3. Diseases of joint
1. Traumatic Arthritis
2. Osteochondosis
3. Infectious (septic)Arthritis
4. Open joint injury
3
4. 1-Traumatic Arthritis
Type 1. Traumatic synovitis and capsulitis
(without disturbance of articular
cartilage or disruption of major
supporting structures.)
4
5. 1-Traumatic Arthritis
Type 2. Disruptive trauma with damage to
the articular cartilage or complete
rupture of major supporting
structures.
This includes
(A) Severe sprains
(B) Meniscal tears
(C) Intra-articular fractures
5
6. 1-Traumatic Arthritis
Type 3. Post-traumatic osteoarthritis (OA).
This includes cases of disruptive
trauma in which major residual
damage is present.
Patients may have deformity, limited motion,
or instability of joints.
6
22. Traumatic synovitis and capsulitis
(Type 1, traumatic arthritis)
Etiology
• Trauma, Single or multiple episodes of trauma
(mainly affect carpal or fetlock J. in young race
horse)
• Predisposing factor like Conformational defect
cause abnormal stresses on joints
Osselets (synovitis and capsulitis of the fibrous joint
capsule of the dorsal aspect of Fetlock J.)
22
24. Treatment
Aim:
Restore and maintain normal joint function by,
1- Alleviating joint pain
2- Decreasing joint inflammation
3- Protecting the cartilage from further injury
24
25. Principles of medical therapy
Rest, exercise and physical therapy program.
1- Rest and Immobilization
1. stall rest
2. Bandage support may also assist
healing of an acutely damaged joint.
3. Complete immoblization (cast) Casting is
only appropriate in cases of destabilizing
injury
25
35. 35
3- Physical therapy
A. Hydrotherapy- cold water for 72hrs?
B. Heat (indication ?) increase bl. Supply
C. Therapeutic ultrasound
(tendinitis, desmitis… )
A. Electromagnitic stimulation
B. Counter irritation (blister, firing,
radiation therapy)
36. 36
Therapeutic ultrasound can heat tendon and ligament
tissues without raising the temperature of the horse’s skin
at the surface.
These thermal effects increase the metabolism of tissues,
which works to promote healing and improve tissue
elasticity (allowing for more beneficial stretching).
Therapeutic ultrasound
37. 37
Benefits of Therapeutic Ultrasound for
Horses
Stimulates cellular repair and collagen synthesis
Reduces pain, edema, and muscle spasms
Increases tissue elasticity and circulation
38. 38
Examples of When Therapeutic Ultrasound is
Used on Horses
• To increase the range of motion of targeted joints
• Treating splints, osteoarthritis, and other bone
conditions
• Reduce scar tissue
39. 4-Nonsteroidal anti-inflammatory drugs
(NSAIDs)
– Phenylbutazone (4.4 mg/kg single daily dosing)
– Flunixin (Finadyne) (1.1 mg/kg iv, im),
– Ketoprofen (2.2 mg/kg once or twice daily
– Meloxican anti COX-2
– Carprofen (A single dose of 0.7 mg/kg iv or PO).
– Ketoprofen (Ketofen) 2.2 mg/kg once or twice daily
– Aspirin (Acetylsalicylic Acid) (25 to 35 mg/kg PO)
39
45. 45
6- Hyaluronan (hyaluronic acid) is a high-
molecular-mass polysaccharide found in
the extracellular matrix, especially of
soft connective tissues.
What Hyaluronic Acid Does ?
•Lubricates joints
•Reduce friction in joints
•Anti-inflammatory properties
49. Type-2 Traumatic arthritis
A- Sprains and Luxations
Sprain (injury of specific ligaments associated with
the joint (from mild to severe damage)
* Mild Sprain (torn of few fibers of lig.)
Trt. by rest and a supportive bandage
* Moderate Sprain (some portion of lig. is torn
and some degree of functional loss
Trt. cast is indicated
* Severe Sprain (total rupture of lig. and complete
loss of function) may result in luxation of joint
Trt. Surgical intervention 49
51. 51
Classification of Luxation
1. Partial (sub-luxation) or complete L.
2. Acute or chronic L.
3. Simple, compound or complicated L.
a. Simple L. (Closed no open wound)
b. Compound L. (with open wound like penetrating wound)
c. complicated L. (with important injuries like
fracture)
4. Recurrent L.
5. Pathological L. (secondary to paralysis or sever
arthritis)
52. Etiology
1- Predisposing factor (congenital, pathological… )
2- trauma
Symptoms
1. Immobility (mechanical impossibility and pain)
2. Deformity (displacement and local inflam. swelling)
3. Crepitation
52
53. (Type -2 traumatic arthritis
B-Meniscal tears
Occurrence. In femoro-tibial joints (Uncommon in horse)
Etiology
Severe trauma (severe sprain to collateral L. and/or cruciate
L.)
Diagnosis
Arthroscopy in acute cases
Radiography in chronic cases (calcification of meniscus
Treatment
Surgical removal of fractured meniscus
53
55. Type -2 traumatic arthritis
C- Intra-articular fracture
Occurrence, in fetlock and carpus in race horses
Etiology trauma (or sudden fast exercise)
Symptoms
Lameness (sever lameness)
Joint effusion
Diagnosis
Clinical signs and radiography
Treatment
Surgical removal of bone fragment (by arthroscopy)
internal fixation in case of slab fracture using lag screw
55
57. 57
Avulsion fracture of the
supraglenoid process with
absence of any reactive bony
(callus) indicating an acute injury Post operative
58. Type 3 traumatic arthritis
Osteoarthritis (OA)
Degenerative Joint Disease (DJD)
58
OA is a degenerative joint disease, in which the
tissues in the joint break down over time.
Osteoarthritis (OA), is a chronic and
progressive joint disease
OA occurs commonly in old animals and can
develop at any age,
59. 59
Degenerative changes of the joint tissues (over time )
Common end-stage related to progressive damage
to articular cartilage accompanied by changes in
bone and soft tissues of joint
An initial cause like intra-articular chip fracture,
overweight, overwork, infection…etc
60. 60
The tarsal (hock) joints are usually the seat of OA in horses
that dispute the western competitive events, due to abrupt
stops and changes in direction required by the exercises
65. 65
As the cartilage
progressively deteriorates,
bony changes around the
joint develop,
With OA,
Joint fluid decreases
and cartilage thins,
Reducing the
joints’ shock-
absorbing
capability.
more inflammation, pain,
stiffness and difficulty
using the joint.
66. 66
OA is a slow, progressive disease of the
joint including damage to the articular
cartilage, the bone underneath the
cartilage, and local soft tissue
structures including the joint capsule
and supporting ligaments.
67. 67
Clinical signs
• may vary from mild to severe based on the
chronicity and number of joints affected.
Signs may include any of the following:
Pain (inflammatory signs in acute cases)
Stiffness
Capsular distension
Lameness ((variable severity)
Decrease in activity or reluctance to walk, run
or exercise
Difficulty getting up from lying down
Muscle wasting
68. Diagnosis
• Clinical signs
• Intra-articular analgesia
• Radiography (changes in advanced cases) or CT,
1- Osteophytes (new bone formation) at articular margin
2- Demineralization (irregularity) of the sagital ridge
3- Concavities of the distal, dorsal and/or palmar cannon bone
4- Narrowing or loss of joint space
5- Subchondral deminarlization
• Arthroscopy allows direct visualization and subjective
evaluation of synovial structures.
68
72. 72
Treatment
The goal of treatment of OA is to:-
Minimize pain,
Slow the progression of damage,
Maintain or develop muscle mass.
73. 1. Treatment initiating or primary cause
2. Rest (3-4 weeks) then gradual exercise
3. Lifestyle changes: Weight control
4. Physical rehabilitation:
Underwater treadmill
Range of motion exercises or other therapeutic
modalities — including acupuncture, LASER
therapy and more
73
Treatment is achieved with a combination of
therapies, which may include any of the following:
74. 74
Manual physio therapy on thoracic limbs. Passive stretching
(A, B, C) with possibility of joint mobilization (B, C); and
active stretching of neck (D, E).
75. 75
5- Pain management:
NSAIDs are commonly prescribed medications to
manage OA pain and inflammation.
6- Intra-articular therapy
I. Corticosteroids
II. Hyalouronic acid-sod hyalouronate
III. Autologous conditioned serum (ACS) (IRAP
(interleukin receptor antagonist protein)
IV. Platelet-rich plasma (PRP)
V. Stem cell therapy (Mesenchymal stem cells)
Regenerative
therapy
78. 78
• Mesenchymal stem cells are isolated from bone
marrow and expanded in tissue culture until
sufficient numbers are reached for treatment.
• This process can take from 3-4 weeks to reach
the optimized dose of 10-25 million stem cells
per treatment.
• The stem cells are then typically injected into
the site of injury under ultrasound guidance.
Stem cell therapy (Mesenchymal stem cells)
79. 79
7- Joint support:
Oral supplements, such as
• Glycosaminoglycan polysulphate
• chondroitin sulfate,
• omega-3 fatty acids
8- Surgery:
May be recommended for some cases that have
underlying causes of OA, such as
• hip dysplasia,
• cranial cruciate ligament rupture
• elbow dysplasia,
• chip fracture
80. Osteochondrosis
(dyschondroplasia)
Refers to a disturbance of cellular differentiation in
the growing cartilage (failure of endochondral
ossification and persistence of hypertrophied)
Affecting the epiphyseal and/or metaphyseal
cartilage.
Two clinical syndromes affect horses:
osteochondrosis dessicans (OCD)
subchondral cyst-like lesions (bone cysts)
80
81. Etiology of osteochondrosis
Unknown cause but various contributing factors;
1-rapid growing animal (6m to 2 years)
2-genetic predisposition
3- nutritional excesses or imbalances
3- superimposed trauma to cartilage
Occurrence: femoropatellar (stifle) and tarscocrural joints
Symptoms
distension of joint, mild lameness (increased with flexion
tests)
Radiography
Irregularity, flattening in subcondral bone
Treatment (management )
Conservative therapy (rest, restricted feed intake)
Surgical intervention
81
86. 86
Symptoms
• Lameness (sever)
• Inflammatory signs (hot,
swelling..) fever , may lead
to cellulitis
• In chronic cases, bony
enlargement
87. What are the physical factors that
cause problems in septic arthritis??
• Joint effusion !
• Fibrin deposition !
• Decreased hyaluronan molecular synthesis !
• Increased proteoglycan loss from articular
cartilage!!
88. What are the sequelae to septic
arthritis??
• Lameness
• Death (euthanasia, laminitis)
90. 90
Joint sepsis is suspected with
• Total protein values above 4.0 g/dL,
• Leukocyte counts >20,000/mL in adults and
>10,000/mL in foals,
• Polymorphonuclear count >90% on cytologic
examination.
• Synovial fluid analysis
91. 91
What are the goals in treatment of
septic arthritis?
Prompt diagnosis
Immediate therapy
Removal of microorganisms
Decrease inflammation
92. Tratment
1- Eliminate the causative organism (s)
2- Eliminate the harmful enzymes that can damage
the articular cartilage
Antibiotic (intraarticular and systemic) prior to
microbiolgical culture and sensitivity test
Joint lavage (two, 12- to 14-gauge needles are
inserted in the joint.) or open lavage (arthrotomy)
In foal with polyarthritis, umbilicus should be
opened and explored for an abscess
92
94. Intravenous regional limb perfusion
(IVRLP) for septic synovitis
Regional limb perfusion (RLP)
• The use of IVRLP, which leads to
significantly higher concentrations at the
site of infection when compared to systemic
therapy
• E.g. Gentamycin
94
97. 97
When a septic joint is non-responsive to
aggressive antibiotic therapy, fungal
causes should be considered.
Immunosuppressed horses are at higher
risk for fungal arthritis.
Cause of immunosuppression range from
intra-articular steroid administration
N.B.!
99. 99
Joint ill (Infectious polyarthritis)
navel ill
Localization of bacteria within joint(s) to cause
an infectious arthritis.
Bacteria enter the bloodstream from the gut
and upper respiratory tract in calves born in poor
sanitary conditions with delayed or inadequate
colostrum intake.
100. 100
Cause
Localisation of bacteria from the bloodstream into
joint(s).
Bacteria enter the bloodstream from the gut and
upper respiratory tract.
The untreated umbilicus is not a common portal for
bacteria.
E. coli and Strep. spp are the common isolates from
infected joints.
101. 101
Clinical signs
The joints most commonly affected are
the fetlock, carpal joints, hock, and stifle joints.
The affected joint(s) are swollen, hot, and
painful.
The drainiage lymph nodes (prescapular or
popliteal) are typically two to four times their
normal size.
Infection causes considerable muscle wastage over
the gluteal/shoulder regions.
102. 102
• Lameness: Moderate (4/10) to non weight-
bearing (10/10).
• Signs from around three to five day-old.
• Rapid muscle atrophy compared to the
unaffected leg.
• Rectal temperature is often within the normal
range.
• The navel may be thickened and painful.
106. 106
Differential diagnoses
• Fracture of a long bone
• Trauma to joint(s)
• Osteomyelitis
• Rickets
• Muscular dystrophy
Diagnosis
• Clinical findings.
• Joint effusion - obtain sample by needle aspiration
• Radiography often underestimates the extent of
joint pathology.
108. 108
Tratment
1- Eliminate the causative organism (s)
2- Eliminate the harmful enzymes that can damage
the articular cartilage
Antibiotic (intraarticular and systemic) prior to
microbiolgical culture and sensitivity test
Joint lavage (two, 12- to 14-gauge needles are
inserted in the joint.) or open lavage (arthrotomy)
In foal with polyarthritis, umbilicus should be
opened and explored for an abscess
109. 109
Prevention and control of navel ill and other
bacterial infections in the neonatal period
1. Adequate passive antibody transfer with a
minimum of 3 litres of good quality colostrum
during the first 6 hours of life but preferably the
first two hours.
2. An oesophageal feeder can be used to administer
colostrum if the calf will not suck.
110. 110
3. Reduce environmental bacterial challenge in
calving boxes by cleaning out between each
calving cow.
4. Umbilicus (navel) must be fully immersed in
strong iodine within the first 15 minutes of life
and repeated 2 to 4 hours later where
possible.
5. Treat all infections promptly
