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Copy of Osteoarthritis of the Knee

A Presentation About the Non-Surgical Therapies for OA of the Knee, With an Emphasis on Pharmacology

James Reising

on 1 July 2011

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Transcript of Copy of Osteoarthritis of the Knee

Osteoarthritis of the Knee Why OA? Because we see it so much! Why the knee? Because we see it so much! And there are certain pharmaceuticals that are FDA Approved for the knee only an estimated 27 million adult had OA in 2005
(as opposed to only 1.7 million with RA) Source: Center for Disease Control (CDC) cdc.gov/arthritis 6.1% of adults over 30 have OA of the knee Source: Farmington OA Study And those are the drugs in which I have a particular interest But first let's review a bit about OA AKA: DJD Most Common Arthritis Loss of hyalin cartilage and changes in the underlying bone Pain swelling stiffness loss of ROM Let's talk about PAIN Joint tissues that have pain innervation are capsule ligaments synovial membrane and subchondral bone The pathophysiology of OA involves the release of a
large number of inflammatory mediators and these directly
act on the nerve endings and reduce their threshold to pain
recognition. Belmonte C: Signal transduction in nocicptors; general principles In:
Belmonte C, Cervero F, editors. Neurobiology of Nociceptors. Oxford,
England: Oxford Unviersity Press. 1996;241–257 HA molecules restrict large plasma
protein from entering into the synovial fluid while facilitating
the passage of small molecules into the joint for maintenance
of nutrition. Goldberg VM, Buckwalter JA: Hyaluronans in the treatment of
osteoarthritis of the knee: evidence for disease-modifying activity.
Osteoarthritis and Cartilage. 2005;31:216–224. In the normal joint: HA provides important viscoelasticity and lubricating
properties to synovial fluid, thereby reducing articular
cartilage wear Balazs EA, Denlinger JL: Viscosupplementation: a new concept in the
treatment of osteoarthritis. J Rheumatol Suppl. 1993;39:3–9 But in the Joint with OA: HA synthesis is disrupted by cytokines, free radicals
and proteinases resulting in an HA with a significantly
reduced molecular weight, and a reduction in synovial fluid viscoelasticity
Proteinases enzymatically breaks HA into a lower-molecular-weight HA which can no longer maintain the mechanical integrity of the joint, accelerating the disease. So what can we do? acetaminophen AKA Tylenol but don't take it and drink,
or if you're on anticonvulsants potential for liver damage blocks pain, but it's not anti-inflamatory OTC NSAIDs like Ibuprofen, AKA Advil or Motrin or.......
a host of other names and not if your on ACE inhibitors
or a Hx of Gastric ulcers Potential for gastrointestinal side effects Or injectable corticosteroids
like Depo-medrol, a glucocorticsteroid Definitely anti-inflamatory
but with what side effects They reduce pain and inflamation but These drugs target cyclooxygenase enzyme
ie, COX inhibitors. The COX enzyme catalyzes the production of prostoglandis which modulate components of inflamation and are involved in pain transmission Prostoglandins are not stored but released on demand and have a very short half life so inhibit the COX enxyme and you decrease inflamation and pain Stringer, Janet L., 2001, Basic Concepts inPharmacology:
A stdents Survival Guide, New York, NY: McGraw-Hill decrease eicosanoid synthesis, decrease antibody production and B lymphocyte function, decrease chemotaxis of leukocytes and macrophages to sites of inflammation, decrease platelet activating factor and tissue necrosis factor and IL1, decrease antigen processing = immunosuppression, Stabilize lysosomal membranes making them less likely to rupture
Catabolic in bone, muscle, connective tissue, and skin Biederman, Ross 2011
Pharmacology for Physical Therapists
Lecture Notes, Pomona, CA Soft tissue atrophy, osteopenia & fractures
Delayed healing (substrate phase) Biederman, Ross 2011
Pharmacology for Physical Therapists
Lecture Notes, Pomona, CA every little thing makes it hurt What about cartilage protection Name: Glucosamine Dosing: 1.5 g/day in single or divided doses Contraindications: No absolute contraindications Interactions: None documented Adverse Reactions: Caution needed in use with fragile diabetes Pharmacology: In OA there is progressive degeneration of the cartilage glycosamnoglycans
the cartilage GAG. The rate of biosynthesis of GAG is limited by the
availability of Glucosamine which is naturally occurring in the body.
The thought is that by taking glucosamine orally there will be more avialable
for synthesis of GAG and thus help regenerate cartilage. Does it work? Depends on how you measure it. Several studies using the Western Ontario and McMaster (WOMAC) indicies show no statistical difference with placebo Several studies using radiographic analysis show positive results for protecting cartilage from further loss of thickness Name: Chondroitin Off Label Use: Studies have been done to test the effect of
glucosamine on viruses and cancer. Towheed TE, Maxwell L, Anastassiades TP, et al. Glucosamine therapy for treating osteoarthritis. Cochrane Database Syst Rev. 2005;(2):CD002946, Pub Med Towheed TE, Maxwell L, Anastassiades TP, et al. Glucosamine therapy for treating osteoarthritis. Cochrane Database Syst Rev. 2005;(2):CD002946, Pub Med Dosing: 800 to 1,200 mg/day Containdications: None Identified Adverse Reactions: Alopecia, constipation, diarrhea, stomach
pain, and may exacerbate asthma Drug Interactions: Possible increase in the INR in patients
taking Coumadin Pharmacokinetics: In a study of health human volunteers the
bioavailability was determined to be 12% Method of Action: Since inflamation and wear altering the matrix of the cartilage and allowing breakdown,
supplementing with chondroitinmay enable chondrocytes to replace proteoglycans,
allowing protection of the cartilage Does it Work: Long tem studies, ie > 1 year seem to show maintainence of joint space.
Short studies show little change in WOMAC scores Off Label Use: Potential use as an antithrombolitic Precautions: Those at risk for prostate cancer secondary to PSA issues What else can we do? First lets look at what's going on. Which takes us to: Hyaluronic Acid Derivatives for Injection or Hyaluronans Brand Names: Euflexxa Hylagan Supartz Synvisc Synvisc-One Indications: Osteoarthritis of THE KNEE FDA approval for the Knee only Dosing: 20 mg qw x 3 20 mg qw x 5 Ortohovisc 30 mg qw x 3 or 4 25 mg qw x 5 16 mg qw x 3 single injection of 48 mg Administration: Intra-articular injection. Not to be used with any other inta-articular injectable Subcutaneous injection of local anesthetic is recommended with Hylagan and Supartz Pharmacology: Naturally occurring GAG (remember the discussion about glucosamine and chondroitin) Derived from the comb of a chicken, except Euflexxa which is derived from bacterial cells If there is a joint effusion it should aspirtated prior to the administration of the hyalronan Cotraindications: As always the obligatory, hypersensitivity to hyaluronan, but also any known allergies to birds or poultry,
or avian derived products, such as feathers or eggs. Except Euflexxa. Off Label Uses: OA of any joint other than the Knee Method of Action: Potential disease-modifying activities of the HA include promotion of healing and repair by
stimulating chondrocyte growth, decreasing apoptosis and stimulating synthesis of cartilage
matrix components: collagen, proteoglycans and endogenous hyaluronans. Goldberg VM, Buckwalter JA: Hyaluronans in the treatment of osteoarthritis of the knee:
evidence for disease-modifying activity. Osteoarthritis and Cartilage. 2005;31:216–224. There are data that suggests a potential inhibition of the synthesis and activity of the chondrodegradating enzymes, eg, metalloproteinases as well as the inhibition of matrix destructive inflammatory processes. Ghosh P, Guidolin D: Potential mechanism of action of intra-articular
hyaluronan therapy in osteoarthritis: are the effects molecular weight
dependent? Semin Arthritis Rheum. 2002;32:10–37. As we discussed earlier the HA in the OA joint degrades through enzymatic action. The Injected Hyaluronan
with its high molecular weigth had better viscoelastic properties to lubricate the joint and provide shock absorption Additionally the injected HA binds with D44 receptors which promotes production of endogenous HA Balazs EA, Watson D, Duff IF, Roseman S. Hyaluronic acid in synovial
fluid. I. Molecular parameters of hyaluronic acid in normal and arthritis
human fluids. Arthritis Rheum. 1967;10(4):357–376. HA binds neuropeptides, creating a boundary layer around nocireceptors which reduces pain. Goldberg VM, Buckwalter JA: Hyaluronans in the treatment of
osteoarthritis of the knee: evidence for disease-modifying activity.
Osteoarthritis and Cartilage. 2005;31:216–224 Side Effects: Temporary pain, especially at injection site. PT Clinical Considerations: All preperations warn against prolonged or strenuous weight bearing activity following treatment. So there go your closed chain exercises, for 48 hours post injection. So open chain, cycle, pool.
Or reschedule for more than 48 hours post injection. It may be best to avoid impact activities for longer, so have patients return to activity gradually.
They may feel much better so you may need to put the brakes on until muscle strength can be increased. The effect reaches max at approx 8 weeks (good time for discharge) and continues on for........6 months. The drawback to postponing: We are frequently the communicators of precautions. James F. Reising, PT
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