, muscles).
  2. Joints may be classified on basis of connective tissues which form the joint... 
    • - fibrous (e.g. symphysis pubis)
    • cartilaginous (e.g. sternum, ribs)
    • or synovial in type.
  3. In synovial type joints.....
    ....articular cartilage covers each bone end, the joint space is filled with synovial fluid, and the joint space is lined by synovium and capsule.

    In some synovial joints discrete structures, fibrocartilaginous discs or ligaments, lie within or across the joint space (e.g. menisci in knee).

    Articular cartilage forms a thin layer over the surface of the articulating bones.

    • Articular cartilage demonstrates a high level of structural organization. Broadly speaking, it has two principal molecular components
    • - fibrillar collagen [mostly type II]
    • - proteoglycans.

    • Synovium forms part of the lining of joints, and also lines tendon sheaths.
    • Lined by cells of two types;
    • - type A synoviocytes (macrophage lineage; phagocytic and secretory functions)
    • - type B synoviocytes, which are of fibroblastic origin.

    Synovial fluid is a viscous liquid tissue with very efficient lubricating properties which facilitates sliding or gliding of articular cartilages under load.
  4. Clinical arthritis is the consequence of loss...? 
    • ....the joint’s normal function.
    • --> assoc w anatomical and physiological alterations.

    Mlfntn of jt can be caused by acute/chronic injuries --> alterations in shapes of articulating surfaces, loss of integrity of supporting structures around the joint e.g. inflammatory processes, or alteration in the mechanical properties of various tissues making up the joint.
  5. Types of arthritis:
    • - non-inflammatory "osteoarthritis" degenerative joint disease,  
    • - various "rheumatic"/ inflammatory syndromes,
    • - infectious arthritis, (see first lecture),
    • - metabolic / crystal associated arthritis (e.g. gout).
  6. Symptoms and Signs of Joint Disease 
    • Symptoms
    • Pain
    • Stiffness
    • Deformity
    • Loss of Function
    • Systemic illness

    • Signs
    • Heat
    • Redness
    • Swelling
    • Loss of movement
    • Deformity
    • Tenderness
    • Crepitus

  7. Pathological changes in arthritis 
    Changes of arthritis -->  alterations in cartilage, synovium and bone. Common to all forms:

    • Cartilage 
    • Clefting/splitting of cartilage
    • "cloning" repair and metaplasia
    • loss of matrix basophilia
    • (uncommonly) cartilage necrosis

    • Synovium
    • Varying degrees of hyperplasia & hypertrophy of synovium haemosiderin deposition
    • rxn to joint wear / breakdown products
    • (possibly) presence of loose bodies

    • Bone 
    • Superficial areas of subchondral necrosis
    • Reactive sclerosis and cystic change
    • Microfractures
    • Formation of osteophytes

    • Synovial Fluid 
    • Examination of synovial fluid v helpful in determining cause and stage of arthritis. Various char's assessed-
    • amount,
    • colour,
    • protein,
    • viscosity,
    • cell count and differential,
    • presence or absence of various substances and crystals, pathogens (culture).
  8. Osteoarthritis
    Functional joint disorder...  altered joint anatomy, esp loss of articular cartilage. Essentially non-inflammatory in nature.

    • Affects all societies and races,
    • more common in women,
    • prevalence increases with age. 
  9. Osteoarthritis patterns of clinical presentation
    • - Disease ltd to large single joint (sometimes bilateral)
    • a generalised process (involving distal and proximal interphalangeal joints, the first carpometacarpal joint, knees, hips and metatarsophalangeal joints)
    • and Charcot joints.

    Often progressive ---> joint failure (may be halted sometimes)

    • Individual risk factors:
    • genetic influences
    • hormonal factors
    • obesity
    • trauma
    • occupation.
  10. Presentation of OA
    • Presentation usu w pain, stiffness
    • On examination --> ltd joint movement. 
    • May be crepitus and small effusions
    • Generally no "inflammatory" signs.
  11. Aetiology of OA
    • OA = heterogenous condition
    • Dif joints have dif risk factors, varying clinical manifestations and natural histories.

    • Individual risk factors:
    • genetic influences
    • hormonal factors
    • obesity
    • trauma
    • occupation.

    Many cases are idiopathic;

    • Causes of ‘secondary osteoarthritis’-
    • Infection
    • inflammatory arthropathies
    • trauma
    • metab jt Ds
    • avascular bone necrosis/osteonecrosis
    • altered loading through the joint due to deranged anatomy, and genetic predisposition.
  12. Pathological changes OA
    • - Damaged cartilage
    • - Alteration and shape of the articular surfaces.

    Initial changes in cartilage are localized. Loss of proteoglycan from superficial articular cartilage followed by damage to the collagen network.

    • Articular cartilage exhibits-
    • fibrillation and clefting,
    • variable loss and thinning
    • sometimes exposing underlying bone - "eburnation’.

    • Subchondral bone reveals
    • sclerosis,
    • cystic change,
    • fractures,
    • exostoses at the joint periphery.

    Osteophyte formation increases joint stability but at the cost of loss of movement.

    • Radiological findings-
    • loss of the joint space,
    • formation of bony osteophytes at the joint periphery, subchondral sclerosis and cystic change.
  13. Osteonecrosis (avascular necrosis)
    AVN- relatively common disorder seen in orthopaedic / rheumatology practice... sig cause of joint pain and disability.

    • Most secondary to trauma; (eg previous displaced fracture)
    • Collapse and fracture of the necrotic subchonral bone markedly disturbs joint anatomy and function. 

    • Non-traumatic AVN occurs primarily in younger adults, and is often bilateral.
    • Clin S&S sim to OA, but often Hx of sudden onset, and patients are generally younger

    • Non-traumatic osteonecrosis assoc w:
    • corticosteroid use
    • alcoholism
    • infections
    • hyperbaric events
    • storage disorders
    • marrow infiltrating diseases
    • coagulation defects
    • some autoimmune diseases
    • large number of cases have no obvious etiologic factor.

    • Skeletal scintigraphy and MRI important for diagnosis. Necrotic bone is recognised by the absence of osteocytes from lacunar spaces.
    • In reaction to the osteonecrosis there is evidence of both osteoblastic, in the form of "creeping apposition" and, to a much lesser extent, osteoclastic activity.

    Creeping apposition represents reactive new bone formation at the surface of necrotic trabeculae. The marrow space is also necrotic.
  14. Charcot joint
    • Extreme form of OA seen in patients with neurol dysfunction    --> rapidly destructive osteoarthritis
    • --> production of loose bodies
    • --> severe subluxation
    • --> and even dislocation of the joint.

    Diabetes and alcohol excess the most common causes, leprosy and late stage syphilis being others.
  15. Spinal arthritis and degenerative disc disease
    The vert column--> important central role in static & dynamic motor functions, and must simultaneously protect the spinal cord / nerve roots and participate in movement.

    Various components of the VC (vertebral bodies, intervertebral discs, muscles and ligaments) contribute in dif ways to its biomechanical functions --> affected by a variety of disease processes.

    The spinal column contains many articulations which include the intervertebral discs and the synovial joints (e.g. posterior articular processes).
  16. Spondylosis (Osteoarthritis of the Spine)
    Spondylosis = degenerative disc disease (osteochondrosis) together with assocd vertebral osteophytes, ligamentous disease, facet joint changes and neurological complications.

    Can occur in any segment of spine, but usu affects the cervical and lumbar segments.

    The disc comprises a central nucleus polposus (water and proteoglycan) ...contained and confined by an annulus of collagen.

    Displacement of disc tissue can occur in any direction (superficially or inferiorly forming Schmorl’s nodes, posteriorly to potentially impinge on nerve roots, or the contents of the spinal canal).

    • Dif forms of displacement include:
    • protrusion
    • prolapse
    • extrusion
    • sequestration.

    Osteochondrosis described the changes in the interverterbral disc and in the adjacent bone as a result of the disruption in the end plates of the disc. Disc components degenerate and are replaced by fibrous tissue. The disc space narrows and new bone forms at the periphery of the disc (marginal osteophytes).

    • Degenerative arthritis of the facet joints of the cervical spine ----> formation of osteophytes --> impinge on intervertebral foramina ---> vascular congestion, irritation of spinal nerve roots.
    • Vertebral artery insufficiency is another complication.
  17. Lumbar spondylosis
    • - affects the lower lumber spine
    • - common cause of low back and leg pain.

    Degen change --> alterations size & shape of vert canal and its recesses --> potential nerve root compression.

    Changes in facet joints are typical of osteoarthritis.

    Degenerative spondylolisthesis = displacement of vertebral body on the one directly below it, is assoc with degen of  facet joints  (may)---> spinal stenosis.
  18. Rheumatoid arthritis
    • Chronic systemic disorder of unknown aetiology
    • Affects females more often than males.
    • Chronic, often symmetric erosive poly-arthropathy...affects all joints, esp small joints of hands feet and cervical spine.

    Peak age onset = 4th - 6th decade.

    • Aetiopathogenesis unclear.
    • Prob an autoimmune disease influenced by genetic and environmental factors. Whilst the cause of rheumatoid disease is unknown, it is clear that there is a immunological reaction and increased formation of degradative enzymes within the joint.

    Rheumatoid factors are immunoglobulins to autologous IgG. Rheumatoid factors complex with IgG. Approximately 70% of patients with rheumatoid have a positive rheumatoid factor.

    No single laboratory test is specific or diagnostic of RA. Rheumatoid factors are found in more than two thirds of adults with RA, but the presence of rheumatoid factor is not specific.

    Rheumatoid factor may be found in healthy individuals, the frequency of its finding increasing in the general population with age. Additionally, several other conditions can be associated with the presence of rheumatoid factor. The level of rheumatoid factor however can be prognostically significant, correlating with disease severity and progression, and is usually found in patients with nodules of vasculitis
  19. RA - Clinical aspects
    • Great clinical heterogeneity
    • Char'd by intermittent/persistent joint inflam & destruction, together with variable extra-articular manifestations.

    Arthritis is typically polyarticular, bilateral and symmetric, and any joint can be affected, although the most commonly affected are the small joints of the hands and feet.

    • Joint specific symptoms usu involve several joints in a symmetric fashion, particularly those of the hands, wrists, knees and feet.
    • In some instances, rapid development of polyarthritis is accompanied by fever, lymphadenopathy and splenomegaly.

    In one third of patients the presenting symptoms may be restricted to one or a small number of joints, and though the involvement may be asymmetric, most ultimately develop a symmetric pattern.

    • Characteristic involvement of specific joints is a feature e.g. PIP and MCPs. Inflamed joints are usually held in flexion. Joint destruction, with ankylosis or soft tissue contractures ultimately leads to fixed deformities. Characteristic deformities of the hand include the Z deformity, Swan–neck deformity, Boutonniere deformity.
    • General malaise, pain and stiffness in the joints, esp in morning.

    Clinical examintn: acutely affected joints hot, swollen and tender. The synovial fluid is milky and turbid.
  20. Pathological Changes in Joints affected by RA 
    • Morph features of RA= joint destruction.
    • Little reparative activity.
    • Synovium chronically inflammed, hypertrophied and hyperplastic--> forms inflam mass - "pannus".

    Synovial pannus encroaches over the surface of the cartilage, ---> prolifs over surface of intrnl & intra-articular structures --> erodes bone, cartilage, capsule, & lig's.

    Inflamed tenosynovium elsewhere --> tendon damage and rupture.

    End result = destruction of the articular surfaces, and sometimes fusion of the joint (ankylosis).

    The capsule and periarticular structures are also destroyed, and this can lead to instability in the joint, with subluxation and dislocation.
  21. Extra-articular manifestations of RA
    Numerous extra-articular manifestations of RA.

    • - Subcutaneous rheumatoid nodules ~ third cases
    • Usu occur on extensor surfaces in relation to periarticular structures or other areas which are subject to mechanical pressure.
    • Typical sites-  olecranon bursa, proximal ulna, achilles and occiput.

    Symptoms - usu related to traumatic disruption/secondary infxn.

    Of the other extra-articular manifestations of rheumatoid, weakness / skeletal muscle atrophy are common.

    Ltd forms of vasculitis not uncommon --> manifest as cutaneous vasculitis, peripheral neuropathies, and ischaemic leg ulcers etc

    Severe vasculitis v rare, but may cause polyneuropathy, mononeuritis multiplex, skin ulceration, digital gangrene, and visceral infarction

    Peuropulmonary disease includes pleuritis, pleural effusion, and less commonly, pulmonary interstitial fibrosis, pleuro-pulmonary, rheumatoid nodules, pneumonitis and vasculitis

    Caplan’s syndrome = combo of pneumoconiosis & rheumatoid nodules.

    Cardiac Ds uncommon, but includes asymptomatic pericarditis.

    • Neurol Ds uncommon... may occur due to vascular/central structural compromise
    • eg spinal joint deformities
    • subluxation
    • vasculitis.

    Ocular disease includes episcleritis and scleritis
  22. Spondylarthropathies
    = group of conditions sometimes referred to as rheumatoid arthritis variants, in which rheumatoid factor is usually negative, (aka ‘seronegative spondyloarthropathies’)

    • Inflam occurs in the spine and peripheral joints in each of these conditions --> referred to as spondylarthropathies Include:
    • 1. Anklyosing spondylitis,
    • 2. Psoriatic arthritis,
    • 3. Enteropathic arthritis and spondylitis,
    • 4. Reactive arthritis (including Reiter’s syndrome)
    • 5. Juvenile idiopathic arthritis.

    • Features common to this group of entities include the following:
    • 1.Enthesopathy (an inflammatory reaction at the site of insertion of ligaments, tendons and muscle into bone).
    • 2. Synovitis.
    • 3. Dactylitis (or "sausage digit") - diffusely swollen fingers or toes.
    • 4. Sacroileitis.
    • 5. Spondylitis - inflammation of the spine (synovitis and enthesopathy)
    • 6. Extra-articular sites of inflammation, often distinctive, e.g. skin, eye e.g. anterior uveitis, or bowel.
    • 7. Greater frequency of the histocompatibility antigen HLA - B27.
    • 8. Family history
    • 9. Absence of classical features of RA such as rheumatoid factor and rheumatoid nodules
  23. Ankylosing spondylitis
    • Peak age of onset = second and third decades
    • Male to female ratio of 5:1
    • Usu low back pain and stiffness
    • frequent HLA-B27
    • Spinal involvement (sacroileitis and spondylitis)
    • +/- peripheral joint involvement (hips, knees, ankles, feet and shoulders).

    • Morphological changes -
    • fibrous/bony ankylosis
    • - SI joints, discs+/- synovial inflammatory changes (Rheumatoid like)
  24. Reactive arthritis
    Infxn of gut or genitourinary tract--> followed weeks later by a sterile synovitis with/wo extra articular manifestations (cutaneous, occular or genitourinary).

    eg. Reiter’s syndrome -  non-specific urethritis, conjunctivitis and arthritis.
  25. Psoriatic arthritis
    ~ 5% of patients w psoriasis ---> psoriatic arthritis

    Psoriasis usu precedes onset of arthritis but may follow or accompany it.

    Markedly heterogenous condition w sevl dif patterns of Ds, some are rheumatoid-like.
  26. Enteropathic arthritis
    • Patients w chronic inflam bowel disease
    • i.e. ulcerative colitis or Crohn’s....
    • can develop a peripheral arthritis, sacroileitis and ankylosing spondylitis.
  27. Crystal Arthropathies
    Crystal jt Ds = spectrum of inflam arthropathies brought about by a cellular rxn to crystals deposited in jt & periarticular tissues.

    Presence of crystals wthn jt --> acute/chronic arthritis, or maybe an incidental finding.

    • 3 most commonly encountered crystals are:
    • monosodium urate (gout),
    • calcium pyrophosphate (pseudogout),
    • and hydroxyapatite.
  28. Gout
    Metabolic disorder affecting jts & soft tissues.

    • Assocd w hyperuricemia.
    • Hyperuricemia is either primary [familial or sporadic] or secondary to an acquired condition, genetic disorder or drug treatment.
    • ~ 10% of individs w hyperuricemia --> gout.

    Primary hyperuricemia accounts for ~90% of all cases of gout and ~90% of these are due to reduced renal excretion of urate.

    Hyperuricaemia may also be secondary to disorders that increase the production of uric acid by cell breakdown, myeloproliferative disorders or disorders that decrease the secretion of uric acid (chronic renal failure).

    Gout char'd by episodic acute attacks of inflam, usu monoarticular arthritis, and chronic deposition of deposits of sodium urate around affected joints.

    Uric acid = end product of purine catab, (component of nucleic acids. Increased synth of uric acid / dc secretion of uric acid by the kidneys --> hyperuricaemia.

    Uric acid not v soluble --> ppts above certain conc's. Prolonged hyperuricaemia --> deposition of urate crystals in joints and tissues.

    Crystals--> provoke acute inflam rxn.

    • Gout divided into various clin stages:
    • - Acute gouty arthritis,
    • - Chronic stage in which diffuse deposits are seen i.e. chronic tophaceous gout.

    The acute arthritis is char'd by swollen painful joint (often the big toe), rapid clinical onset, low grade fever and leucocytosis.

    • Microscopic examination of synovial fluid reveals inflam exudate and presence of -vely birefringent needle shaped crystals and polymorphs.
    • The chronic chalky tophi are deposited around joint.

    The crystalline deposits are ringed by characteristic collections of histiocytes and multinucleate giant cells

    Examination under polarised light ---> needle shaped crystals...typical birefringence pattern of monosodium urate. Alcohol preservation allows visualisation of crystals.

    • Complications:
    • chronic urate nephropathy
    • uric acid calculi.
  29. Calcium pyrophosphate deposition disease - pseudo gout, chondrocalcinosis 
    • Clin presentation of CPPD sim to OA.
    • Joints of involvement include knees, ankles, wrist, elbows, hips and shoulder.

    May occur sporadically or as a hereditary condition, and may be assoc w other metabolic disorders.

    • Ds may present incidentally, as an acute synovitis or as a chronic arthritis.
    • Clin signs = those of OA, with varying degrees of synovitis.

    Crystals are rhomboidal in shape (in contrast to urate) and macroscopically appear as chalky white deposits.
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