Anatomy and physiology of the synovial joint Flashcards
Anatomy of diarthrodial joint (out to in ish)
Soft tissue
Bone
Joint capsule - largely fibrous
Articular cartilage
Synovial membrane - usually very thin
Synovial cavity with synovial fluid - important for bathing articular cartilage (avascular)
Articular cartilage
Made of chondrocytes and extracellular matrix (largely collagen)
Breakdown of extracellular matrix of cartilage
Inflammatory insult
Pro-inflammatory cytokines
Net effect is cartilage destruction and changes to underlying subchondral bone
Synovial fluid
Fundamental role in boundary lubrication
Plasma dialysate supplemented with
- hyaluronan from synovial fibroblasts
- lubricin from chondrocytes
Provides glucose, other electrolytes, protein and CO2/O2 for cartilage metabolism
Non-inflammatory joint disease
DJD
Trauma
Neoplastic
Osteochondrosis
Inflammatory joint disease
Infectious and immunological joint disease
Osteochondral or full thickness defect
Right down to the cancellous bone
Chondral or partial thickness defect
Down to the subchondral bone
Degenerative joint disease (DJD), osteoarthritis, osteoarthrosis
Inherently non-inflammatory disease of synovial joints
CHaracterised by deterioration of articular cartilage and formation of new bone at joint margins
VERY COMMON
Clinical signs of Degenerative joint disease (DJD), osteoarthritis, osteoarthrosis
Usually a decreased range of motion
Pain (variable)
Joint swelling (fibrosis or effusive)
Crepitus
Pathology of DJD
Cartilaginous abnormalities:
- loss of matrix constituents and chondrocytes
- flaking
- fibrillation
Osteophytes develop at margin between joint capsule and articular cartilage
Synovial membrane changes:
- thickening
- mild inflammation
- joint capsule fibrosis
Radiographic changes indicative of DJD
Osteophytes formation
Soft tissue swelling
Joint effusion (often mild)
Subchondral sclerosis
Subchondral bone cysts - v rare in SA
Primary DJD
No identifiable cause
Rarely recognised in SAs (maybe aged beagles)
Secondary DJD
Secondary to:
- congenital problem e.g. dwarfism or achondroplasia
- Developmental disease e.g. hip dysplasia, osteochondrosis
- Acquired e.g. after articular fractures, luxations, cranial cruciate rupture etc.
Categories of inflammatory joint disease
Infectious
Non-infectious
- Immunological - erosive or non-erosive
- non-immnuological - crystal induced or chronic haemathrosis
Causes of infectious (septic) joint disease
External trauma and bite wounds
Iatrogenic
Endocarditis or remote infections
Immunodeficiency
Secondary to omphalophlebitis in puppies
Haematogenous spread in large breed dogs with estabilshed DJD
Clinical signs of infectious (septic) joint disease
Sudden onset
Pain
Swollen, effusive joint
Distal limb oedema
Lameness
More commonly a signle joint rather than multiple
Diagnosis of infectious (septic) joint disease
Radiographs to rule out other disease.
- soft tissue swelling and joint effusion
- later changes: periosteal bone reaction and discrete lucencies
Arthrocentesis
- turbid
- decreased viscosity
- increased volume
- high no. neutrophils, often degenerative
Techniques to increase success of culturing bacteria from joints
Incubation of synovial fluid in blood culture media for 24 hours
Submit a sample of synovial membrane for culture
Direct culture of synovial fluid - rarely successful
Treatment of infectious (septic) joint disease
Evacuate exudate
Treat with antibiotics - high dose IV
If no response consider lavaging with sterile saline
Prognosis of infectious (septic) joint disease
Acute infection: usually good
Chronic cases: much more guarded
Criteria to diagnose rheumatoid arthritis
- morning stiffness
- pain or tenderness on motion of at least one joint
- swelling of at least one joint
- swelling of one joint within a three month period
- symmetrical joint swelling
- subcutaneous nodules (not in dog)
- destructive radiological changes
- serological evidence of rheumatoid factor (IgG, IgM, IgA)
- abnomal synovial fluid
- characteristic histological changes in the synovial membrane
Definite rheumatoid arthritis- diagnosis
Can be diagnosed if 5 criteria are met - including at least the presence of two criteria 7, 8, or 10
Classical rheumatoid arthritis - diagnosis
can be diagnosed if 7 criteria are met - including at least the presence of two criteria 7, 8, or 10
Signalment of rheumatoid arthritis
Small breeds, female, middle aged
Clinical signs of rheumatoid arthritis
Most commonly affects the carpus and tarsus and distal joints
Present with collapse and deformity
May be palmigrade or plantigrade
Laxity, subluxation, and crepitus
May be pyrexic with lymphadenopathy
Radiography of rheumatoid arthritis
Subchrondral erosions, soft tissue swelling, subluxations, disuse osteoporosis
Laboratory features of rheumatoid arthritis
Rheumatoid factor test: RF is an autoantibody of the IgM (IgG) class against IgG.
Not specific
Titre greater than 1 in 40 may be significant, but negative result doesn’t exclude
Treatment of rheumatoid arthritis
Waxes and wanes so in quiescent stages treatment may not be necessary
Acute exacerbations can be treated with NSAIDs, steroids, or immunosuppression
SUrgical therapy such as cranial crutiate ligament rupture repair or arthrodesis
Prognosis of rheumatoid arthritis
Guarded
Rarely is a cure obtained
May be managed successfully for variable lengths of time
Rare erosivejoint conditions
Periosteal porliferative polyarthritis - in young male cats
Mycoplasmal polyarthritis - greyhounds, seen in Australia
Feltys syndrome - Rheumatoid arthritis, splenomegaly, and neutropenia
Idiopathic immune mediated polyarthritis
Most common inflammatory joint disease
Non-erosive polyarthritis
Pathophysiology of idiopathic mediated polyarthritis
Thought to involve the deposition of immune complexes - or a type III hypersensitivity
4 types:
1. uncomplicated
2. associated with a remote infection e.g. pyometra
3. associated with GIT disease
4. associated with neoplasia e.g. lymphoma in cats
Signalment of idiopathic mediated polyarthritis
Often large breeds, spaniels, shelties, young adults
Clinical signs of idiopathic mediated polyarthritis
Waxing and waning
Lameness, distal joints such as carpus and tarsus most commonly affected, joint effusions, pain on flexion/extension of joints, migratory problem, lethargy, and pyrexia
Radiology of idiopathic mediated polyarthritis
Soft tissue swelling, effusion, no erosions, no DJD
Image thorax and abdomen to rule out GI disease (type III) and neoplasia
Laboratory investigations of idiopathic mediated polyarthritis
Mild anaemia, leucocystosis
Negative for ANA and RF
Synovial fluid: low viscosity, increased volume, cell count increased neutrophils
Treatment of idiopathic mediated polyarthritis
Treat underlying cause e.g. pyometra
Immunosuppressive therapy using corticosteroids in a gradually decreasing dosing regime
DO NOT taper dose too quickly and continue treatment for several months past remission
Prognosis of idiopathic mediated polyarthritis
Type I - in 50% of cases a cure should be obtained, in the other 50% continual therapy may be needed
In a few cases medication may be ineffective and euthanasia may be requested
Systemic lupus erythematosus
Very rare
An inflammatory non-erosive joint disease associated with involvement of other body systems
Diagnostic criteria of systemic lupis erythematosus
- a significant titre of serum anti nuclear antibody (ANA)
- involvement of more than one body system - e.g. dermatological lesions, AIHA, IMT, IML, glomerulonephritis, NM disease, GIT disease
- Immunopathological features consistent with clinical involvement should be demonstrable e.g. IMT should be matched by presence of antibodies to platelets
Signalment of systemic lupis erythematosus
GSDs, Afghans, Irish setters, OES may be represented
Female
Any age
Clinical signsof systemic lupis erythematosus
Involvement of symmetrical joints, pyrexia, lethargy, inappetant, lymphadenopathy
Disease often phasic
Labratory findings of systemic lupis erythematosus
Anti nuclear antibody test positive (titre >1:64 - use fluorescent antibody test)
Coombs positive if AIHA
RF negative
Anaemia, leucopenia, thrombocytopaenia, hyperglobulinaemia
Treatment of systemic lupis erythematosus
Corticosteroids
Cytotoxic drugs
Prognosis of systemic lupis erythematosus
Guarded
Other very rare inflammatory non-erosive diseases
Canine polyarthritis/polymyositis
Canine polyarthritis/meningitis
Canine sjorgrens syndrome - KCS, dry mouth (xerostomia) and polyarthritis
Polyarteritis nodosa - vasculitis, beagles
Plasmacytic lymphocytic gonitis - recognised with cranial cruciate rupture in small breeds
Vaccination reaction - calicivirus in cats
Drug reactions - potentiated sulphonamides in Dobermanns and Weimaraners
Shar-pei fever (familial renal amyloidosis) - sharpei, swollen hocks and pyrexia
Heritable polyarthritis in Akitas - young Akitas. Guarded prognosis
Management of DJD
Usually multi-modal appraoch needed
Surgery critical for end-stage disease
Regenerative medicine for the future
Most frequently encountered joint disease in general practice
DJD A.K.A oestoarthritis/osteoarthrosis
Treatment considerations for DJD
Exercise modulation
Weight loss
Physical therapy and hydrotherapy
Drugs (e.g. NSAIDs, anti-NGF)
Surgical options (e.g. osteotomy, arthrodesis, total joint replacement)
What causes damage in DJD?
Abnormal wear on normal cartilage
Normal wear on abnormal cartilage
Age-related ‘wear and tear’
Exercise for DJD
Eliminate long periods of inactivity
Short and frequent periods of gentle controlled exercise
Physical therapy for DJD
Massage - stimulates circulation and disperses oedema, relaxes muscles in spasm and prevents or breaks down adhesions
Passive range of motion (PROM) exercises - aim to maintain or restore a normal range of motion in affected limbs and may help prevent tendon contractures
Hydrotherapy for DJD
Allows joint movement in a non-weight bearing mode - improves joint range of motion, improves muscle strength and general fitness
NSAIDs for DJD
Analgesic due to inhibition of prostaglandin synthesis
Some studies show that it actually abolishes cartilage synthesis
Possible side effects: vomiting, diarrhoea, gastrointestinal ulceration, nephropathy
Corticoid steroids for DJD
Potent anti-inflammatort effects
Should be reserved for cases that are unresponsive to NSAIDs
Repeat injections can cause cartilage degeneration
Surgical options for DJD
Correct inciting cause
Joint stabilisation
Ensure normal joint loading
Salvage procedures for chronic arthritis: joint fusion, arthrodesis, joint replacement
Chondroprotectants for DJD
Better defined as disease-modifying OA drugs
Hyaluronic acid
- IV or IA
- used in synovitis and early DJD
PSGAGs
- SC or IM (horse)
- Reduces PG degredation and MMP synthesis
Regenerative medicine for OA
Platelet rich plasma (PRP)
- autologous concentrated platelets
- increased PDGF, VEGF, FGF-2, TGF-B
- Widely used in management of soft tissue injuries, esp. ligament and tendon
Librela and solensia for DJD
Monoclonal antibodies to Nerve Growth Factor (NGF) - implicated in pain in OA
Administered by SC injection once monthly
Simple, long-lasting, safe
Cost reasonable (about £70 pm)
Efficacy (in long term) remains unproven
