Gingivitis is one of the most common oral health problems in Canada. It starts off with a little redness in the gums but without proper attention and care, the situation can worsen leading to bleeding, puffiness, bad breath, and over time, what is known as periodontitis, more commonly known as gum disease. The consequences can be dire with loosening or loss of the teeth.
The main culprit behind the condition is bacterial growth, usually called plaque. Although several different types of species are detrimental to gum health, some are more troublesome than others. One particular enemy is known as Porphyromonas gengivalis . Having high amounts of this bacterium can significantly increase the potential for periodontitis.
Researchers tried for decades to figure out what makes this bacterium so problematic. Back in the 1990s, studies revealed the bacteria had the ability to invade our gum cells. This led to the potential for bleeding and cell death leading to gum recession.
This was bad news indeed yet the results only offered half of the story. As with many chronic infections, there had to be some involvement of the immune system. By 2001, the effect of this bacterium on immunity was finally discovered. Its presence led to a cellular form of inflammation in the gum area. What was worse was the fact the type of response prompted immune cells to destroy cells in that area.
Even with this rather unsavory thought, there was still a missing piece to the puzzle. No one quite knew what was actually causing the inflammation. Some research had suggested the physical components of the bacterial cells was enough to cause this problem. Yet these results revealed only short term effects.
Now the guilty party may have been found. An international group of researchers have used a combination of microbial and human cell cultures, they have identified a particular protein, aptly named Gingipain, as the source for the long term inflammation occurring in the gums. The results of this research suggest the bacteria are most troublesome not when the protein is active, but when it is dormant.
The initial experiments behind this discovery were relatively straightforward. Cultures of immune cells were infected by the bacterium in the hopes of finding cellular markers of inflammation. Sure enough, the cells reacted to the microbial presence. But there was a surprise in store. When Gingipain was active, there was relatively little inflammation. On the other hand, when the enzyme was dormant, inflammation took off.
This strange twist led the researchers to think there may be more than an infection going on. Answering that required a different type of experiment. The team had to add the infected cells to an artificial immune system to find out the effects of the enzyme on a systematic level.
When they looked at the effect of infection on the immune system, the team was shocked to find the inactive or dormant form of the enzyme led to the most troublesome effects. In this case, inflammation was increased and sustained. This meant a lack of enzyme activity was making the situation worse.
Though the results appeared to make little sense, the team persevered to identify a reason. They looked at the various proteins involved in inflammation in the hopes of finding one that might interact with the enzyme. The best candidate was a molecule known as interleukin six (IL-6). If the group was right, blocking this molecule might halt inflammation regardless of the enzyme's activity.
Sure enough, when the group blocked IL-6, inflammation went down in all cases. The team had found the lynchpin of the periodontitis mystery. Perhaps more importantly, the results revealed the trouble wasn't being caused some previously unknown entity but a biological factor known for being involved in long-term inflammation.
Based on the identification of IL-6 as the culprit, the authors suggest the potential to slow and possibly stop the progression of gingivitis may not be too far away. A pharmaceutical route to achieve this goal already exists although it only is approved for another IL-6 based chronic condition, rheumatoid arthritis. Still, the existence of an approved therapeutic means the potential for periodontitis treatment may be years rather than decades away.
While we wait for medicine to catch up to the research, the best way to reduce the chances for this IL-6 based route of gum inflammation is to ensure your teeth and gums are healthy. This means brushing at least twice a day and making sure to visit your dentist regularly. While research may be able to help us find routes to resolve gum disease, these oral health professionals can help you prevent and manage troubles before they go too far.
via HuffPost Canada
Gingivitis is one of the most common oral health problems in Canada. It starts off with a little redness in the gums but without proper attention and care, the situation can worsen leading to bleeding, puffiness, bad breath, and over time, what is known as periodontitis, more commonly known as gum disease. The consequences can be dire with loosening or loss of the teeth.
The main culprit behind the condition is bacterial growth, usually called plaque. Although several different types of species are detrimental to gum health, some are more troublesome than others. One particular enemy is known as Porphyromonas gengivalis . Having high amounts of this bacterium can significantly increase the potential for periodontitis.
Researchers tried for decades to figure out what makes this bacterium so problematic. Back in the 1990s, studies revealed the bacteria had the ability to invade our gum cells. This led to the potential for bleeding and cell death leading to gum recession.
This was bad news indeed yet the results only offered half of the story. As with many chronic infections, there had to be some involvement of the immune system. By 2001, the effect of this bacterium on immunity was finally discovered. Its presence led to a cellular form of inflammation in the gum area. What was worse was the fact the type of response prompted immune cells to destroy cells in that area.
Even with this rather unsavory thought, there was still a missing piece to the puzzle. No one quite knew what was actually causing the inflammation. Some research had suggested the physical components of the bacterial cells was enough to cause this problem. Yet these results revealed only short term effects.
Now the guilty party may have been found. An international group of researchers have used a combination of microbial and human cell cultures, they have identified a particular protein, aptly named Gingipain, as the source for the long term inflammation occurring in the gums. The results of this research suggest the bacteria are most troublesome not when the protein is active, but when it is dormant.
The initial experiments behind this discovery were relatively straightforward. Cultures of immune cells were infected by the bacterium in the hopes of finding cellular markers of inflammation. Sure enough, the cells reacted to the microbial presence. But there was a surprise in store. When Gingipain was active, there was relatively little inflammation. On the other hand, when the enzyme was dormant, inflammation took off.
This strange twist led the researchers to think there may be more than an infection going on. Answering that required a different type of experiment. The team had to add the infected cells to an artificial immune system to find out the effects of the enzyme on a systematic level.
When they looked at the effect of infection on the immune system, the team was shocked to find the inactive or dormant form of the enzyme led to the most troublesome effects. In this case, inflammation was increased and sustained. This meant a lack of enzyme activity was making the situation worse.
Though the results appeared to make little sense, the team persevered to identify a reason. They looked at the various proteins involved in inflammation in the hopes of finding one that might interact with the enzyme. The best candidate was a molecule known as interleukin six (IL-6). If the group was right, blocking this molecule might halt inflammation regardless of the enzyme's activity.
Sure enough, when the group blocked IL-6, inflammation went down in all cases. The team had found the lynchpin of the periodontitis mystery. Perhaps more importantly, the results revealed the trouble wasn't being caused some previously unknown entity but a biological factor known for being involved in long-term inflammation.
Based on the identification of IL-6 as the culprit, the authors suggest the potential to slow and possibly stop the progression of gingivitis may not be too far away. A pharmaceutical route to achieve this goal already exists although it only is approved for another IL-6 based chronic condition, rheumatoid arthritis. Still, the existence of an approved therapeutic means the potential for periodontitis treatment may be years rather than decades away.
While we wait for medicine to catch up to the research, the best way to reduce the chances for this IL-6 based route of gum inflammation is to ensure your teeth and gums are healthy. This means brushing at least twice a day and making sure to visit your dentist regularly. While research may be able to help us find routes to resolve gum disease, these oral health professionals can help you prevent and manage troubles before they go too far.
via HuffPost Canada
