Skeletal Muscle Atrophy and Dysfunction Following Total Knee Arthroplasty
| Status: | Recruiting |
|---|---|
| Conditions: | Arthritis, Osteoarthritis (OA), Neurology |
| Therapuetic Areas: | Neurology, Rheumatology |
| Healthy: | No |
| Age Range: | 50 - 75 |
| Updated: | 5/3/2018 |
| Start Date: | January 1, 2017 |
| End Date: | June 30, 2021 |
| Contact: | Michael J Toth, PhD |
| Email: | michael.toth@uvm.edu |
| Phone: | 802-656-7989 |
Total knee replacement, or arthroplasty, is the final clinical intervention available to
relieve pain and functional limitations related to advanced stage knee osteoarthritis.
Despite its beneficial effects, the early post-surgical period is characterized by the
erosion of lower extremity muscle size and strength that cause further disability and slow
functional recovery. While the detrimental effects of this period on muscle are widely
recognized, the mechanisms underlying these adaptations are poorly understood and there are
currently no widely-accepted clinical interventions to counter them
relieve pain and functional limitations related to advanced stage knee osteoarthritis.
Despite its beneficial effects, the early post-surgical period is characterized by the
erosion of lower extremity muscle size and strength that cause further disability and slow
functional recovery. While the detrimental effects of this period on muscle are widely
recognized, the mechanisms underlying these adaptations are poorly understood and there are
currently no widely-accepted clinical interventions to counter them
Total knee arthroplasty (TKA) is currently the most common elective surgery in the US and
will increase in frequency nearly five-fold by 2030 to 3.5 million surgeries annually. This
surgery is most prevalent among older adults with advanced knee osteoarthritis (OA) and its
increase is explained primarily by growth in this population. Although TKA reliably reduces
joint pain, it fails to correct objectively-measured functional disability due, in part, to
dramatic declines in lower-extremity neuromuscular function during the early, postsurgical
period. These deficits are never fully remediated, remaining for years after surgery and
contributing to persistent disability. Despite these detrimental effects of TKA, the
fundamental skeletal muscle adaptations that occur in the early, post-surgical period are
poorly defined and understudied and there is currently no widely-accepted, evidence-based
intervention to counter these changes. To address this clinical problem, the investigators
goals in this application are to define the skeletal muscle structural and functional
adaptations following TKA at the whole body, tissue, cellular, organellar and molecular
levels in humans in an effort to identify factors contributing to functional disability and
to assess the utility of neuromuscular electrical stimulation (NMES) to counter post-surgical
muscle adaptations at these same anatomic levels. We hypothesize that TKA fails to remediate
physical disability in patients, in part, because of the profound skeletal muscle myofilament
and mitochondrial loss and dysfunction that develops during the early, post-surgical period.
Moreover, the investigators posit that NMES will improve functional recovery following TKA by
countering these early skeletal muscle adaptations. To test this model, the investigators
will evaluate participants with knee OA prior to and following TKA for skeletal muscle
structure and function at multiple anatomic levels, with patients randomized to receive NMES
or sham control intervention during the first 5 weeks post-surgery.
will increase in frequency nearly five-fold by 2030 to 3.5 million surgeries annually. This
surgery is most prevalent among older adults with advanced knee osteoarthritis (OA) and its
increase is explained primarily by growth in this population. Although TKA reliably reduces
joint pain, it fails to correct objectively-measured functional disability due, in part, to
dramatic declines in lower-extremity neuromuscular function during the early, postsurgical
period. These deficits are never fully remediated, remaining for years after surgery and
contributing to persistent disability. Despite these detrimental effects of TKA, the
fundamental skeletal muscle adaptations that occur in the early, post-surgical period are
poorly defined and understudied and there is currently no widely-accepted, evidence-based
intervention to counter these changes. To address this clinical problem, the investigators
goals in this application are to define the skeletal muscle structural and functional
adaptations following TKA at the whole body, tissue, cellular, organellar and molecular
levels in humans in an effort to identify factors contributing to functional disability and
to assess the utility of neuromuscular electrical stimulation (NMES) to counter post-surgical
muscle adaptations at these same anatomic levels. We hypothesize that TKA fails to remediate
physical disability in patients, in part, because of the profound skeletal muscle myofilament
and mitochondrial loss and dysfunction that develops during the early, post-surgical period.
Moreover, the investigators posit that NMES will improve functional recovery following TKA by
countering these early skeletal muscle adaptations. To test this model, the investigators
will evaluate participants with knee OA prior to and following TKA for skeletal muscle
structure and function at multiple anatomic levels, with patients randomized to receive NMES
or sham control intervention during the first 5 weeks post-surgery.
Inclusion Criteria:
- symptomatic, primary knee osteoarthritis (OA)
- being considered for total knee arthroplasty
Exclusion Criteria:
- knee OA secondary to inflammatory/autoimmune disease
- untreated/uncontrolled hypertension, diabetes or thyroid disease
- chronic heart failure, actively-treated malignancy, exercise-limiting peripheral
vascular disease, stroke or neuromuscular disease
- body mass index >38 kg/m2
- lower extremity blood clot or known coagulopathies
- implanted pacemaker/ICD
We found this trial at
1
site
1 South Prospect Street
Burlington, Vermont 05401
Burlington, Vermont 05401
802-656-8990
Phone: 802-847-4545
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