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Spirochaetes in periodontal disease
1177
EDITORIALS
periodontal pocket. Whether or not they are causal, however, spirochaetes are valuable indicator organisms for monitoring the status of disease.All the oral spirochaetes so far identified have been assigned to the genus Treponema. The best-known species associated with chronic periodontal disease is Treponema denticola, which in one study accounted for 90% of subgingival spirochaetes.3About 5% were T socranskii and the remaining 5 % were hitherto undescribed species.3At least ten treponemal species have been detected in periodontitis,4of which T pectinovorum and T socranskii are the most thoroughly characterised. There is some doubt whether T denticola is really the principal organism present or merely the most easily cultured. Lately,
Spirochaetes The
in
periodontal disease
periodontal disease covers conditions from acute ranging necrotising ulcerative gingivitis to chronic gingivitis and chronic inflammatory periodontal disease. These disorders can cause distress and can be difficult, expensive, and timeconsuming to treat. In many cases chronic periodontal disease is refractory to therapy and, by destroying supporting bone, causes loss of teeth. In the aetiology of periodontal disease, dental plaque bacteria are clearly important,! but which specific microorganisms or groups of microorganisms are relevant? In the subgingival plaque of patients with disease, a wide range of organisms may be observed by dark-field or phase-contrast microscopy. The most distinctive are the spirochaetes, which may be the predominant type of organism seen.2Various morphotypes of spirochaete can be observed but many of these have resisted culture in vitro. As a group, their properties are therefore poorly characterised and there are many unanswered questions about their taxonomic relationships, antigenic and physiological properties, and virulence factors. Current developments in ribosomal RNA sequencing and the design of specific genetic probes should complement immunocytochemical methods in the identification of non-cultivable organisms as well as the resolution of questions about term
taxonomy. We do
yet know whether spirochaetes contribute to the disease process or are simply opportunists exploiting the new anaerobic, nutrientrich, ecological niche created in the developing not
monoclonal antibodies to T denticola have been used in assays of plaque samples from patients with chronic adult periodontitis, and there was a positive correlation between numbers of a particular serotype of T denticola and severe disease.5,6Raised serum antibodies to T denticola in affected patients, particularly antibodies to certain polypeptide antigens, likewise speak for an association."’ However, we cannot say whether such antibody was induced by T denticola itself or by a cross-reacting spirochaete. Spirochaetes can be acquired in childhood and are also commonly associated with acute necrotising ulcerative gingivitis (otherwise known as Vincent’s disease or trench mouth), 12 but again difficulties in the culture and enumeration of the organisms have made their importance hard to assess.
Of the species of oral spirochaetes that have been studied in detail, it is clear that some could contribute to the pathogenic process. Electron microscopy of periodontal pockets has shown spirochaetes of subgingival plaque in direct contact with the pocket epithelium and with polymorphonuclear leucocytesevidence that they have specific binding sites. 13 T denticola also produces a wide range of enzymes capable of degrading substrates including collagen, fibrin, keratin, and glycosaminoglycans, and may thereby take part in the destruction of soft tissue and bone. Suppression of lymphocyte responses and fibroblast proliferation14,15 may likewise be important. Another observation is that in some forms of periodontal disease spirochaetes are capable of invading the epithelium, though the invading species remain unidentified. Riviere et al 16,17 report that infected gingival tissue and plaque from periodontitis patients contain spirochaetes that do not seem to react with the monoclonal antibodies to T denticola but do react with monoclonal antibodies to T pallidum, the agent of syphilis. These differences are the more impressive because the two species have much in common: they share surface structural similarities18 and several surface cross-reactive antigens; and although their guanosine and cytidine contents differ, the 16S ribosomal RNA sequences cluster them
together.19
1178
The new results are therefore noteworthy for several reasons-the identification of an apparently novel oral species, the demonstration of its ability to penetrate tissue, and the evidence of a relationship between an oral organism and a species with known pathogenic effects at many sites. Besides providing information directly related to periodontal disease, work on the cultivable species of oral spirochaetes such as T denticola may thus prove valuable in exploration of the structure and function of components that have analogues in Tpallidum. 1.
Socranksy SS, Haffajee AD. Microbial mechanisms in the pathogenesis of destructive periodontal diseases: a critical assessment. J Periodont
Res 1991; 26: 195-212. WJ. The role of spirochaetes in periodontal disease. Adv Dent Res 1988; 2: 275-83. 3. Salvador SL, Syed SA, Loesche WJ. Comparison of three dispersion procedures for quantitative recovery of cultivable species of subgingival spirochaetes. J Clin Microbiol 1987; 25: 2230-32. 4. Moore WEC. Microbiology of periodontal disease. J Periodont Res 1987; 22: 335-41. 5. Simonson LG, Goodman CH, Morton HE. Quantitative immunoassay of Treponema denticola serovar C in adult periodontitis. J Clin Microbiol 1990; 28: 1493-96. 6. Simonson LG, Goodman CH, Bial JJ, Morton HE. Quantitative relationship of Treponema denticola to severity of periodontal disease. Infect Immun 1988; 56: 726-28. 7. Jacob E, Meiller TF, Nanman RK. Detection of elevated serum antibodies to Treponema denticola in humans with advanced periodontitis by an enzyme-linked immunosorbent assay. J Periodont Res 1982; 17: 145-53. 8. Mangan DF, Langon BE, Bower B, Lopatin DE. In vitro lymphocyte blastogenic responses and titers of humoral antibodies from periodontitis patients to oral spirochete isolates. Infect Immun 1982; 37: 445-51. 9. Tew JG, Smibert RM, Scott EA, Burmeister JA, Rannay RR. Serum antibodies in young adult humans reactive with periodontitis associated treponemes. J Periodont Res 1985; 20: 580-90. 10. Lai C-H, Listgarten MA, Evian CI, Dougherty P. Serum IgA and IgG antibodies to Treponema vincentii and Treponema denticola in adult periodontitis, juvenile periodontitis and periodontally healthy subjects. J Clin Periodontol 1986; 13: 752-57. 11. Umemoto T, Zambon JJ, Genco RJ, Namikawa I. Major antigens of human oral spirochaetes associated with periodontal disease. Adv Dent Res 1988; 2: 292-96. 12. Johnson BD, Engel D. Acute necrotizing ulcerative gingivitis: a review of diagnosis, etiology and treatment. J Periodontol 1986; 57: 141-50. 13. Dawson JR, Ellen RP. Tip-oriented adherence of Treponema denticola to fibronectin. Infect Immun 1990; 58: 3924-28. 14. Boehringer H, Taichman NS, Shenker BJ. Suppression of fibroblast proliferation by oral spirochetes. Infect Immun 1984; 45: 155-59. 15. Shenker BJ, Listgarten MA, Taichman NS. Suppression of human lymphocyte responses by oral spirochetes: a monocyte dependent phenomenon. J Immunol 1984; 132: 2039-45. 16. Barron SL, Riviere GR, Simonson LG, Lukehart SA, Tira DE, O’Neil DW. Use of monoclonal antibodies to enumerate spirochaetes and identify Treponema denticola in dental plaque of children, adolescents and young adults. Oral Microbiol Immunol 1991; 6: 97-101. 17. Riviere GR, Wagoner MA, Baker-Zander SA, et al. Identification of spirochetes related to Treponema pallidum in necrotising ulcerative gingivitis and chronic periodontitis. N Engl J Med 1991; 325: 539-43. 18. Cockayne A, Sanger R, Ivic A, et al. Antigenic and structural analysis of Treponema denticola. J Gen Microbiol 1989; 135: 3209-18. 19. Paster BJ, Dewhirst FE, Weisburg WG, et al. Phylogenetic analysis of the spirochetes. J Bacteriol 1991; 173: 6101-09. 2. Loesche
Pacemakers—practice and paradox The speed of advance in many branches of medicine tends to outrun the production time of the standard textbook, so it is often difficult to distinguish the orthodox view or treatment of a particular
condition from the hullabaloo of conflicting opinions. In the September issue of the British Heart Journal) Brugadal takes issue with the use of the word "conventional" to describe one of the more recent techniques for ablation of atrioventricular conduction. Clear statements of practices that are currently believed to be optimum are especially necessary at a time when the potentially conflicting requirements of clinical versus budgetary audit are uppermost in many minds. This need was well appreciated in the USA over a decade ago when the American College of Cardiology and the American Heart Association (ACC/AHA) established a joint task force on assessment of cardiovascular procedures in 1980. The task force subcommittee on pacemaker implantation first reported in 19842 and introduced three classes for the various conditions that might require permanent pacemaker implantation: class 1 consists of conditions that are generally accepted as requiring a pacemaker; class 2 of conditions often treated with pacing but where there is some controversy; and class 3 of conditions not requiring pacemaker implantation. The report ended by suggesting the most appropriate type of device for different conditions. In July this year the ACC/AHA published a revised version of their 1984 report.3A month later came the recommendations of a working party of the British Pacing and Electrophysiological Group,4mainly concerned with the type of pacemaker ("pacemaker prescription") most suited to different bradycardiaproducing conditions. In general, the British group accepted the indications for pacing put forward by the 1984 ACC/AHA report but chose to differ with respect to the management of the carotid sinus and malignant vasovagal syndromes and some forms of second-degree atrioventricular block. The revised American report was more favourably disposed towards pacing for carotid sinus syndrome and vasovagal syndrome, thereby approaching the British view, but made no change for high atrioventricular (Wenckebach) second degree block.3 In the absence of symptoms, this condition was regarded as benign and not an indication for pacing. Such a view was orthodox in 1984 but was questioned the following year with the publication of a long-term follow-up study which showed that pacer implantation lengthened the survival of elderly patients with chronic second degree atrioventricular block, irrespective of its site.5,6The ACC/AHA report gave qualified support (class 2) to pacing symptomfree patients with Wenckebach second degree block within the His bundle, but this condition can only be diagnosed by His bundle electrography, which is seldom carried out routinely. Moreover, even when this technique is used, it can be difficult to detect both elements of the "split His" potential.’ There is much to be said for the British group’s recommendation that elderly patients with chronic second degree block, whether Wenckebach or Mobitz 2 (ie, distal), should qualify for pacemaker implantation.
EDITORIALS
periodontal pocket. Whether or not they are causal, however, spirochaetes are valuable indicator organisms for monitoring the status of disease.All the oral spirochaetes so far identified have been assigned to the genus Treponema. The best-known species associated with chronic periodontal disease is Treponema denticola, which in one study accounted for 90% of subgingival spirochaetes.3About 5% were T socranskii and the remaining 5 % were hitherto undescribed species.3At least ten treponemal species have been detected in periodontitis,4of which T pectinovorum and T socranskii are the most thoroughly characterised. There is some doubt whether T denticola is really the principal organism present or merely the most easily cultured. Lately,
Spirochaetes The
in
periodontal disease
periodontal disease covers conditions from acute ranging necrotising ulcerative gingivitis to chronic gingivitis and chronic inflammatory periodontal disease. These disorders can cause distress and can be difficult, expensive, and timeconsuming to treat. In many cases chronic periodontal disease is refractory to therapy and, by destroying supporting bone, causes loss of teeth. In the aetiology of periodontal disease, dental plaque bacteria are clearly important,! but which specific microorganisms or groups of microorganisms are relevant? In the subgingival plaque of patients with disease, a wide range of organisms may be observed by dark-field or phase-contrast microscopy. The most distinctive are the spirochaetes, which may be the predominant type of organism seen.2Various morphotypes of spirochaete can be observed but many of these have resisted culture in vitro. As a group, their properties are therefore poorly characterised and there are many unanswered questions about their taxonomic relationships, antigenic and physiological properties, and virulence factors. Current developments in ribosomal RNA sequencing and the design of specific genetic probes should complement immunocytochemical methods in the identification of non-cultivable organisms as well as the resolution of questions about term
taxonomy. We do
yet know whether spirochaetes contribute to the disease process or are simply opportunists exploiting the new anaerobic, nutrientrich, ecological niche created in the developing not
monoclonal antibodies to T denticola have been used in assays of plaque samples from patients with chronic adult periodontitis, and there was a positive correlation between numbers of a particular serotype of T denticola and severe disease.5,6Raised serum antibodies to T denticola in affected patients, particularly antibodies to certain polypeptide antigens, likewise speak for an association."’ However, we cannot say whether such antibody was induced by T denticola itself or by a cross-reacting spirochaete. Spirochaetes can be acquired in childhood and are also commonly associated with acute necrotising ulcerative gingivitis (otherwise known as Vincent’s disease or trench mouth), 12 but again difficulties in the culture and enumeration of the organisms have made their importance hard to assess.
Of the species of oral spirochaetes that have been studied in detail, it is clear that some could contribute to the pathogenic process. Electron microscopy of periodontal pockets has shown spirochaetes of subgingival plaque in direct contact with the pocket epithelium and with polymorphonuclear leucocytesevidence that they have specific binding sites. 13 T denticola also produces a wide range of enzymes capable of degrading substrates including collagen, fibrin, keratin, and glycosaminoglycans, and may thereby take part in the destruction of soft tissue and bone. Suppression of lymphocyte responses and fibroblast proliferation14,15 may likewise be important. Another observation is that in some forms of periodontal disease spirochaetes are capable of invading the epithelium, though the invading species remain unidentified. Riviere et al 16,17 report that infected gingival tissue and plaque from periodontitis patients contain spirochaetes that do not seem to react with the monoclonal antibodies to T denticola but do react with monoclonal antibodies to T pallidum, the agent of syphilis. These differences are the more impressive because the two species have much in common: they share surface structural similarities18 and several surface cross-reactive antigens; and although their guanosine and cytidine contents differ, the 16S ribosomal RNA sequences cluster them
together.19
1178
The new results are therefore noteworthy for several reasons-the identification of an apparently novel oral species, the demonstration of its ability to penetrate tissue, and the evidence of a relationship between an oral organism and a species with known pathogenic effects at many sites. Besides providing information directly related to periodontal disease, work on the cultivable species of oral spirochaetes such as T denticola may thus prove valuable in exploration of the structure and function of components that have analogues in Tpallidum. 1.
Socranksy SS, Haffajee AD. Microbial mechanisms in the pathogenesis of destructive periodontal diseases: a critical assessment. J Periodont
Res 1991; 26: 195-212. WJ. The role of spirochaetes in periodontal disease. Adv Dent Res 1988; 2: 275-83. 3. Salvador SL, Syed SA, Loesche WJ. Comparison of three dispersion procedures for quantitative recovery of cultivable species of subgingival spirochaetes. J Clin Microbiol 1987; 25: 2230-32. 4. Moore WEC. Microbiology of periodontal disease. J Periodont Res 1987; 22: 335-41. 5. Simonson LG, Goodman CH, Morton HE. Quantitative immunoassay of Treponema denticola serovar C in adult periodontitis. J Clin Microbiol 1990; 28: 1493-96. 6. Simonson LG, Goodman CH, Bial JJ, Morton HE. Quantitative relationship of Treponema denticola to severity of periodontal disease. Infect Immun 1988; 56: 726-28. 7. Jacob E, Meiller TF, Nanman RK. Detection of elevated serum antibodies to Treponema denticola in humans with advanced periodontitis by an enzyme-linked immunosorbent assay. J Periodont Res 1982; 17: 145-53. 8. Mangan DF, Langon BE, Bower B, Lopatin DE. In vitro lymphocyte blastogenic responses and titers of humoral antibodies from periodontitis patients to oral spirochete isolates. Infect Immun 1982; 37: 445-51. 9. Tew JG, Smibert RM, Scott EA, Burmeister JA, Rannay RR. Serum antibodies in young adult humans reactive with periodontitis associated treponemes. J Periodont Res 1985; 20: 580-90. 10. Lai C-H, Listgarten MA, Evian CI, Dougherty P. Serum IgA and IgG antibodies to Treponema vincentii and Treponema denticola in adult periodontitis, juvenile periodontitis and periodontally healthy subjects. J Clin Periodontol 1986; 13: 752-57. 11. Umemoto T, Zambon JJ, Genco RJ, Namikawa I. Major antigens of human oral spirochaetes associated with periodontal disease. Adv Dent Res 1988; 2: 292-96. 12. Johnson BD, Engel D. Acute necrotizing ulcerative gingivitis: a review of diagnosis, etiology and treatment. J Periodontol 1986; 57: 141-50. 13. Dawson JR, Ellen RP. Tip-oriented adherence of Treponema denticola to fibronectin. Infect Immun 1990; 58: 3924-28. 14. Boehringer H, Taichman NS, Shenker BJ. Suppression of fibroblast proliferation by oral spirochetes. Infect Immun 1984; 45: 155-59. 15. Shenker BJ, Listgarten MA, Taichman NS. Suppression of human lymphocyte responses by oral spirochetes: a monocyte dependent phenomenon. J Immunol 1984; 132: 2039-45. 16. Barron SL, Riviere GR, Simonson LG, Lukehart SA, Tira DE, O’Neil DW. Use of monoclonal antibodies to enumerate spirochaetes and identify Treponema denticola in dental plaque of children, adolescents and young adults. Oral Microbiol Immunol 1991; 6: 97-101. 17. Riviere GR, Wagoner MA, Baker-Zander SA, et al. Identification of spirochetes related to Treponema pallidum in necrotising ulcerative gingivitis and chronic periodontitis. N Engl J Med 1991; 325: 539-43. 18. Cockayne A, Sanger R, Ivic A, et al. Antigenic and structural analysis of Treponema denticola. J Gen Microbiol 1989; 135: 3209-18. 19. Paster BJ, Dewhirst FE, Weisburg WG, et al. Phylogenetic analysis of the spirochetes. J Bacteriol 1991; 173: 6101-09. 2. Loesche
Pacemakers—practice and paradox The speed of advance in many branches of medicine tends to outrun the production time of the standard textbook, so it is often difficult to distinguish the orthodox view or treatment of a particular
condition from the hullabaloo of conflicting opinions. In the September issue of the British Heart Journal) Brugadal takes issue with the use of the word "conventional" to describe one of the more recent techniques for ablation of atrioventricular conduction. Clear statements of practices that are currently believed to be optimum are especially necessary at a time when the potentially conflicting requirements of clinical versus budgetary audit are uppermost in many minds. This need was well appreciated in the USA over a decade ago when the American College of Cardiology and the American Heart Association (ACC/AHA) established a joint task force on assessment of cardiovascular procedures in 1980. The task force subcommittee on pacemaker implantation first reported in 19842 and introduced three classes for the various conditions that might require permanent pacemaker implantation: class 1 consists of conditions that are generally accepted as requiring a pacemaker; class 2 of conditions often treated with pacing but where there is some controversy; and class 3 of conditions not requiring pacemaker implantation. The report ended by suggesting the most appropriate type of device for different conditions. In July this year the ACC/AHA published a revised version of their 1984 report.3A month later came the recommendations of a working party of the British Pacing and Electrophysiological Group,4mainly concerned with the type of pacemaker ("pacemaker prescription") most suited to different bradycardiaproducing conditions. In general, the British group accepted the indications for pacing put forward by the 1984 ACC/AHA report but chose to differ with respect to the management of the carotid sinus and malignant vasovagal syndromes and some forms of second-degree atrioventricular block. The revised American report was more favourably disposed towards pacing for carotid sinus syndrome and vasovagal syndrome, thereby approaching the British view, but made no change for high atrioventricular (Wenckebach) second degree block.3 In the absence of symptoms, this condition was regarded as benign and not an indication for pacing. Such a view was orthodox in 1984 but was questioned the following year with the publication of a long-term follow-up study which showed that pacer implantation lengthened the survival of elderly patients with chronic second degree atrioventricular block, irrespective of its site.5,6The ACC/AHA report gave qualified support (class 2) to pacing symptomfree patients with Wenckebach second degree block within the His bundle, but this condition can only be diagnosed by His bundle electrography, which is seldom carried out routinely. Moreover, even when this technique is used, it can be difficult to detect both elements of the "split His" potential.’ There is much to be said for the British group’s recommendation that elderly patients with chronic second degree block, whether Wenckebach or Mobitz 2 (ie, distal), should qualify for pacemaker implantation.