Degenerative Joint Disease Flashcards
What do joints allow for?
Predictable and energy efficient motion
-transfer of load
What properties of joints encourage joint stability?
Geometric shape of articular surfaces, ligaments, joint capsule, tendons, muscle, menisci, synovial membranes
Where are menisci present in the body?
At the stifle and the TMJ
Define osteoarthritis
Progressive and permanent deterioration of the articular cartilage
- a group of disorders characterized by deterioration of the articular cartilage, changes in the subchondral bone, and changes in the soft tissues of the joint
What are the main causes of OA?
Abnormal stress on normal cartilage
-due to joint incongruence, loss of stability (ligament tear or fracture) or athletic trauma
Normal stress on abnormal cartilage
-due to osteochondrosis, aging, synovitis
Describe the pathogenesis of OA
-abnormal stress on normal cartilage causes cell injury and direct damage to the cartilage matrix, leading to loss of PGs from matrix, enzymatic breakdown of PGs and collagen as well as decreased synthesis of PGS and collagen
-normal stress on abnormal cartilage causes the same as the above minus the losses from the matrix
-all of this leads to the morphological breakdown of articular cartilage
Describe how articular cartilage repairs itself
Not well- no cells for proliferation or blood supply
-it has a limited capacity for regeneration or healing
-natural repair processes by adjacent tissues are incapable of producing tissue with morphologic, biochemical and biomechanical properties of articular cartilage
-cartilage defect –> fibrous tissue –> fibrocartilage
-fibrocartilage is weaker–> will wear and byproducts will cause inflammation of the joint
What is the etiopathogenesis of OA?
Physical forces lead to biomaterial failure (traumatic injuries)
-chondrocyte response to insult (degradation and repair) leads to chronic synovitis
-extra cartilaginous factors cause secondary cartilage changes (bony remodeling, synovial responses, microfractures, vascular changes, and others)
What are the cytokines associated with OA produced by both the synovial membrane and bone that lead to inflammation associated with OA?
Interleukin 1 and TNF alpha
-these induce bone resorption, and inflammation in joint response
What other compounds are released by the synoviocytes when they are damaged?
Free radicals, prostaglandins and metalloproteinases, and aggrecanase (breaks down proteoglycans of cartilage)
Name some of the changes associated with OA in joints?
Swelling of the joint due to synovitis, trabecullar modelling of subchondral bone, erosion of cartilage, inflammation of joint capsule and structures around the joint, new bone formation (enthesophytes) and osteophytes
-goal of all of this is to fuse the joint-body does a poor job of this though
What are some of the first signs of articular cartilage degeneration?
Discoloration due to loss of PGs (turns yellow), fibrillation, erosion, wear lines, eburnation
What changes occur with degeneration of the articular cartilage?
Decreased prostaglandins, reduced PG aggregation with GAGS, increased or decreased water content, change in collagen structure
-all results in reduced compressive and tensile strength
What is the chondrocytic response in arthritis?
Normally chondrocytes maintain a balance between turnover of the ECM or the cartilage and synthesis
- in this case there are more enzymes created and less synthesis (more IL1 and TNF, less IGF and TGF)
How do mechanical factors contribute to the pathogenesis of OA?
They affect cartilage indirectly by insult to the subchondral bone, synovial membrane or chondrocytes
What happens to the subchondral bone in OA?
Thickens (sclerosis) leading to reduced shock absorption
-can lead to lysis- shear induced tensile failure of collagen cross-links
What are the targets in treatment of OA?
Reduce inflammation of the joints (synovitis)
-treat traumatic injury
-correct for developmental orthopedic disease
-prevent infection
Decrease inflammations of the soft tissues and cartilage, alleviate pain, lubricate joint, restore normal environment, improve cartilage repair
What are some challenges associated with medical management of OA?
Chance of success depends on specific joints involved, stage of lesions, work of horse, age of horse, finances, response to therapy and regulations for competing
What are the components of medical management in OA cases?
Exercise modification, weight reduction, anti-inflammatories, slow acting and disease modifying antiosteroarthritis agents, and supportive care
What are the levels of OA treatment?
Oral: supplements and systemic anti-inflammatories
Topicals: surpass
Injectables: hyaluronic acid, polysulfated glycosaminoglycans
Joint injections: corticosteroids, hyaluronic acid, polysulfated glycosaminoglycans, regenerative therapies
Name the nonsteroidals commonly used in horses
Phenylbutazone, flunixin meglumine, firocoxib, diclofenac sodium, acetaminophen (not a true NSAID- no side effects)
What glycosaminoglycan is FDA approved?
Adequan IM
What does adequan promote in joints? What does it inhibit?
Stimulates production of HA by synoviocytes, increases synthesis of proteoglycans and collagen by chondrocytes and inhibits metalloproteases
What are some advantages and disadvantages to intraarticular corticosteroids?
Advantages: decreases MMP, decreases IL-1, TNFa, decreases fibrin deposition, causes pain relief, cheap, helps with chondrocyte nutrition
Disadvantages: pain relief, laminitis
Why is Depo-Medrol not recommended for use in joints in most cases?
It can cause articular degeneration, chondrocyte damage, decreased matrix production, worsening arthritis (steroid arthropathy)
What are the two times Depo might be preferred?
Sacroiliac joint and intertransverse joint
What are the guidelines in terms of dose of steroids in order to reduce the risk of laminitis?
Triamcinolone <18 mg
Methylprednisolone (depo) <200 mg
Betamethasone <30 mg
T/F: Betamethasone is more potent than triamcinolone
True
Describe post injection flare after intraarticular steroid administration?
Acute inflammatory response within 24 hours of injection
-causes heat, pain, swelling lameness (even at walk)
-hard to tell difference between this and infection- should treat like infection
What is the problem with diagnosing infections after intraarticular steroids?
Steroids will decrease the immune response and keep White cell counts low
-wont see classic signs of inflammation until possibly weeks later
What are some tips for steroid injections in horse?
Choose drugs wisely! Rest after use, limit repeated doses, keep doses low
What is the standard cocktail used in inflamed joints
Hyaluronic acid and triamcinolone
T/F: triamcinolone is chondroprotective
True- at low doses
What are the options for hyaluronic acid administration?
IV- legend
IA- legend IA, hyvisc (best as higher molecular weight), hyalovet
T/F: HA is better at treating arthritis than it is at treating synovitis
False- better for synovitis
- provides lubrication, binds inflammatory proteins
What are some potential adverse effects of PSGAG?
Increases partial thromboplastin, prothrombin and activated clotting times
- can possibly lead to thrombocytopenia
- can make joint more susceptible to infection (dont ever use with steroids)
Describe the properties of polyglycan
Not FDA approved
-mixture of HA, chondroitin, and glucosamine
-use as lavage post arthroscopic surgery
Describe autologous conditioned serum
Take patients own blood and mix in vial with chromium treated glass beads which cause the monocytes to release interleukin 1 antagonist protein
-outcompetes IL-1
-after clotting, use serum to treat joints
-includes IRAP and IRAP II
How is Platelet rich plasma produced?
Take patients blood and concentrate platelets but don’t clot them
- contains plasma, fibrinogen, and platelets
-can also get a form that concentrates the WBC- LPRP (dont use for joint injections as it can lead to release of pro-inflammatory cytokines)
Describe bone marrow aspirate concentrate?
Taking bone marrow from patient and concentrating supernatant
Describe adipose stomal vascular fraction cells?
Have to send out to vet stem
What are the two different types of stem cells used in horse joints?
Bone marrow or adipose derived
What is prostride?
Autologous protein solution
-concentrates WBCs, platelets and proteins
-increases IRAP, IL-10 and TNF receptor 1
-does not require overnight incubation
What is alpha2EQ
A new option for joint injections
- a high molecular weight protein present in blood- binds proteolytic enzymes and inhibits them
-created through running serum through a filter that holds back high molecular weight proteins and lets low through
-doesnt actually concentrate that well
Are stem cell therapies FDA approved?
NO -but they should be
Describe peripheral blood stem cells.
Allogenic aka from a donor
- off the shelf
-approved to treat OA in Europe
-not yet available in US
What is the recommended treatment for OA on presentation?
Start with triamcinolone and hyvisc, follow with IRAP II 3-6 mo later
T/F: PRP with steroids better than PRP or steroids alone
True
What is the purpose of diagnostic arthroscopic surgery?
To see inside joint to assess cartilage damage- cant see everything on imaging
-if case is nonresponsive to treatment can help determine diagnosis and prognosis, can treat at same time
How can arthroscopy be used for surgery?
Removal of loose cartilage or OA fragments
-stimulation of fibrocartilage repair (curettage, microfracture)
-remove diseased bone
-cartilage resurfacing techniques
-arthroscopic lavage
What is a unique thing that can be done during fetlock arthroscopy?
Hyperextension of fetlock joint can cause inflammation of villonodular pad and bone loss on distal MC III
-can remove excess tissue via arthroscopy
What is the prognosis for tearing of the intercarpal ligaments of the carpus?
BAD- occurs in racehorses
What can be observed well in stifle arthroscopy?
Cruciate ligaments, menisci, meniscal ligaments, large cartilage erosions
How do you enhance repair of arthritis lesions via arthroscopy?
Local manipulation or cell/tissue transplantation
What are the types of repair of cartilage?
Matrix flow- marginal migration (can only cover <3 mm of distance)
Intrinsic repair- limited repair within the cartilage
- for partial thickness injuries
Extrinsic repair- mesenchymal ingrowth from below the subchondral plate
-for full thickness defects
What are the steps to extrinsic repair of cartilage?
- Remove calcified cartilage (allows fibrocartilage formation)
- Make punctate defects in the subchondral bone until it bleeds (place 2-3 mm apart)
-allows access to vasculature, maintains subchondral bone contour, leads to better quality fibrocartilage healing
-increases type II cartilage
What are some of the tissue transplantation techniques for repair?
- Mosaicplasty-get plugs from non-weight bearing part and transplant to weight bearing
- Autologous cartilage implantation
- Allogenic chondrocyte implantation
- Stem cell implantation
What are the options with end stage DJD?
Arthrodesis of low motion joints
- can eliminate pain
- can be done in DIT, TMT, PIP
-carpal or fetlock arthrodesis can be done for salvage
Name some of the methods to encourage arthrodesis of joints
Injection
Laser
Drilling
Open approach (remove cartilage, lag screws, bone graft)
T/F: arthrodesis of pastern has better prognosis in the front compared to the hind?
False- better in the rear
Why is fetlock arthrodesis avoided if possible?
High motion joint, difficult surgery, biomechanics work against plate
