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Collagen and periodontal disease: report from the annual AAAS meeting
Collagen and periodontal disease: report from the annual AAAS meeting
David L. Dreier, Chicago
Until a few years ago, most dental researchers believed that the destruction o f gingival collagen in periodontal disease must be the direct result o f action by bacterial plaque. That theory has largely given way to the view that the loss of collagen cells, which in aggregate serve as connective fibers in the periodontium, is also caused by substances released by the body’s own immune reaction to bacterial products. Further support for this newer theory was of fered recently in San Francisco at the 140th an nual meeting of the American Association for the Advancement o f Science, held Feb 24March 1 at the San Francisco Hilton Hotel. The session on biochemical lesions o f perio dontal disease was organized by Howard M. Myers, professor of biochemistry at the Univer sity of the Pacific School of Dentistry in San Francisco, and the late Isadore Zipkin, profes sor at the University of California at San Fran cisco School of Dentistry.
cells into an immune reaction by which so-called hypersensitive cells are formed. Dr. Page said other researchers have shown that the blood of periodontal patients carries lymphocytes that have been sensitized to the plaque antigens. The lymphocytes release sub stances to combat the products of the plaque bacteria, but those substances are also damaging to the cells of the periodontium. The professor said research data strongly in dicate that gingival collagen is lost through the
D ouble m echanism Roy C. Page, associate professor of pathology and periodontology at the University of Wash ington School of Dentistry in Seattle, empha sized that he still believes plaque formation is the primary first step in the chain o f events lead ing to tooth loss. H owever, he said, it is still very unclear just how the disease progresses from here. It appears likely, he added, that plaque bacteria release substances into the gingiva that spur the gingival 698 ■ JAD A, V o l. 88, A p ril 1974
HOWARD M. MYERS
double m echanism of the release of bacteria prod ucts and the immune reaction by the gingival cells to those substances. D r. Page said he believes the cells of the gin giva produce a great deal of collagen each day to enable the tissues around the teeth to be con stantly rejuvenated and revam ped. T he unused portion of newly created collagen undergoes nor mal destruction, he said. H ow ever, he added, in periodontal disease, this regular m echanism for maintaining the health of the supporting structures of the teeth is disrupted. H e explained that possibly m ore col lagen is destroyed, less is m ade, or the nature of the collagen is changed; or a com bination of these actions may be occurring. R esearch indicates the latter possibility; that is, a variety of factors operate to produce the 70% loss of collagen around the necks of teeth in patients with severe periodontal disease. With regard to the change in the nature of col lagen, D r. Page reported that he has found an unusual form of collagen in diseased periodontal tissues. H e said the characteristics of that col lagen and its role in the disease have not yet been determ ined. T he possibility that the body’s immune m ech anism could initiate a series of chemical reac tions resulting in the production of altered forms of collagen was substantiated by M arcel E. Nim ni, associate professor in the U niversity of Southern C alifornia’s departm ent of medicine and biochem istry. D r. Nim ni dem onstrated that with some types of arthritis, the body stops forming the type of collagen associated with cartilage and instead forms the type characteristic o f skin. H e sug gested the sam e sort of change may operate with periodontal disease. Com menting on research findings presented by the two scientists, D r. M yers said, “ R eplace ment of one type of collagen by another alters its function and this in turn may be responsible for the conditions seen in periodontal disease. In stead of forming the correct type of collagen that acts as fibrous bands to hold the gingiva close to the teeth, a different type of collagen is form ed.” H e added, “ T he purpose of the collagen in gingival tissue is to make a seal against the oral environm ent and failure to do this properly means that bacteria from the oral cavity can pen etrate the seal and lead to destruction of the sup porting tissues of the te e th .” Reiterating Dr. P age’s conclusions, D r. M yers said, “ T he changes that occur in periodontal dis-
ROY C. PAGE
ease evidently are not those produced by the at tacking microorganisms. This m eans that the products and toxins and toxic m aterials that mi croorganism s create do not directly produce periodontal disease. Instead, the changes are produced by the efforts of the host to fight off the microorganisms. T he substances produced by the defense mechanisms of the host may be re sponsible for the disease.”
Polysaccharides A nother com ponent of gingival tissue that ap parently plays a role in periodontal disease is a group of carbohydrates called polysaccharides, which serve as a sort of glue or filler betw een collagen fibers and which are destroyed along with the collagen. T he nature of the destruction of polysacchar ides, also referred to by the m ore technical name of glycosam inoglycans, was discussed by A udre W. L overde, assistant resident neuroscientist in the departm ent of neurosciences at the U niver sity of California, La Jolla. D r. L overde said that normal destruction of polysaccharides is a very com plicated series of steps and that it is not know n yet w hether poly saccharide destruction m ust necessarily accom pany the breaking down of collagen, although the two are usually seen together. She said that since collagen and polysaccharD re ie r: AAAS M E ETING ■ 699
gingival cells, but under certain conditions, such as in an immune reaction, they are produced in excess. Dr. G oodson said that prostaglandins, when overproduced by gingival cells, are capable of breaking down bone. H e said that that may be occurring at the same time that other substances are destroying collagen and polysaccharides. W ILLIA M A. PAYNE
P o lym orp honu clea r leukocytes
ides are found together in gingival tissue, it has not yet been ascertained which of the substances is destroyed first by the products that are formed against bacteria by the host, assuming that that is indeed what occurs.
P rostaglandins D estruction o f periodontal bone may be caused by prostaglandins, it was suggested by J. Max G oodson, associate professor in the departm ent o f oral biology, U niversity of California at San Francisco. Prostaglandins, which are a type of cellular horm one, have only recently been found in gin gival tissue. D r. G oodson said prostaglandins apparently are produced in m oderate am ounts by healthy
700 ■ JADA, V o l. 88, A p ril 1974
Thom as R. Tem pel, chief of periodontal re search with the maxillofacial sciences division of the Letterm an Arm y Institute of R esearch in San Francisco reported that periodontal tissues being irritated by plaque bacteria give off a sub stance that attracts polym orphonuclear leuko cytes, a type of white blood cell. D r. Tem pel said the leukocytes produce an enzyme that can be destructive to their periodontium . H ow ever, another researcher, William A. Payne, assistant professor of periodontics in the University of the Pacific School of D entistry, San Francisco, said his histologic studies have shown that polym orphonuclear leukocytes ap parently do not play a major role in the altera tion of collagen. H e said the collagen changes may be due to the release of toxins by lym phocytes. Also speaking at the session was Philip Per son, chief of the special research laboratory in the departm ent of biochem istry of the Brooklyn (NY ) V eterans Adm inistration H ospital. H e m ade introductory rem arks on the current state of biochemical research and how it relates to studies of periodontal disease.
M r. D re ie r is a s s o c ia te e d ito r o f th e AD A NEWS.
David L. Dreier, Chicago
Until a few years ago, most dental researchers believed that the destruction o f gingival collagen in periodontal disease must be the direct result o f action by bacterial plaque. That theory has largely given way to the view that the loss of collagen cells, which in aggregate serve as connective fibers in the periodontium, is also caused by substances released by the body’s own immune reaction to bacterial products. Further support for this newer theory was of fered recently in San Francisco at the 140th an nual meeting of the American Association for the Advancement o f Science, held Feb 24March 1 at the San Francisco Hilton Hotel. The session on biochemical lesions o f perio dontal disease was organized by Howard M. Myers, professor of biochemistry at the Univer sity of the Pacific School of Dentistry in San Francisco, and the late Isadore Zipkin, profes sor at the University of California at San Fran cisco School of Dentistry.
cells into an immune reaction by which so-called hypersensitive cells are formed. Dr. Page said other researchers have shown that the blood of periodontal patients carries lymphocytes that have been sensitized to the plaque antigens. The lymphocytes release sub stances to combat the products of the plaque bacteria, but those substances are also damaging to the cells of the periodontium. The professor said research data strongly in dicate that gingival collagen is lost through the
D ouble m echanism Roy C. Page, associate professor of pathology and periodontology at the University of Wash ington School of Dentistry in Seattle, empha sized that he still believes plaque formation is the primary first step in the chain o f events lead ing to tooth loss. H owever, he said, it is still very unclear just how the disease progresses from here. It appears likely, he added, that plaque bacteria release substances into the gingiva that spur the gingival 698 ■ JAD A, V o l. 88, A p ril 1974
HOWARD M. MYERS
double m echanism of the release of bacteria prod ucts and the immune reaction by the gingival cells to those substances. D r. Page said he believes the cells of the gin giva produce a great deal of collagen each day to enable the tissues around the teeth to be con stantly rejuvenated and revam ped. T he unused portion of newly created collagen undergoes nor mal destruction, he said. H ow ever, he added, in periodontal disease, this regular m echanism for maintaining the health of the supporting structures of the teeth is disrupted. H e explained that possibly m ore col lagen is destroyed, less is m ade, or the nature of the collagen is changed; or a com bination of these actions may be occurring. R esearch indicates the latter possibility; that is, a variety of factors operate to produce the 70% loss of collagen around the necks of teeth in patients with severe periodontal disease. With regard to the change in the nature of col lagen, D r. Page reported that he has found an unusual form of collagen in diseased periodontal tissues. H e said the characteristics of that col lagen and its role in the disease have not yet been determ ined. T he possibility that the body’s immune m ech anism could initiate a series of chemical reac tions resulting in the production of altered forms of collagen was substantiated by M arcel E. Nim ni, associate professor in the U niversity of Southern C alifornia’s departm ent of medicine and biochem istry. D r. Nim ni dem onstrated that with some types of arthritis, the body stops forming the type of collagen associated with cartilage and instead forms the type characteristic o f skin. H e sug gested the sam e sort of change may operate with periodontal disease. Com menting on research findings presented by the two scientists, D r. M yers said, “ R eplace ment of one type of collagen by another alters its function and this in turn may be responsible for the conditions seen in periodontal disease. In stead of forming the correct type of collagen that acts as fibrous bands to hold the gingiva close to the teeth, a different type of collagen is form ed.” H e added, “ T he purpose of the collagen in gingival tissue is to make a seal against the oral environm ent and failure to do this properly means that bacteria from the oral cavity can pen etrate the seal and lead to destruction of the sup porting tissues of the te e th .” Reiterating Dr. P age’s conclusions, D r. M yers said, “ T he changes that occur in periodontal dis-
ROY C. PAGE
ease evidently are not those produced by the at tacking microorganisms. This m eans that the products and toxins and toxic m aterials that mi croorganism s create do not directly produce periodontal disease. Instead, the changes are produced by the efforts of the host to fight off the microorganisms. T he substances produced by the defense mechanisms of the host may be re sponsible for the disease.”
Polysaccharides A nother com ponent of gingival tissue that ap parently plays a role in periodontal disease is a group of carbohydrates called polysaccharides, which serve as a sort of glue or filler betw een collagen fibers and which are destroyed along with the collagen. T he nature of the destruction of polysacchar ides, also referred to by the m ore technical name of glycosam inoglycans, was discussed by A udre W. L overde, assistant resident neuroscientist in the departm ent of neurosciences at the U niver sity of California, La Jolla. D r. L overde said that normal destruction of polysaccharides is a very com plicated series of steps and that it is not know n yet w hether poly saccharide destruction m ust necessarily accom pany the breaking down of collagen, although the two are usually seen together. She said that since collagen and polysaccharD re ie r: AAAS M E ETING ■ 699
gingival cells, but under certain conditions, such as in an immune reaction, they are produced in excess. Dr. G oodson said that prostaglandins, when overproduced by gingival cells, are capable of breaking down bone. H e said that that may be occurring at the same time that other substances are destroying collagen and polysaccharides. W ILLIA M A. PAYNE
P o lym orp honu clea r leukocytes
ides are found together in gingival tissue, it has not yet been ascertained which of the substances is destroyed first by the products that are formed against bacteria by the host, assuming that that is indeed what occurs.
P rostaglandins D estruction o f periodontal bone may be caused by prostaglandins, it was suggested by J. Max G oodson, associate professor in the departm ent o f oral biology, U niversity of California at San Francisco. Prostaglandins, which are a type of cellular horm one, have only recently been found in gin gival tissue. D r. G oodson said prostaglandins apparently are produced in m oderate am ounts by healthy
700 ■ JADA, V o l. 88, A p ril 1974
Thom as R. Tem pel, chief of periodontal re search with the maxillofacial sciences division of the Letterm an Arm y Institute of R esearch in San Francisco reported that periodontal tissues being irritated by plaque bacteria give off a sub stance that attracts polym orphonuclear leuko cytes, a type of white blood cell. D r. Tem pel said the leukocytes produce an enzyme that can be destructive to their periodontium . H ow ever, another researcher, William A. Payne, assistant professor of periodontics in the University of the Pacific School of D entistry, San Francisco, said his histologic studies have shown that polym orphonuclear leukocytes ap parently do not play a major role in the altera tion of collagen. H e said the collagen changes may be due to the release of toxins by lym phocytes. Also speaking at the session was Philip Per son, chief of the special research laboratory in the departm ent of biochem istry of the Brooklyn (NY ) V eterans Adm inistration H ospital. H e m ade introductory rem arks on the current state of biochemical research and how it relates to studies of periodontal disease.
M r. D re ie r is a s s o c ia te e d ito r o f th e AD A NEWS.