Diseases of the Musculoskeletal Disease Flashcards
NORMAL JOINT STRUCTURE AND CLASSIFICATION
A joint consists of the ends of contiguous bones together with their surrounding soft tissue components, ligaments, tendons, and synovium.
Joints can be classified according to the type of tissue present at the articulating interface as follows: (These are all SOLID joints)
1. Bony joints (skull sutures) (synostosis)
2. Fibrous joints (pubis symphysis) (syndesmosis)
3. Cartilaginous joints - most joints in our body, hip bone, knee, etc. (symphsis)
There is a CAVITATED joint that is synovial
- i.e. the knee
- synovial cells make fluid, allowing the joint to move fluidly and also provides nutrients
- Normal synovium has a few layers of synovial lining cells at the top and then blood vessels below
- the synovium also has adipocyte, mast cells, fibroblasts, and macrophages
Cartilage in joints
Cartilage is firm yet pliable and changes shape under increasing loads such that the surfaces of the joint come into increasing contact thereby distributing the load more equitably.
Cartilage is also elastic by virtue of its abundant extracellular matrix which retains water.
When forces are transmitted from one bone to the adjacent bone, the cartilage of the joint is compressed and extracellular water is extruded.
- Upon removal of the force, the extracellular matrix draws the water back in and the cartilage recovers its original shape.
Cartilage is avascular and therefore receives all nourishment from synovial fluid.
Because joints are not perfectly congruous, during compression, flow of synovial fluid occurs.
Like bone, the articular surfaces (cartilage and subchondral bone) are dynamic and are constantly undergoing remodeling in order to optimize load distribution.
Normal functioning of a joint
The normal functioning of a joint is dependent on three features:
1) the maintenance of stability during use
2) freedom of opposed articular surfaces to move painlessly over one another within a normal range of motion
3) correct distribution of load across joint tissues in order to avoid damage.
These aspects of joint function are governed by the shape of the articulating surfaces of the joint, the integrity of the supporting tissues of the joint, and the biologic cellular control of the mechanical properties of the tissues forming the joint.
Disturbances of any one of these may lead to joint disease.
Diseases of the joint
Diseases of the joint can essentially be grouped into 3 categories:
a) ARTHRITIS - most common (inflammation/degradation) (arthritides)
b) INFECTIONS (septic arthritis)
c) TUMOURS - least common
CLASSIFICATION OF ARTHRITIS
- Non-inflammatory arthritis
a. Osteoarthritis - Inflammatory arthritis
a. Infectious
b. Non-Infectious
i. Rheumatoid arthritis
ii. Seronegative arthropathies
iii. Crystal induced arthritis
Distinction of the arthritides requires good clinical information, by the time a joint has been affected many of the morphological and histological changes are the same for the various entities.
In the majority of cases, the etiology is at best unclear.
Osteoarthritis (Degenerative Joint Disease) - clinical features
Osteoarthritis (OA) is the most common form of arthritis in the Western world affecting nearly 10% of individuals greater than 60 years of age.
Typically the disease is limited to a single or only a few, large, weight-bearing joints, usually the knee or hip.
- single, asymmetrical
Patients with OA usually complain of decreased mobility of the affected joint(s), stiffness, and pain that worsens with use and is relieved with rest.
Key features
- very common
- one/few large joints, asymmetric
- narrowing of joint space (x ray)
- increased bone production (osteophytes)
- no inflammation
- not systemic
- interfere with function
- treatment - symptomatic
Osteoarthritis (Degenerative Joint Disease) - radiographic features
Radiologically, there is loss of the joint space, osteophyte formation, increased density of the bone immediately beneath the articular cartilage (subchondral bone sclerosis), and subchondral cyst formation.
Osteoarthritis (Degenerative Joint Disease) - gross pathologic features
The articular surface and bone are misshapen with the formation of peripherally located bone spurs (osteophytes).
Rather than being smooth, pearly-blue, and shiny, the articular cartilage will show areas of thinning, roughening (fibrillation), red-brown discoloration, and often areas of complete loss of articular cartilage with exposure of the underlying bone which becomes quite smooth resembling polished marble (eburnation).
After cross-sectioning the articular surface and bone, subchondral bone sclerosis and subchondral cysts may be identified.
Despite the loss of cartilage, regenerative changes at the periphery exceed loss such that the joint is actually larger than the normal joint.
Osteoarthritis (Degenerative Joint Disease) - microscopic pathologic features
These include duplication and irregularity of the tidemark (the line where cartilage begins to undergo endochondral ossification), chondrocyte clones (large clusters of chondrocytes trying to replace the lost articular cartilage), synovial cell hyperplasia/hypertrophy, villous change of the synovium, and nil to minimal chronic inflammation.
If present, the inflammation is negligible in comparison to that present in the inflammatory arthritides.
Osteoarthritis (Degenerative Joint Disease) - pathophysiology
The sequence of events (pathophysiology) leading to OA is as follows:
i) The earliest change in the articular cartilage is loss of proteoglycans from the extracellular matrix.
- This can only be appreciated histologically by the use of special stains.
- This alteration is indicative of abnormal biochemical functioning of the chondrocytes.
ii) Small numbers of chondrocytes die and groups of enlarged chondrocytes (chondrocyte clones) develop in an attempt to replace the damaged cartilage.
iii) As the cartilage weakens, superficial cracks develop (fibrillation).
- With time, these cracks become quite deep (fissures).
- These cracks may be vertical or horizontal and may result in the breaking off of fragments of the articular cartilage which may float freely within the joint space (joint mice, loose bodies).
- The chondrocytes within the loose bodies remain viable as they get sufficient nutrition from the synovial fluid.
- The lost hyaline cartilage is often replaced to some extent by fibrocartilage.
- End-stage degenerative changes
— loss of lots of articular cartilage
— will try to make new cartilage, but it is not very good at doing so
— when it DOES eventually make cartilage, it tends to be a different type. It tends to be fibrocartilage and hyaline cartilage. So it doesn’t do as well as a job compared to the normal cartilage.
iv) Loss of articular cartilage exceeds replacement resulting in exposure of the underlying (subchondral) bone.
- This bone remodels, becoming thickened (sclerotic) in an attempt to handle the transmitted forces and often becomes smooth and polished in appearance (eburnated).
v) The subchondral bone cracks (microfractures), allowing synovial fluid to enter into the bone marrow cavity and form subchondral cysts.
vi) The loss of articular cartilage and retransmission of forces results in osteophyte formation at the lateral portion of the joint.
- These are masses of bone and cartilage formed by the mesenchymal cells of the synovium.
- They are also called bone spurs.
- In the fingers they are called Heberden and Bouchard’s nodes.
Osteoarthritis (Degenerative Joint Disease) - etiology
Many underlying conditions may result in the development of OA (secondary OA) including congenital hip dysplasia, fracture, infection, avascular necrosis, metabolic diseases, etc.
More commonly, however, the exact etiology is unknown (primary OA).
While OA increases with increasing age, OA is not an inevitability of aging.
On the contrary, many joints remain essentially normal even into extreme old age.
OA is not simply a result of wear and tear, although this may play a significant role.
OA may result from any condition that affects the articular surfaces of the joint, the bones of the joint, or the tissues supporting the joint (ligaments, tendons, capsule).
It is an end stage of multiple processes
Rheumatoid Arthritis (RA) - clinical features
RA is the most common of the inflammatory arthritides.
RA is a chronic, systemic disease of unknown etiology that primarily attacks the synovial lining of the peripheral joints.
- The synovitis results in the secondary destruction of the articular cartilage.
- chronic meaning that it occurs over years
RA is characterized by bouts of remission and exacerbation and affects women more than men (3-5:1).
Peak incidence is 20-40 years old
Affects all races
Extra-articular features are common and include arteritis, neuropathy, pericarditis, pleuritis, lymphadenopathy, and rheumatoid nodules.
Patients complain of malaise, and pain and stiffness of the joints which is typically worse in the morning and improves throughout the day.
RA usually involves multiple joints, bilaterally and symmetrically.
- Although any joint may be involved, the small joints of the hands and feet are most commonly affected.
The joints are usually swollen, painful, hot, and red.
Synovial fluid analysis of an acute joint frequently reveals neutrophils however, no organisms grow on culture.
Advanced RA:
- in hands, the fingers will point towards ulnar side aka away from the thumb
Rheumatoid Arthritis (RA) - radiographic features
The typical findings are: periarticular loss of bone (osteopenia), bone erosion, narrowing of the joint space,
subluxations, dislocations, and soft tissue swelling.
Rheumatoid Arthritis (RA) - gross pathologic features
One sees joint destruction but, unlike OA, there is little reparative activity, and osteophytes and new bone formation are not prominent.
The synovium is hyperplastic and thickened and extends over the articular surface (pannus).
Rheumatoid Arthritis (RA) - Microscopic pathologic features
The synovial lining cells increase in number (hyperplasia) and size (hypertrophy).
The synovium is expanded by edema, increased numbers of blood vessels (angiogenesis), and chronic inflammatory cells (lymphocytes and plasma cells – not neutrophils) which frequently form lymphoid follicles with germinal centres.
This expansion causes the synovium to form finger-like extensions (papilla/villi) that extend into the joint space and over the surface of the articular cartilage (pannus).
Rheumatoid Arthritis (RA) - Pathophysiology
After the initial injury, there is attack of the synovial lining. This results in:
- leaky vessels causing edema and makes tissues expand, and also causes large components (like fibrin) to cross, possibly causing fibrin deposition leaking out and causing grains in the synovial space within the joints
- influx of lymphocytes, histiocytes, and plasma cells, NOT neutrophils.
- inflammatory mediators cause synovial lining cells to undergo hypertrophy and hyperplasia
- neovascularization
- synovial hyperplasia
Lymphocytes will be arranges in many prominent lymphoid nodules
Fibrin will coat the surface
Synovium is thick due to hyperplasia, forming finger-like extensions that form over the articular cartilage.
- called pannus
Pannus
- associated with fibrin, so there will be white deposition on it
- pannus gets trapped in joint space and sheared by bones in the articular cartilage and that causes tearing and bleeding; and this breakdown of blood leads to iron deposition, giving it a brown-red color
Inflammation will form lymphoid follicles with germinal centres
The pannus grows in joint space, burrows into bone, and destroys the underlying cartilage by several mechanisms:
1) The pannus physically covers the cartilage thereby preventing it from receiving adequate nutrition from the synovial fluid,
2) The pannus releases enzymes that directly destroy cartilage and,
3) The pannus releases inflammatory mediators that activate osteoclasts which destroy bone and cartilage.
Pannus may cause joint to fuse and be unable to move properly
- fusion is termed ankylosis
- if the pannus is ossified or turned into a bone, it is called bony ankylosis
there is loss of articular cartilage and periarticular bone at the joint
The end result is destruction of the articular surface and loss of bone with joint subluxation and instability.
There is PMN leukocytes in synovial fluid
Joint findings: rice bodies
- fibrin bodies floating around in space
- fibrin bodies contains neutrophils; but neutrophils are not within the pannus; neutrophils do not destroy the joint
Rheumatoid Arthritis (RA) - etiology
- Autoimmunity (cellular - CD4+, humoral - RF)
RA is believed to be an immune mediated disease.
Most patients have rheumatoid factor (auto-antibodies to autologous IgG).
Rheumatoid factor complexes with IgG and deposits in the synovium where an immune reaction takes place inciting damage via released enzymes and pro-inflammatory mediators.
Inflammation causes pleuritis that can deposit in tissues and organs to make things called rheumatoid nodules. Rheumatoid nodules:
- it is necrosis in tissue and inflammation around necrosis, creating large circular nodules around the joint
- firm, non tender
- round, oval nodule
- micro: central fibrinoid necrosis surrounded by histiocytes, lymphocytes, and plasma cells
- Microbial agents acting synovial lining
- EBV
- parvovirus
- retrovirus
- mycobacteria - Genetic susceptibility
- familial
- twin studies
- HLA-D
Bone function
Locomotion
Protection
- heart
- lungs
- brain (skull)
Hematopoiesis
- RBC, WBC, platelets
Metabolic (bone is made of these components and also stores them)
- Ca2+
- PO4
Energy (inside of bone has fat tissue)
- fat
Morphological classification of bones
206 bones
axial/appendicular
Tubular
- long
- short
Flat
Cuboidal
Bone anatomy - long tubular bones
Middle is diaphysis
Ends are epiphysis
Order: epiphysis, growth plate, metaphysis, diaphysis
