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    Anonymous
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    The evidence of a specific bacterial cause of dental caries and of the function of the salivary glands as an effector site of the mucosal immune system has provided a scientific basis for the development of a vaccine against this highly prevalent and costly oral disease. Research efforts towards developing an effective and safe caries vaccine have been facilitated by progress in molecular biology, with the cloning and functional characterization of virulence factors from mutans streptococci, the principal causative agent of dental caries, and advancements in mucosal immunology, including the development of sophisticated antigen delivery systems and adjuvants that stimulate the induction of salivary immunoglobulin A antibody responses. Cell-surface fibrillar proteins, which mediate adherence to the salivary pellicle, and glucosyltransferase enzymes, which synthesize adhesive glucans and allow microbial accumulation, are virulence components of mutans streptococci, and primary candidates for a human caries vaccine. Infants, representing the primary target population for a caries vaccine, become mucosally immunocompetent and secrete salivary immunoglobulin A antibodies during the first weeks after birth, whereas mutans streptococci colonize the tooth surfaces at a discrete time period that extends around 26 months of life. Therefore, immunization when infants are about one year old may establish effective immunity against an ensuing colonization attempts by mutans streptococci. The present review critically evaluates recent progress in this field of dental research and attempts to stress the protective potential as well as limitations of caries immunization.
    Source: Hajishengallis and Michalek-1999-Current status of a mucosal vaccine against dental caries.-Oral Microbiol Immunol-14-1

    #13621
    sushantpatel_doc
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    For most of the twentieth century, the only way dentists could treat cavities was to “drill and fill.” But what if cavities never formed to begin with, thanks to a vaccine painlessly squirted into the nostrils in the first few years of a child’s life?

    Harvard Medical School faculty members working at the Forsyth Institute in Boston, an independent research and educational organization focused on oral and craniofacial science, have discovered the basis for a vaccine that could someday end tooth decay in children. Professor of oral biology Martin Taubman, who heads Forsyth’s immunology department, and associate clinical professor of oral biology and pathophysiology Daniel Smith, a senior member of the Forsyth immunology department, say their vaccine could prevent decay-causing bacteria from gaining a foothold in the mouth.

    Although it has been common knowledge among dental scientists since the 1950s, most people are still startled to learn that tooth decay is merely a symptom of a chronic infectious disease called dental caries (Latin for “rot”). The germs that cause caries, a group of bacteria called the mutans streptococci, amass in significant numbers in the presence of sugar-sucrose, specifically. As mutans break down sugar, they manufacture lactic acid, which strips away tooth enamel and eventually produces cavities.

    Rotting teeth are now nearly epidemic around the world, caused in part by the spread of sugary Western foods, including infant formula. In China, 75 percent of five-year-olds have tooth decay. And in the United States, dental caries affects permanent teeth in almost half of all children between the ages of five and 17, most of them poor. Lacking the money to drill and fill, poor children are more likely to see their cavities progress to excruciating tooth infections and to have decaying teeth extracted rather than undergo costly treatments like root canals or crowns.

    The Forsyth team aims to pull the rug out from under the cavity-causing mutans germs by making it impossible for them to stick to teeth to begin with. Like other active vaccines, theirs works by introducing a foreign substance, called an antigen, into the body. Antigens trigger the immune system to produce antibodies, which attack the antigens and stay in the system indefinitely, providing long-term immunity.

    The new caries vaccine uses an antigen called glucosyltransferase, or GTF-an enzyme that allows decay-causing bacteria to accumulate on teeth and, Taubman says, arouses a greater immune response than other previously tested antigens. By stimulating immunity to the enzyme, the vaccine makes it impossible for the decay-producing microorganisms to cling to the teeth.

    Unlike many vaccines that work through the bloodstream, this one triggers immunity in saliva and mucous tissues-hence it could be squirted or swabbed into the nostrils. The researchers believe the best way to provide long-term protection against caries is to vaccinate children at about the age of one, after baby teeth have begun to emerge, but before the mutans bacteria have started to amass in destructive numbers. At this age, Taubman explains, children’s immune systems are developed enough to produce the needed antibodies. (Once the bacteria have begun to build up, usually when a child is between 18 and 36 months of age, antibodies still form, but are powerless to interfere with mutans streptococci that have already established themselves on teeth; in high-sucrose conditions, these bacteria can still cause decay.) Since antibodies remain in the saliva-and can be “boosted”-they could conceivably provide lifelong immunity, although this has yet to be proven.

    That is the next step: human clinical trials. Taubman and Smith have successfully tested the new vaccine on rats (which, like humans, love to gobble sweets) and also showed positive effects and safety with an orally administered form of the vaccine tested 10 years ago in a Phase I trial involving young men. The researchers are now seeking to partner with institutions that could provide the initial financial support (perhaps $400,000 to $500,000, Taubman estimates) and/or research facilities to help make enough vaccine to test in wider controlled studies.

    Alternatively, we could simply give up our love affair with sugar.

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