Turmeric supplement more effective than placebo for osteoarthritis knee pain

Turmeric supplement more effective than placebo for osteoarthritis knee pain

An extract of Curcuma longa (CL), commonly known as turmeric, was found to be more effective than placebo for reducing knee pain in patients with knee osteoarthritis.

#arthritis #pain #turmeric

Wang Z, Jones G, Winzenberg T, Cai G, Laslett LL, Aitken D, Hopper I, Singh A, Jones R, Fripp J, Ding C, Antony B. Effectiveness of Curcuma longa Extract for the Treatment of Symptoms and Effusion-Synovitis of Knee Osteoarthritis : A Randomized Trial. Ann Intern Med. 2020 Sep 15. doi: 10.7326/M20-0990. Epub ahead of print. PMID: 32926799.

https://www.acpjournals.org/doi/10.7326/M20-0990

turmeric, curcumin longa, curcumin, osteoarthritis, knee pain, arthritis, pain effusion, synovitis, effusion synovitis

Adenosine Helps Regrow Cartilage in Osteoarthritis

Injections of a natural ‘energy’ molecule prompted regrowth of almost half of the cartilage lost with aging in knees, a new study in rodents shows.

#arthritis #osteoarthritis #adenosine

Carmen Corciulo, Cristina M. Castro, Thomas Coughlin, Samson Jacob, Zhu Li, David Fenyö, Daniel B. Rifkin, Oran D. Kennedy, Bruce Neil Cronstein. Intraarticular injection of liposomal adenosine reduces cartilage damage in established murine and rat models of osteoarthritis. Scientific Reports, 2020; 10 (1) DOI: 10.1038/s41598-020-68302-w

https://www.nature.com/articles/s41598-020-68302-w

Rheumatoid Arthritis resolved with a newly discovered peptide

Rheumatoid Arthritis resolved with a newly discovered peptide

A peptide was recently discovered that completely resolved Rheumatoid Arthritis in all animals tested within 15 days.

Citation: Suppression and resolution of autoimmune arthritis by rhesus θ-defensin-1, an immunomodulatory macrocyclic peptide. PLOS ONE, 2017; 12 (11): e0187868 DOI: 10.1371/journal.pone.0187868

New study proves that pain is not a symptom of arthritis, pain causes arthritis

2008 study posted for filing

Contact: Greg Williams
Greg_Williams@urmc.rochester.edu
585-273-1757
University of Rochester Medical Center

New treatments will seek to interrupt ‘crosstalk’ between joints and the spinal cord

Pain is more than a symptom of osteoarthritis, it is an inherent and damaging part of the disease itself, according to a study published today in journal Arthritis and Rheumatism. More specifically, the study revealed that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis. In addition, researchers found that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends.

Technically, pain is a patient’s conscious realization of discomfort. Before that can happen, however, information must be carried along nerve cell pathways from say an injured knee to the pain processing centers in dorsal horns of the spinal cord, a process called nociception. The current study provides strong evidence that two-way, nociceptive “crosstalk” may first enable joint arthritis to transmit inflammation into the spinal cord and brain, and then to spread through the central nervous system (CNS) from one joint to another.

Furthermore, if joint arthritis can cause neuro-inflammation, it could have a role in conditions like Alzheimer’s disease, dementia and multiple sclerosis. Armed with the results, researchers have identified likely drug targets that could interfere with key inflammatory receptors on sensory nerve cells as a new way to treat osteoarthritis (OA), which destroys joint cartilage in 21 million Americans. The most common form of arthritis, OA eventually brings deformity and severe pain as patients loose the protective cushion between bones in weight-bearing joints like knees and hips.

“Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and inevitable part of aging,” said Stephanos Kyrkanides, D.D.S., Ph.D., associate professor of Dentistry at the University of Rochester Medical Center. “Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing, and suggests the mechanisms behind the effect,” said Kyrkanides, whose work on genetics in dentistry led to broader applications. The common ground between arthritis and dentistry: the jaw joint is a common site of arthritic pain.

Study Details

Past studies have shown that specific nerve pathways along which pain signals travel repeatedly become more sensitive to pain signals with each use. This may be a part of ancient survival skill (if that hurt once, don’t do it again). Secondly, pain has long been associated with inflammation (swelling and fever).

In fact, past research has shown that the same chemicals that cause inflammation also cause the sensation of pain and hyper-sensitivity to pain if injected. Kyrkanides’ work centers around one such pro-inflammatory, signaling chemical called Interleukin 1-beta (IL-1β), which helps to ramp up the bodies attack on an infection.

Specifically, Kyrkanides’ team genetically engineered a mouse where they could turn up on command the production of IL-1β in the jaw joint, a common site of arthritis. Experiments showed for the first time that turning up IL-1β in a peripheral joint caused higher levels of IL-1β to be produced in the dorsal horns of the spinal cord as well.

Using a second, even more elaborately engineered mouse model, the team also demonstrated for the first time that creating higher levels of IL-1β in cells called astrocytes in the spinal cord caused more osteoarthritic symptoms in joints. Past studies had shown astrocytes, non-nerve cells (glia) in the central nervous system that provide support for the spinal cord and brain, also serve as the immune cells of CNS organs. Among other things, they release cytokines like IL-1β to fight disease when triggered. The same cytokines released from CNS glia may also be released from neurons in joints, possibly explaining how crosstalk carries pain, inflammation and hyper-sensitivity back and forth.

In both mouse models, experimental techniques that shut down IL-1β signaling reversed the crosstalk effects. Specifically, researchers used a molecule, IL-1RA, known to inhibit the ability of IL-1β to link up with its receptors on nerve cells. Existing drugs (e.g. Kineret® (anakinra), made by Amgen and indicated for rheumatoid arthritis) act like IL-1RA to block the ability IL-1β to send a pain signal through its specific nerve cell receptor, and Kyrkanides’ group is exploring a new use for them as osteoarthritis treatment.

The implications of this process go further, however, because the cells surrounding sensory nerve cell pathways too can be affected by crosstalk. If 10 astrocytes secrete IL-1β in response to a pain impulse, Kyrkanides said, perhaps 1,000 adjacent cells will be affected, greatly expanding the field of inflammation. Spinal cord astrocytes are surrounded by sensory nerve cells that connect to other areas of the periphery, further expanding the effect. According to Kyrkanides’ model, increased inflammation by in the central nervous system can then send signals back down the nerve pathways to the joints, causing the release of inflammatory factors there.

Among the proposed, inflammatory factors is calcitonin gene related peptide (CGRP). The team observed higher levels calcitonin-gene related peptide (CGRP) production in primary sensory fibers in the same regions where IL-1β levels rose, and the release of IL-1β by sensory neurons may cause the release of CGRP in joints. Past studies in Kyrkanides reveal that CGRP can also cause cartilage-producing cells (chondrocytes) to mature too quickly and die, a hallmark of osteoarthritis.

Joining Kyrkanides in the publication from the University of Rochester School of Medicine and Dentistry were co-authors M. Kerry O’Banion, M.D., Ph.D., Ross Tallents, D.D.S., J. Edward Puzas, Ph.D. and Sabine M. Brouxhon, M.D. Paolo Fiorentino was a student contributor and Jennie Miller was involved as Kyrkanides’ technical associate. Maria Piancino, led a collaborative effort at the University of Torino, Italy. This work was supported in part by grants from the National Institutes of Health.

“Our study results confirm that joints can export inflammation in the form of higher IL-1β along sensory nerve pathways to the spinal cord, and that higher IL-1β inflammation in the spinal cord is sufficient in itself to create osteoarthritis in peripheral joints,” Kyrkanides said. “We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor.”

N-acetyl glucosamine and niacinamide, significantly reduced the amount and appearance of hyperpigmentation, age spots and uneven melanin distribution

Contact: Shirley Johnson shirley.johnson@mslpr.com 212-468-3292 Manning Selvage & Lee

Science finds new fix for UV-damaged skin in arthritis treatment

IMAGE:Researchers found that the topical application of a N-acetyl glucosamine (4 percent) and niacinamide (2 percent) complex produced visible improvement in pigmentation after 8 weeks. Photos were taken under polarized…

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Cincinnati, OH – For many women, accumulated sun exposure has already permanently damaged their skin cells, causing them to overproduce pigment that shows up as unsightly dark splotches and uneven skin tone over time. But new research indicates that glucosamine – a compound best known for treating arthritis – can actually help stop the formation of new age spots, and help fade existing ones.

“These findings on glucosamine may impact the way dermatologists treat UV-related skin damage in the future. Right now we have prescription and surgical options, which some people aren’t willing to try,” says Alexa Kimball, M.D., assistant professor of dermatology, Harvard Medical School and lead researcher on one of the studies testing glucosamine. “It’s exciting to see this level of research being done on topical cosmetic applications of glucosamine, and the promising results.”

IMAGE:N-acetyl glucosamine and niacinamide block melanin production by interfering in the process at two different points – reducing formation and appearance of age spots. A key enzyme in melanin biosynthesis…

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An International Consensus on Glucosamine Skin Benefits

In early 2006, a group of leading dermatologists from around the world and Procter & Gamble Beauty scientists convened in Rome to review and discuss the glucosamine data.  The panel determined that n-acetyl glucosamine, a more stable form of glucosamine, reduced the amount of melanin in skin cells, meaning there was less excess pigment in the skin to cause age spots.  Additionally, the panel concluded that a formulation of n-acetyl glucosamine and niacinamide, a vitamin B derivative, significantly reduced the amount and appearance of hyperpigmentation, age spots and uneven melanin distribution. Researchers paired n-acetyl glucosamine with niacinamide because they knew that niacinamide had similar effects on slowing down pigment production and hypothesized that the two might work better together.

The panel reviewed data from three studies involving the n-acetyl glucosamine /niacinamide formulation.  Tissue studies showed a reduction in melanin and an increase in collagen – a key structural protein in skin. Three double-blinded placebo- controlled clinical studies involving more than 200 subjects, including a study supervised by Dr. Kimball, showed improvement in hyperpigmentation and skin tone and a decrease in the size of age spots. The research is set to be presented in July at the “Academy ’06” meeting of the American Academy of Dermatology (AAD), and was first presented at the AAD annual meeting in March 2006.

IMAGE:A series of events occur within pigment cells to trigger the production of melanin.  The process can be activated by both external influences, such as UV radiation or irritants,…

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Skin Biology Gives Researchers Clues for Developing New Treatments The interest in glucosamine as a possible treatment comes in part from what scientists already know happens on a cellular level when skin is exposed to UV radiation. Chronic UV exposure can damage melanocytes, cells in the skin responsible for producing melanin, in a variety of different ways. Often, this damage can lead to a loss of cellular control, and the production of chemicals that allow the cells to keep producing more and more melanin – which eventually leads to age spots and uneven discoloration. Additionally, as skin ages, cell turnover slows down and melanin “dust” – microscopic particles of melanin – can become trapped in the upper layers of skin, resulting in a duller appearance.

Researchers are familiar with these processes and that has helped them focus on substances – such as n-acetyl glucosamine – that are known to interrupt the UV-triggered chemical signals that turn on melanin production. Skin care products that utilize signal-blocking ingredients currently exist in the marketplace, but products with n-acetyl glucosamine/niacinamide  – which block melanin at two different points in the pigment producing process – are among the newest and most studied.

“Pigmentation is an appearance issue that strikes an emotional chord for women, and even though we’re constantly telling our patients about the importance of UV-protection, once the damage is done, we need to be able to provide them with ways to help,” says Dr. Kimball.  “The level of research and validation on topical cosmetic application of glucosamine will help it stand apart from other ingredients when it comes to improving tone and treating hyperpigmentation.”

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Reposted for Filing