Abstract
Osteoarthritis (OA) is a degenerative joint disease and a leading cause of adult disability. Since there is no cure for OA and no effective treatment to slow its progression, current pharmacologic treatments, such as analgesics and non-steroidal anti-inflammatory drugs (NSAIDs), only alleviate symptoms, such as pain and inflammation, but do not inhibit the disease process. Moreover, chronic intake of these drugs may result in severe adverse effects. For these reasons, patients have turned to the use of various complementary and alternative approaches, including diverse dietary supplements and nutraceuticals, in an effort to improve symptoms and manage or slow disease progression. The present study was conducted to evaluate the anti-osteoarthritic effects of FlexPro MD® (a mixture of krill oil, astaxanthin, and hyaluronic acid; FP-MD) in a rat model of OA induced by monosodium iodoacetate (MIA). FP-MD significantly ameliorated joint pain and decreased the severity of articular cartilage destruction in rats that received oral supplementation for 7 days prior to MIA administration and for 21 days thereafter. Furthermore, FP-MD treatment significantly reduced serum levels of the articular cartilage degeneration biomarkers cartilage oligomeric matrix protein (COMP) and crosslinked C-telopeptide of type II collagen (CTX-II), and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), as well as mRNA expression levels of inflammatory mediators, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and matrix-degrading enzymes, matrix metalloproteinase (MMP)-2 and MMP-9, in the knee joint tissue. Our findings suggest that FP-MD is a promising dietary supplement for reducing pain, minimizing cartilage damage, and improving functional status in OA, without the disadvantages of previous dietary supplements and medicinal agents, including multiple adverse effects.
Highlights
Osteoarthritis (OA), called degenerative joint disease, is a universal debilitating joint disease, and is the most prevalent type of arthritis characterized by synovial inflammation, the gradual loss of articular cartilage and degenerative changes in other surrounding tissues, including the synovium, menisci, ligaments, and subchondral bone, that are caused by multiple risk factors such as age, weight, excessive joint usage, and metabolic or genetic factors [1,2]
FlexPro MD® (FP-MD) sample consisted of 70% krill oil, 7% Haematococcus pluvialis extract, and 7% sodium hyaluronate, along with 16% various excipients, as determined by high-performance liquid chromatography (HPLC) and gas chromatography (GC), using the methods recommended by the United States Pharmacopeia (USP) and Korean Pharmacopoeia (KP), respectively
The monosodium iodoacetate (MIA)-induced OA control (MIA) group animals showed a quick reduction of weight-bearing distribution in the OA-induced limbs compared to non-OA-induced knees due to pain induced by MIA injection, while the weight distribution did not change in the sham control group
Summary
Osteoarthritis (OA), called degenerative joint disease, is a universal debilitating joint disease, and is the most prevalent type of arthritis characterized by synovial inflammation, the gradual loss of articular cartilage and degenerative changes in other surrounding tissues, including the synovium, menisci, ligaments, and subchondral bone, that are caused by multiple risk factors such as age, weight, excessive joint usage, and metabolic or genetic factors [1,2]. Recommended treatments include aerobic exercise, strengthening exercises, and medicinal agents, including non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or acetaminophen, which treat OA primarily by reducing pain and inflammation [9] These medications cannot prevent progressive cartilage degradation or repair the damaged cartilage of OA patients, and long-term use of these drugs can lead to various adverse effects, including renal toxicity, gastrointestinal disturbances, diarrhea, nausea, vomiting, or increased cardiovascular risks [10,11,12]. A recent clinical study reported that chronic but not short-term use of NSAIDs was associated with no clinical improvement in pain and a minimal, non-statistically significant improvement in clinical outcomes in persons with stiffness and functional and structural changes due to OA [13].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
