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He showed that while a healthy lifestyle won’t help us live much longer, it can stave off chronic disease and disability until our final years.James F. Fries majored in philosophy as an undergraduate, so it’s no surprise that as a medical researcher he was obsessed with how to lead a good life, even though his interest was more about physical than moral well-being.His focus, starting in the mid-1970s, was on what Dr. Fries (pronounced freeze) and other scientists called the failure of success. They noted that one great achievement of the 20th century was the rapid increase in life expectancy, thanks to improvements in vaccinations and sanitation that dramatically reduced deaths from acute, transmissible disease.But that increase in life span did not mean an accompanying increase in “healthspan,” or the duration of one’s life free from chronic conditions like hypertension, diabetes and heart disease.Dr. Fries, who trained as a rheumatologist and spent his entire teaching career at Stanford University, was a data guy, long before large data sets became a common tool in medical research. He was among the first to create an international database of patients that tracked their health over time, an enormous effort that began in 1975 with a grant from the National Institutes of Health.“He was thinking about electronic health records and data mining in the 1970s,” Michael Joyner, a physiologist at the Mayo Clinic, said in a phone interview. “I wouldn’t call him an early adopter. I would call him a pioneer.”Early on, Dr. Fries noticed something strange in the numbers: While the average life span of patients didn’t change much depending on their lifestyle, the rates of morbidity — that is, affliction by chronic disease and disability — varied greatly between those who exercised and ate a healthy diet and those who smoked, overate and exercised infrequently, if at all.Put differently, exercise and a healthy diet don’t help you live longer, but they can help you postpone the onset of debilitating disease until close to the end of your life, a phenomenon that Dr. Fries called “compression of morbidity.”He died at 83 on Nov. 7 at an assisted living home in Boulder, Colo. His son, Greg, said the death, which was not widely reported at the time, was attributed to end-stage dementia.Dr. Fries outlined his compression of morbidity hypothesis in an article in The New England Journal of Medicine in 1980, then spent the rest of his career trying to prove it, using longitudinal studies of both large groups of people and so-called natural experiments, like a runners’ club, as measured against a control population.He practiced what he preached. In high school he ran the mile and pole-vaulted; as an adult, he took up jogging, running an average of 500 miles a year. An avid outdoorsman, he climbed the highest peaks on six continents, though at Mount Everest he had to turn back when a snowstorm endangered his crew just 3,000 feet from the summit.Dr. Fries was not without his critics. Some pushed back against his assumption that there was a limit to human beings’ natural maximum life span; others insisted that chronic disease was here to stay, and that lifestyle choices mattered little in the grand scheme of things.But he said he had the data to support his claims, and over time his core insight became a cornerstone of a new approach to healthy living, one that spilled out of the medical laboratory and into the pages of countless self-help books. Dr. Fries was the author of some himself; one, “Take Care of Yourself” (1979), which he wrote with Dr. Donald M. Vickery, has sold some 20 million copies.Another of his books, “Taking Care of Your Child” (1977), briefly made headlines in 1992. After an insurance provider announced that it would distribute copies to some 275,000 federal workers, President George Bush’s administration insisted that a chapter on contraception be removed lest it offend some parents.Dr. Fries took his approach to healthy living out of the laboratory and into the pages of self-help books, including this one from 1979, written with a colleague. It has sold some 20 million copies.Dr. Fries was careful to insist that the compression of morbidity was not inevitable, and he urged policymakers to develop tools to encourage healthy living and to make it easier for people to pursue interventions like statins and joint-replacement surgery, to help them stave off chronic disease and disability.But, ever the philosopher, he also recognized that staving off morbidity was ultimately a personal choice, and those who failed to follow his advice would have to live with the results.“Anguish arising from the inescapability of personal choice and the inability to avoid personal consequences may become a problem for many,” he wrote in a 2011 paper. “For others, exhilaration may come from recognizing that the goal of a vigorous long life may be an attainable one.”James Franklin Fries was born on Aug. 25, 1938, in Normal, Ill., the son of Albert and Orpha (Hair) Fries. His mother taught middle school English, and his father was a college business professor. The family soon moved to Evanston, Ill., where Albert Fries taught at Northwestern University, and then to California, where he taught at several institutions, including the University of Southern California.Jim Fries attended Stanford University and graduated with a degree in philosophy in 1960, the same year he married Sarah Tilden, whom he had met in a freshman history course.Weeks after their wedding ceremony, the Frieses drove east to Baltimore, where Dr. Fries attended medical school at Johns Hopkins University. He graduated in 1964 and stayed another four years as a resident before returning to Stanford, where he joined the faculty.His daughter, Elizabeth, died of breast cancer in 2005, the same year that his wife developed metastatic melanoma. She survived, but the disease left her disabled. Dr. Fries insisted that she remain active, and the two continued to travel extensively, taking cruises and walking tours around the world. At one point he carried her across a bridge in the Himalayas.Mrs. Fries died in 2017. Along with his son, Dr. Fries is survived by his brother, Ken, and five grandchildren.Dr. Fries retired in 2017, after his wife’s death and after he suffered a debilitating stroke. A few months later, he moved to Colorado to be near his son.

SharecloseShare pageCopy linkAbout sharingAn 11-year-old has become the first patient in the country to have kidney surgery using specialist 3D equipment.Libby, from Watchet, Somerset, was suffering from kidney and bladder complications which meant she was often in severe pain.Surgeons were able to operate on her faster and with greater accuracy using 3D technology during keyhole surgery.Hundreds more children across the country could now have faster surgery.One in 200 children are born with stretched kidneys, but in Libby’s case it was not detected until she was older.She had a blockage in her ureter, the tube that connects kidneys to the bladder.Libby said she often had a pain in her side and felt sick, and the painful episodes were becoming more frequent and stronger.Her mother Holly said the family had found Libby’s situation “quite worrying” the more it escalated.Using the 3D laparoscopic equipment, which is only 4mm wide and more commonly used for brain surgery, the problem was corrected at Bristol Children’s Hospital.Libby’s paediatric urologist Mark Woodward said the 3D equipment, which costs £20,000, had enabled him to be more precise during the operation, as the equipment creates a better image on screen and enables surgeons to perform the operation faster and with greater accuracy.”All my training has been with non-3D, and you learn tricks to gauge depth and angle, particularly for suturing.”Then when you flick it over to 3D – people will know themselves from going to the cinema – you suddenly know really well what your needle angle is.”Dr Woodward said the equipment would increase precision and help trainee surgeons learn operating skills more quickly.Libby’s surgery would normally take between two to three hours but using 3D equipment doctors think that can be reduced by 20%.Follow BBC West on Facebook, Twitter and Instagram. Send your story ideas to: bristol@bbc.co.ukBristol Royal Hospital for ChildrenThe BBC is not responsible for the content of external sites.

Scientists have found a way to prove that biochemical signals sent from cell to cell play an important role in determining how those cells develop.
The study from researchers at the USC Dornsife College of Letters, Arts and Sciences was published in the journal Development on Dec. 22.
A little background All cells within the body begin as stem cells. In simplest terms, blood forms when stem cells in bone marrow develop along one of three paths to become either oxygen-carrying red cells, immune-system white cells, or platelets, which clot to stop bleeding. Scientists have long accepted that communication between cells can affect their fate, but they have largely found it too complex to study directly. Cells can communicate by sending growth factors, hormones or other molecules back and forth.What’s new USC Dornsife’s Adam MacLean, assistant professor of quantitative and computational biology, and doctoral candidate Megan Rommelfanger, found a way to better understand how cell-to-cell communication affects the way blood stem cells develop. The scientists discovered that the communication process can change the formation of blood cell types dramatically. They also found that distance between cells matters.”We discovered that the communication process can change the formation of blood cell types dramatically, and that cells that are closer to one another have a greater influence on each other’s fate,” MacLean said.
A controversy resolved
Researchers trying to determine what early factors nudge a cell down one developmental path or another have wondered if random fluctuations within the cell are enough to decide which path is taken. Many models have suggested they were, but recent breakthrough studies showed that random fluctuations were not enough, that something else drives cells toward their fate.

Scientists investigating the DNA outside our genes — the ‘dark genome’ — have discovered recently evolved regions that code for proteins associated with schizophrenia and bipolar disorder.
They say these new proteins can be used as biological indicators to distinguish between the two conditions, and to identify patients more prone to psychosis or suicide.
Schizophrenia and bipolar disorder are debilitating mental disorders that are hard to diagnose and treat. Despite being amongst the most heritable mental health disorders, very few clues to their cause have been found in the sections of our DNA known as genes.
The scientists think that hotspots in the ‘dark genome’ associated with the disorders may have evolved because they have beneficial functions in human development, but their disruption by environmental factors leads to susceptibility to, or development of, schizophrenia or bipolar disorder.
The results are published today in the journal Molecular Psychiatry.
“By scanning through the entire genome we’ve found regions, not classed as genes in the traditional sense, which create proteins that appear to be associated with schizophrenia and bipolar disorder,” said Dr Sudhakaran Prabakaran, who was based in the University of Cambridge’s Department of Genetics when he conducted the research, and is senior author of the report.

Some people are resigned to another season of restrictions and plan to forge ahead with celebrations. Others are trying to overcome a sense of perpetual fear.A single mother of two girls, Katherine Sargent is accustomed to working hard to ensure Christmas is a wonderful time, baking cookies and shopping with her children to find new ornaments for the tree.She had hoped that this season would be more cheerful than in 2020, when schools were shuttered and the Covid-19 vaccine rollout had barely begun.But it hasn’t turned out that way.Even though more people are returning to normal life in her hometown, Portland, Maine, they’re finding there’s little normal about it. “They lack the energy to get together, to celebrate,” Ms. Sargent said. “So many people I know say they’re stressed.”This year is indeed bringing a new layer of stressors, especially now that the highly contagious Omicron variant is casting a chill on travel and everyday routines. Once again, we’re dialing back on plans to attend parties, concerts and movies. We’re Googling the variant’s symptoms and taking our temperatures. And the nation’s mental health is at a precarious level.On top of pandemic pressures, inflation has driven up the prices of many gifts. Shelves remain barren in many toy stores as popular dolls and games sit aboard container ships in traffic jams offshore from the nation’s ports.Add to that the traditional hassles of tangled light strings and fraught family relations, and it’s no wonder that holiday Grump Trees are selling fast at Trader Joe’s.“We entered into this winter feeling more optimistic, and now it’s clear the uncertainty continues,” said Vaile Wright, a clinical psychologist and senior director for health care innovation at the American Psychological Association. A recent study for the group showed that people were having trouble making the most basic decisions.And the rules keep changing for family gatherings, with rapid virus tests in higher demand than gifts in some places. “Covid definitely adds a complexity to the holidays that wasn’t there a few years ago,” said Tracey Kim Snow, a clinical psychologist in the Chicago area.Even among the closest of relatives, the vaccination divide has caused hurt and isolation. Some families have forbidden immediate relatives from visiting if they aren’t immunized against Covid. And some have gone even further by demanding their relatives get booster shots for inclusion around the tree to enjoy the collective excitement of unwrapping presents.“Once again, we’re looking at other humans as a risk, and we weren’t trained to do that, except in battle,” said Dr. Cynthia Ackrill, a lifestyle medicine physician in Asheville, N.C.Ms. Sargent, 37, shifted to remote work to avoid exposure to the virus these past few weeks, so that she could be with her grandmother along with her parents, her brother and his family for the holiday.Divorced six years ago, she finds that being a single mother adds extra strain to her planning for a second Christmas in the pandemic.“It’s a lot of pressure to want to give your children so much magic and warmth right now, with so many limitations, and I don’t have a partner to share it with,” Ms. Sargent said. One survey conducted for the American Psychiatric Association found that women were feeling more stress this holiday season compared with last year’s.The same was true for adults ages 18 to 44, Republican and Independent voters and those with incomes under $50,000, according to the poll of 2,119 adults conducted last month.Ena Sargent donned a bow during present-wrapping.Tristan Spinski for The New York TimesThe tensions are evident in national warnings about the nation’s mental health and as counselors have been hearing from and seeing more patients and newcomers. Ms. Snow, the Chicago area psychologist, said appointments started increasing in numbers right after Thanksgiving.Dr. Itai Danovitch, chairman of the psychiatry and behavioral neurosciences department at Cedars-Sinai Medical Center in Los Angeles, said patients were experiencing twin worries from the pandemic and the holidays. “Those two things colliding increase the background stress,” he said.In counseling patients about Covid, Dr. Danovitch added, “I see both people who have resigned themselves to the new norm, and also people who are in a perpetual state of fear.”Therapists offer a variety of tips and exercises to ease stress, often advising simple tasks like looking for activities to distract people from the pandemic and not watching anxiety-producing news.Drinking too much and smoking too much cannabis should be avoided, Dr. Danovitch said. He suggests searching for ways to be of service in your community by volunteering for a worthy cause or checking in with an older neighbor.Because holiday meals are well-known minefields for family tension, try to plan ahead for how to defuse those arguments, said Dr. Ackrill, a fellow with the American Institute of Stress and an editor of its magazine Contentment.“Maybe a long walk before dinner,” she said. “If you can get outside, that’s a great idea. Play a game together. Build in some fun.”And if the family starts discussing divisive topics over the cranberry sauce? Merely point out that people at the table have different viewpoints, she said.Other simple steps can ease stress: going to bed 15 minutes earlier, taking breaks during the day — even if it’s just walking around or doing jumping jacks — or watching a funny four-minute video for a laugh, she advised.Another tool is breath work, a technique of using controlled breathing to calm yourself.For some, the holidays can stir up painful memories that require regular counseling.“If that anxiety is really spinning out of control, there’s a threshold where you should seek help,” Dr. Danovitch said.The Coronavirus Pandemic: Key Things to KnowCard 1 of 4New C.D.C. guidelines

New data from Britain suggests that booster protection against symptomatic Covid caused by the Omicron variant wanes within 10 weeks.There have not yet been enough severe cases of Omicron to calculate how well boosters protect against severe disease, but experts believe the shots will continue to provide significant protection against hospitalization and death.“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” the new report, from Britain’s Health Security Agency, noted. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”In the weeks since Omicron was discovered, multiple studies have suggested that the variant is skilled at evading the antibodies that are produced after vaccination or after infection with the coronavirus.The new report from Britain, which included data on people who had received the AstraZeneca, Pfizer or Moderna shots, confirmed that the vaccines — both the initial two-shot series and booster doses — were less effective and waned faster against Omicron than against Delta.Among people who received two doses of the AstraZeneca vaccine, a booster with one of the mRNA vaccines, made by Pfizer and Moderna, was 60 percent effective at preventing symptomatic disease two to four weeks after the shot. After 10 weeks, however, the Pfizer booster was just 35 percent effective. The Moderna booster was 45 percent effective at up to nine weeks. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology.)For people who were given three Pfizer doses, vaccine effectiveness dropped from 70 percent one week after the booster to 45 percent after 10 weeks. Pfizer recipients who received a Moderna booster, on the other hand, seemed to fare better; their vaccine regimen remained up to 75 percent effective at up to nine weeks.The report, which was based on an analysis of about 148,000 Delta cases and 68,000 Omicron cases, also included recent data suggesting that Omicron infections are less likely to lead to hospitalizations than Delta infections. The findings should be interpreted cautiously, the agency noted, because there have still not been many Omicron cases, relatively speaking, and the people who have contracted the variant may not be representative of the broader population.The Biden administration has been encouraging all eligible Americans to receive booster shots as Omicron spreads.In a recent interview on WCBS-AM, a New York radio station, Dr. Anthony S. Fauci, the nation’s leading infectious disease doctor, said that officials were monitoring the effectiveness of mRNA boosters against Omicron.“I do think it’s premature, at least on the part of the United States, to be talking about a fourth dose,” he said. Israel is weighing whether to give a fourth shot to its citizens.Some scientists have warned against a fourth shot, noting that there is not yet evidence that it is necessary and that some immune cells might eventually stop responding to the shots if too many doses are given.

The agency issued revised guidelines as Omicron cases climb, and hospitals grapple with worker shortages that have left wards understaffed.With rising concern over hospital staffing shortages as Omicron cases rapidly spread, the Centers for Disease Control and Prevention on Thursday shortened isolation periods for health care workers who contract Covid-19.The agency recommended that health care workers who are asymptomatic return to work after seven days and a negative test, adding that “isolation time can be cut further if there are staffing shortages.”The agency also said that those workers who had received all recommended vaccine doses, including boosters, do not need to quarantine at home following high-risk exposures.Many major hospital systems had already been forced to move ahead on their own in recent days, creating a patchwork of guidelines regarding infected workers in anticipation of a winter surge.The shortest such policy for returning to work — five days, with some other preconditions — is half the 10-day standard set earlier by the C.D.C. Other hospitals have settled on seven days as a safe window for infected staff members to return to work.The agency’s new recommendations do not apply to the public. Early in the pandemic, the C.D.C. had set a 14-day isolation period for infected Americans, to lower the risk of contagion, but then winnowed that back as more research confirmed that typical patient would be infectious for a shorter amount of time.Criticized for shifting guidance and mixed messaging, the C.D.C. decision to recommend the changes in isolation only to health care workers is likely to add to the confusion among Americans, especially since Britain issued a broad recommendation for shortened isolation on Wednesday that applies to everyone.Britain’s Health Security Agency cut the period for all infected individuals to seven days from 10 days, if they have twice tested negative with rapid antigen tests.Some medical experts pointed to limited evidence regarding when a person infected with the Omicron variant might no longer be contagious. But other researchers have been urging shorter periods and said that the C.D.C. revisions were overdue.“They are consistently behind in updating recommendations that are needed now, especially as we face the daunting prospect of a sudden surge in cases,” said Angela Rasmussen, a virologist at the Vaccine and Infectious Disease Organization at the University of Saskatchewan in Canada.Dr. Ashish Jha, dean of the Brown University School of Public Health, said it would make sense to shorten isolation times for the public, as well — especially for those who are vaccinated.“Given that a large proportion of health care workers, like other Americans, are going to get infected, finding a shorter period of time for isolation is critical,” said Dr. Jha.“I think we have reasonably good evidence with Delta that vaccinated people clear the virus far more quickly. There is no reason to believe that wouldn’t be true for Omicron.”Hospital administrators have stressed that the new changes allowing employees to resume work sooner would not put patients at risk.Given that health care workers are tested frequently, are largely vaccinated, and must be masked, “the chances of causing a significant amount of infections seem very low” if isolation periods are shortened, said Dr. Bob Wachter, chairman of the department of medicine at the University of California, San Francisco.“The consequences of keeping them out of the work force are massive when you think about the impact on health,” he added. U.C.S.F. also is weighing whether to reduce the isolation period to five days for workers: “I don’t know if five days saves us, but it’s better than seven and better than 10.”Dr. Jha stressed, though, that more research is needed to definitively answer questions regarding how long a person with an Omicron infection may remain infectious. The variant is far more contagious than previous versions of the coronavirus.Many of the new hospital policies also include requirements regarding testing, vaccination status and symptoms.In New York State, which has reported a seven-day average of more than 4,600 hospitalizations as Omicron cases soar, major hospitals recently changed isolation protocols for vaccinated employees.N.Y.U. Langone shortened its return-to-work policy to five days after a worker receives a positive test, or three days after a fever has subsided, whichever is longer. NewYork-Presbyterian reduced its isolation period to seven days. On Thursday, the Mount Sinai Health System also shifted to seven days from 10.“Guided by the latest science, our current protocols allow fully vaccinated employees to return to work after seven days,” said Joy Valenzuela, a spokesman for NewYork-Presbyterian. “Nothing is more important to us than the health and safety of our patients, visitors and staff.”Northwell Health’s guidelines now allow fully vaccinated workers to return to work eight days after a positive test or after symptom onset, if their symptoms are improving and they have not had a fever for 24 hours.The Coronavirus Pandemic: Key Things to KnowCard 1 of 5The holiday season.

Infection-fighting B cells retain better memory of the coronavirus spike protein in University Hospital patients who recover from less-severe cases of COVID-19 than in those recovering from severe COVID-19, a new study suggests. Findings by scientists from The University of Texas Health Science Center at San Antonio were published Wednesday (Dec. 22) in the journal PLOS ONE.
Evelien Bunnik, PhD, corresponding author of the paper, said the results hint of subtle differences in the quality of immune response based on COVID-19 severity. Dr. Bunnik is an assistant professor of microbiology, immunology and molecular genetics at the health science center, also referred to as UT Health San Antonio.
The study focused on memory B cells that react against the SARS-CoV-2 spike protein. Blood samples were analyzed one month after symptom onset and five months post-onset. After one month, a significant proportion of spike-specific B cells were active.
However, samples from eight individuals who recovered from less-severe disease showed increased expression of markers associated with durable B cell memory as compared to individuals who recovered from severe disease, the authors wrote. The markers include T-bet and FcRL5.
T-bet-positive, spike-specific B cells nearly disappeared from the blood samples five months post-symptom onset, the authors noted. Overall, a more dysfunctional B cell response is seen in severe disease cases, they wrote.
Non-severe cases were defined as not requiring supplemental oxygen or invasive ventilation, while severe cases needed invasive mechanical ventilation or extracorporeal membrane oxygenation (ECMO). “The definition of severe disease was made based on the need for mechanical ventilation or ECMO, because this distinguishes the most critical patients, who are the most likely to develop impaired immune responses,” said study senior author Thomas Patterson, MD, professor and chief of infectious diseases at UT Health San Antonio who leads COVID-19 care at clinical partner University Health.
Study participants were enrolled in the Adaptive COVID-19 Treatment Trial (ACTT)-1 or ACTT-2 clinical trials. Samples were from University Health patients co-enrolled in the UT Health San Antonio COVID-19 Repository.
“The increased percentage of B cells associated with long-lived immunity in non-severe COVID-19 patients may have consequences for long-term immunity against SARS-CoV-2 re-infection or severity of the resulting disease,” the authors wrote.
Acknowledgments
This work was supported by a COVID-19 pilot award from the UT Health San Antonio Joe R. and Teresa Lozano Long School of Medicine (10009547 to Dr. Evelien Bunnik). Raphael A. Reyes was supported by Translational Science Training award TL1 TR002647. Data were generated in the Flow Cytometry Shared Resource Facility, which is supported by UT Health San Antonio, NIH-NCI P30 CA054174-20 (Mays Cancer Center, home to UT Health San Antonio MD Anderson) and UL1 TR001120 (Clinical Translational Science Award grant). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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A new study from Columbia researchers, in collaboration with scientists at the University of Hong Kong, adds more evidence that the omicron variant can evade the immune protection conferred by vaccines and natural infection and suggests the need for new vaccines and treatments that anticipate how the virus may soon evolve.
The study was led by David Ho, MD, director of the Aaron Diamond AIDS Research Center and the Clyde’56 and Helen Wu Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons. The findings were published in Nature.
A striking feature of the omicron variant is the alarming number of changes in the virus’s spike protein that could pose a threat to the effectiveness of current vaccines and therapeutic antibodies.
Large drop in omicron neutralization by antibodies from vaccines
The new study tested the ability of antibodies generated by vaccination to neutralize the omicron variant in laboratory assays that pitted antibodies against live viruses and against pseudoviruses constructed in the lab to mimic omicron.
Antibodies from people double-vaccinated with any of the four most widely used vaccines — Moderna, Pfizer, AstraZeneca, Johnson & Johnson — were significantly less effective at neutralizing the omicron variant compared to the ancestral virus. Antibodies from previously infected individuals were even less likely to neutralize omicron.

Blocking function of a blood-clotting protein prevented bone loss from periodontal (gum) disease in mice, according to research led by scientists at the National Institute of Dental and Craniofacial Research (NIDCR), part of the National Institutes of Health. Drawing on animal and human data, the researchers found that buildup of the protein, called fibrin, triggers an overactive immune response that damages the gums and underlying bone. The study, which was published in Science, suggests that suppressing abnormal fibrin activity could hold promise for preventing or treating periodontal disease, as well as other inflammatory disorders marked by fibrin buildup, including arthritis and multiple sclerosis.
Periodontal disease affects nearly half of Americans over age 30, and 70% of those 65 and older. It is a bacterial infection of the tissues supporting the teeth. In its early stages, periodontal disease causes redness and swelling (inflammation) of the gums. In advanced stages, called periodontitis, the underlying bone becomes damaged, leading to tooth loss. While scientists have known that periodontitis is driven in part by an exaggerated immune cell response, until now, it was unclear what triggered the response, and how it caused tissue and bone damage.
“Severe periodontal disease can lead to tooth loss and remains a barrier to productivity and quality of life for far too many Americans, especially those lacking adequate access to dental care,” said NIDCR Director Rena D’Souza, D.D.S., Ph.D. “By providing the most comprehensive picture yet of the underlying mechanisms of periodontal disease, this study brings us closer to more effective methods for prevention and treatment.”
At sites of injury or inflammation, fibrin normally plays a protective role, helping to form blood clots and activating immune cells to fight infection. But too much fibrin has been linked with health problems, including a rare form of periodontitis due to a condition called plasminogen (PLG) deficiency. In affected people, mutations in the PLG gene lead to fibrin buildup and disease at various body sites, including the mouth.
To explore the connection between abnormal fibrin buildup and periodontitis, the scientists, led by NIDCR investigators Niki Moutsopoulos, D.D.S., Ph.D., and Thomas Bugge, Ph.D., studied PLG deficiency in mice and analyzed human genetic data.
Like humans with the condition, PLG-deficient mice developed periodontitis, including periodontal bone loss and elevated levels of fibrin in the gums. The mice’s gums were crowded with immune cells called neutrophils, which are also found at high levels in common forms of periodontitis.