Finding a connection between osteoarthritis and gut bacteria seems unlikely. But, a new study concludes that they could, actually, be tied. New research, published in the journal JCI Insight, probes bacteria in our guts and their role in osteoarthritis.
People with excess weight put extra stress on their joints. This explained the increased risk of osteoarthritis which comes with obesity. Therefore, new research looked at a more interesting mechanism which might link these two conditions.
In the U.S, osteoarthritis affects approximately 31 million people. Furthermore, it is a leading cause of disability, worldwide.
Obesity comes with a range of related health hazards including cardiovascular disease and diabetes. It is also closely related to osteoarthritis. Often stated as the “wear and tear” arthritis, osteoarthritis comprises the slow cartilage degradation or the stuffing between bones in a joint.
We have billions of bacteria living in our guts. They are critical for good health. Scientists from the University of Rochester Medical Center in New York set out to discover what associations there might be between gut bacteria, diet, obesity, and osteoarthritis.
What did the researchers do?
For this purpose, the scientists fed mice a high-fat diet over a 12-week period. The mice quickly became obese and diabetic. Then, the bacterial residents of their colons were assessed.
As estimated, the microbiomes of the guts were off-kilter; their bowels were filled with pro-inflammatory bacteria. Moreover, it had a distinct lack of healthy, probiotic bacteria, such as Bifidobacteria.
Simultaneously, the researchers also observed body-wide inflammation in obese mice, comprising the knee joints. To induce osteoarthritis, the researchers tore the menisci of mice which is the cartilage cushion between the shin and thigh bones. This type of injury generally causes osteoarthritis.
Researchers of the study found that, in the obese mice, osteoarthritis developed more quickly than in the control mice. Actually, within 12 weeks, nearly all of the obese mice’s cartilage had disappeared.
According to the researchers, cartilage is both a cushion and lubricant which support friction-free joint movements. When you lose that its bone on bone or rock on rock. Thus, it is the end of the line, and you may need to replace the whole joint.
What did the researchers conclude?
For the next stage of the research, the researchers started the procedure again. They fattened up mice with a high-fat diet for 12 weeks. However, this time, they involved a prebiotic called oligofructose. Prebiotics cannot be broken down by mouse or human guts. However, many useful bacteria, like Bifidobacteria, flourish in their presence.
This important change in diet encouraged the growth of beneficial bacteria and made a marked decrease in pro-inflammatory bacteria.
Notably, it also reduced joint inflammation, and the knee cartilage of the obese mice was vague from that of the non-obese control mice. Further, the addition of a prebiotic also reduced diabetic symptoms. But it made no change to the amount of weight that the mice gained.
Thus, even though the joints of the mice were subjected to the same amount of stress, they were healthier. This supports the idea that inflammation, rather than mechanical stress, is the crucial driver of osteoarthritis.
A note of caution
It is noteworthy to remind ourselves that, though the study outcomes are exciting, there are considerable differences between the mouse microbiome and our own. Therefore, the next step will be to move this route of an investigation into humans.
The leaders of this study hope to compare the microbiomes of veterans with and without obesity-related osteoarthritis. They will supplement some of these members with prebiotics to estimate how much advantage this involvement might have in humans.