646
Letters to the Editor To the Editor: re: Antibiotic Prophylaxis for Medical-Risk Patients (J Periodontol 1991; 62:227-231) The above cited article reported the new recommendations of the American Heart Association concerning prophylactic antibiotic regimens for bacterial endocarditis. The American Heart Association recommendations contained an error in that 1600 mg of erythromycin ethylsuccinate should be taken 2 hours before the appointment rather than the 800 mg listed as 400 mg of EES is equivalent to 250 mg of erythromycin stéarate. This was printed incorrectly in the Journal of the American Medical Association (1990;264— 2919-2922) and the Journal of the American Dental Association (1991; 122:87-91).— Steven M. Pollack, University of Mississippi Medical Center.
Antibiotic Prophylaxis for Medical-Risk patients It is with great interest that I have read the above cited article. I think that letters to the editor should only be written on very rare occasions and only if a controversy of arguments could have misleading sequels. In the mentioned article such a paragraph is included on page 228: re:
Local application of Chlorhexidine may itself induce bacteremia and should only be used immediately before the dental procedure and after systemic prophylaxis is in place. Prolonged use of Chlorhexidine prior to the dental procedure is not recommended as this may result in the selection of antibiotic-resistant oral streptococci, enteric Gram-negative rods, and a
pseudomonads. After searching through the
literature I am not aware of any scientific evidence which would support this statement. On the contrary, Chlorhexidine rinses have been used in several instances for prolonged periods of time in medically compromised patients, such as bone marrow transplantation and AIDS patients. As reported at the 4th International Conference on AIDS in Stockholm, Sweden, 1988, Grassi et al. demonstrated the great beneficial effects of Chlorhexidine application in AIDS patients (Abstract 7579). If bacteremia would be a problem following the use of Chlorhexidine no such effects or even exacerbation of infection would have to be expected. I therefore think that the above statement is grossly misleading the profession. If statements of that nature are made, they should at least be documented with adequate references.— N. P. Lang, University of Berne.
Regarding Dr. Pollock's issue of the erythromycin ethylsuccinate dosage, in early January 1991, our pharmacist at the USC School of Dentistry contacted the American Heart Association (AHA) in Dallas regarding our impression that this dose was not fully bioavailable (800 mg resulting in only 500 mg of drug actually absorbed and active). We were told that the matter would be addressed at some future time. We recognized a potential problem but did not feel compelled to change the AHA recommendations unilaterally. We again contacted the AHA (Los Angeles Chapter) on June 3, 1991 and were told that the AHA had not changed the erythromycin ethylsuccinate dose and had no immediate plan for doing so. To date, neither the AHA nor the ADA has provided any written statements on this issue. Dr. Pollock is then correct that the current dosages of the ethylsuccinate salt may not be fully bioavailable. The practitioner may then choose to: 1) double the dose of erythromycin ethylsuccinate (for which we see no objection); or 2) use the stéarate salt form at 1000 mg initially and 500 mg for the second dose thereby avoiding the entire issue. Dr. Lang takes issue with our discussion of the bacteremic potential of topical Chlorhexidine and its selection of resistant microorganisms. Bender et al.1 cautioned that the subgingival application of Chlorhexidine by irrigation may itself induce a bacteremia (as acknowledged by the AHA2), thereby necessitating prior systemic antibiotic prophylaxis. MacFarlane et al.3 demonstrated that 16/20 patients receiving a saline irrigation of the gingival sulcus prior to dental extractions experienced a bacteremia. The issue then appears settled that active gingival irrigation with antiseptic fluids requires prior antibiotic prophylaxis for patients at high risk from bacteremia. Dr. Lang's concerns appear more directed towards the prolonged use of Chlorhexidine in patients at-risk from oral bacteremias. Unfortunately, the current AHA recommendations in this regard are vague: "Individuals who are at risk for developing bacterial endocarditis should establish and maintain the best oral health to reduce potential sources of bacterial seeding. Dentists should make every attempt to reduce gingival inflammation in patients who are at risk by means of brushing, flossing, fluoride rinse, Chlorhexidine gluconate mouth rinse, and professional cleaning before proceeding with routine dental procedures. Chlorhexidine that is painted on isolated and dried gingiva 3 to 5 minutes prior to tooth extraction has been shown to reduce postoperative bacteremia." These statements could be interpreted to endorse the prolonged use of Chlorhexidine or to primarily advocate its use immediately before dental treatment.
Authors' Response: We thank Drs. Pollock and Lang for their interest in our article and welcome the opportunity to address their concerns.
There is little doubt that good oral hygiene may reduce the incidence and magnitude of orally-induced bacteremias. It is also very likely Chlorhexidine can aid in this regard.
Volume 62 Number 10
647
However, several questions remain. If Chlorhexidine or any
other liquid is employed in a vigorous manner, this might be analagous to gingival irrigation. Whether gentle supragingival rinsing with oral liquids induces a bacteremia is open to speculation since, to our knowledge, no controlled clinical studies have been performed. Of possibly greater concern is the potential for Chlorhexidine, while suppressing many viridans streptococci, to allow for the greater dominance of other bacteremic microorganisms. Such potential would likely increase with prolonged use. If Chlorhexidine does not alter the microbial ratio and composition of the targeted indigenous flora, it would be unique among antimicrobials. In 1975, Johansen et al.4 demonstrated that prolonged Chlorhexidine use (beyond 6 months) has little plaque and gingivitis-reducing effect probably due to growth of resistant organisms. Chlorhexidine rinses seem unable to suppress various enteric species, pseudomonads and enterococci in the human mouth5 8 and may even cause overgrowth of enteric rods in beagle dogs9 and certain compromised
patients.10-11
These above organisms can induce infective endocarditis and in such cases are associated with higher endocarditis mortality rates than viridans streptococci.12'13 The issue then appears to be the benefit of reducing major oral organisms
responsible for infective endocarditis (viridans streptococci) versus the potential for selection of possibly more lethal bacteremic organisms (pseudomonads, enterococci, and enteric species). Until the patient risk-benefit ratio is fully addressed in large study populations, since infective endocarditis is such
event, it appears best to stay within the confines of generally accepted principles of antibiotic prophylaxis. The guidelines for antibiotic prophylaxis to prevent infective endocarditis are much the same as for antimicrobial therapy of active infections: high doses for as short a time as possible to achieve optimum antibiotic activity during the period of patient risk and to reduce toxicity, allergy, and the selection of drug-resistant microorganisms. It is our opinion that the rules of antibiotic endocarditis prophylaxis are the same whether the antimicrobials are used systemically or topically. Individuals who favor some other protocol should gather laboratory and clinical evidence to substantiate their thesis that such rules do not apply to Chlorhexidine under the experimental and clinical conditions that surround infective endocarditis. Until such data become available, we caution against a prolonged use of Chlorhexidine or any other antimicrobial agent in infective endocarditis prophylaxis.—Thomas J. Pallasch, Jorgen Slots, University of Southern California.
docarditis: Recommendations by the American Heart Association. J Amer Med Assn 1990;264:2919-2922. 3. MacFarlane TW, Ferguson MM, Mulgrew CJ. Post-extraction bacteremia: Role of antiseptics and antibiotics. Brit Dent] 1984;156:179184. 4. Johansen JR, Gjermo P, Eriksen HM. Effect of 2-year's use of chlorhexidine-containing dentifrices on plaque, gingivitis and caries. Scand J Dent Res 1975;83:288-292. 5. Emilson CG, Fornell J. Effect of toothbrushing with Chlorhexidine gel on salivary microflora, oral hygiene and caries. Scand J Dent Res
1976;84:308-319. TE, Babalola OO, Slots J. Subgingival occurrence of enteric rods, yeasts and staphylococci after systemic doxycycline therapy. Oral Microbio! Immunol 1990;5:166-168. 7. Spijkervet FKL, van Saene HKF, Panders AK, et al. Effect of Chlor6. Rams
hexidine rinsing on the oropharngeal ecology in patients with head and neck cancer who have irradiation mucositis. Oral Surg Oral Med OralPathol 1989;67:154-161. 8. Wahlin YB, Holm -K. Changes in the oral microflora in patients with acute leukemia and related disorders during the period of induction therapy. Oral Surg Oral Med Oral Pathol 1988;65:411^117. 9. Hamp S-E, Emilson CG. Some effects of Chlorhexidine on the plaque flora of the Beagle dog. / Periodont Res 1973: 8(Suppl 12):28-35. 10. Ferretti GA, Ash RC, Brown AT, et al. Control of oral mucositis and candidiasis in marrow transplantation: A prospective, double blind trial of Chlorhexidine gluconate oral rinse. Bone Marrow Transp
1988;3:483-494.
11. Ferretti GA, Raybould TP, Brown AT, et al. Chlorhexidine prophylaxis for chemotherapy- and radiotherapy-induced stomatitis: A randomized double-blind trial. Oral Surg Oral Med Oral Pathol
1990;69:331-338. 12. Weinstein L. Infective endocarditis. In: Heart Disease: A Textbook of Cardiovascular Medicine, 2nd ed. Braunwald E, ed. Philadelphia: W.B. Saunders, 1984. 13. Durack DT. Infective and noninfective endocarditis. In: The Heart, 7th ed. Hurst JW, Schlant RC, Rackley CE, Sonnenblick EH, Wenger NK, eds. New York: McGraw-Hill, 1990.
a rare
References 1. Bender IB, Naidorf IJ, and Garvey GJ. Bacterial endocarditis:
A
consideration for physicians and dentists. / Amer Dent Assn 1984; 109:415^120. 2. Dajani AS, Bisno AL, Chung KJ, et al: Prevention of bacterial en-
To the Editor: re:
Guest Editorial: Diabetes and Periodontal Disease
(J Periodontol 1991;62:161-163) Dr. Robert Gottsegen's recent editorial on the role of diabetes mellitus in periodontal disease raises some interesting
questions.
As a member of two ADA's, the American Diabetes Association and the American Dental Association, I know that both groups are aware of the interconnection between the oral cavity and the rest of the body. But this awareness is marginal, at best. In the 1990 1991 Clinical Practice Recommendations the Diabetes American Association, no mention of the of of oral health be found. The position statecan importance ments range from somewhat general to quite specific. There is a position statement on the use of non-caloric sweeteners, but not on the need for dental check-ups. In no way can the blame for this be placed on the American Diabetes Association. It has done an excellent job of formulating and updating this information. Clinicians and researchers have input. Unfortunately, dentists do not join in any great number. The American Dental Association appears to be unaware of any need for input and dialogue. —
648
J Periodontol October 1991
LETTERS TO THE EDITOR
The recommendations and guidelines should be formulated by a committee of dentists familiar with the diabetic's problems. We are aware that diabetics may need more intensive dental treatment to maintain oral health and comfort. There may be times when treatment should be deferred. There are many questions to be addressed. These guidelines should be updated as needed. In diabetic individuals with infection, blood sugar rises. The higher the blood sugar, the more difficult it is to control infection. The destabilized insulin-blood sugar balance makes the goals of treatment-normoglycemia even more difficult to achieve. We, as dentists, treat Periodontitis, a disease of the oral tissues intimately connected with the infective process. It is a disease afflicting diabetic individuals with greater frequency, earlier in life, and with more destructiveness, than the general population. I see occasional review articles but little new research is being done in this area. The research which is done usually investigates (and confirms) the statistical significance of the relation between diabetes and periodontal disease. The other side of the coin is being neglected. We need to quantify the degree to which elimination of oral infection improves diabetic control and reduces insulin requirements. For instance, back in 1960 (!) Williams and Mahan reported their findings in the Journal of the American Medical Association. They found, after treatment for Periodontitis, 7 of 9 patients had reduced insulin needs. As far as I am aware, little has been published since then. Further, as pointed out in the Guest Editorial the level of standardization of the research leads to confusion. The 2 studies Dr. Gottsegen referred to may appear somewhat
conflicting.
Now, many of the problems inherent in periodontal recan be dealt with adequately and easily. In addition,
search
technological
advances have improved the ability of the researcher to monitor blood glucose levels. Home blood glucose monitoring units which can easily record and store the time and result of a test are more readily available. The memory chip can be retrieved and replaced by the research team. We should foster awareness in the dental profession of the requirement for greater awareness of diabetic needs and more research into dental infection and its relation to glycémie control. Research teams should be led by dentists. There should be greater communication by the dentist with the treating endocrinologist and with the diabetic educators. I would like to see the diabetic community better served by my fellow professionals and more meaningful input by
dentists into the daily lives of diabetic individuals.—Joanne Eisen, Old Bethpage, NY.
D.
To the Editor: re: Treatment of Periodontal Defects With an Absorbable Membrane (Polyglactin 910) With and Without Osseous Grafting (J Periodontol 1991; 276-
283)
Some
questions need to be raised about the 12 clinical case
reports published in the above article by Gager and Schultz.
There is considerable documentation in the literature and
experience indicating that the type of periodontal lesion described by the authors heal quite routinely and completely following debridement and curettage of the osseous defects. One need not go further than to refer to the early work of
Prichard and other clinicians who achieved considerable repair and regeneration in similar lesions with simple "clean out" procedures. While guided tissue regeneration may be considered by some a viable approach to treatment of periodontal lesions such as furcation involvements which continue to remain a challenge in periodontal therapy, the concept of using barrier membranes and/or grafts for treatment of lesions that heal spontaneously following simple curettage remains enigmatic to vat.—Bernard S. Moskow, Columbia University School of Dental and Oral Surgery.
Authors' Response: As Dr. Moskow has pointed out, some periodontal lesions do heal partially with techniques other than guided tissue regeneration. As clinicians we have observed this in isolated cases, and our patients have benefited. However, we could disagree with Dr. Moskow's impression that lesions such as we have treated heal "routinely and completely" following curettage alone. One need go no further than the carefully controlled reports in the literature comparing various regenerative methods. The control sites are often treated with flap debridement alone, and they do not heal "completely." Indeed, if curettage (open or closed) were such a predictable procedure, Periodontitis might not be the leading cause of tooth loss which it is. Much needs to be learned about GTR, and hopefully in the future we will have even better methods. However its current use is hardly enigmatic. The preponderance of the literature and clinical practice indicate that GTR is the best we have at this time.—Arthur H. Gager, Wells, ME and Allen J. Schultz, Mission Viejo, CA.
Letters to the Editor To the Editor: re: Antibiotic Prophylaxis for Medical-Risk Patients (J Periodontol 1991; 62:227-231) The above cited article reported the new recommendations of the American Heart Association concerning prophylactic antibiotic regimens for bacterial endocarditis. The American Heart Association recommendations contained an error in that 1600 mg of erythromycin ethylsuccinate should be taken 2 hours before the appointment rather than the 800 mg listed as 400 mg of EES is equivalent to 250 mg of erythromycin stéarate. This was printed incorrectly in the Journal of the American Medical Association (1990;264— 2919-2922) and the Journal of the American Dental Association (1991; 122:87-91).— Steven M. Pollack, University of Mississippi Medical Center.
Antibiotic Prophylaxis for Medical-Risk patients It is with great interest that I have read the above cited article. I think that letters to the editor should only be written on very rare occasions and only if a controversy of arguments could have misleading sequels. In the mentioned article such a paragraph is included on page 228: re:
Local application of Chlorhexidine may itself induce bacteremia and should only be used immediately before the dental procedure and after systemic prophylaxis is in place. Prolonged use of Chlorhexidine prior to the dental procedure is not recommended as this may result in the selection of antibiotic-resistant oral streptococci, enteric Gram-negative rods, and a
pseudomonads. After searching through the
literature I am not aware of any scientific evidence which would support this statement. On the contrary, Chlorhexidine rinses have been used in several instances for prolonged periods of time in medically compromised patients, such as bone marrow transplantation and AIDS patients. As reported at the 4th International Conference on AIDS in Stockholm, Sweden, 1988, Grassi et al. demonstrated the great beneficial effects of Chlorhexidine application in AIDS patients (Abstract 7579). If bacteremia would be a problem following the use of Chlorhexidine no such effects or even exacerbation of infection would have to be expected. I therefore think that the above statement is grossly misleading the profession. If statements of that nature are made, they should at least be documented with adequate references.— N. P. Lang, University of Berne.
Regarding Dr. Pollock's issue of the erythromycin ethylsuccinate dosage, in early January 1991, our pharmacist at the USC School of Dentistry contacted the American Heart Association (AHA) in Dallas regarding our impression that this dose was not fully bioavailable (800 mg resulting in only 500 mg of drug actually absorbed and active). We were told that the matter would be addressed at some future time. We recognized a potential problem but did not feel compelled to change the AHA recommendations unilaterally. We again contacted the AHA (Los Angeles Chapter) on June 3, 1991 and were told that the AHA had not changed the erythromycin ethylsuccinate dose and had no immediate plan for doing so. To date, neither the AHA nor the ADA has provided any written statements on this issue. Dr. Pollock is then correct that the current dosages of the ethylsuccinate salt may not be fully bioavailable. The practitioner may then choose to: 1) double the dose of erythromycin ethylsuccinate (for which we see no objection); or 2) use the stéarate salt form at 1000 mg initially and 500 mg for the second dose thereby avoiding the entire issue. Dr. Lang takes issue with our discussion of the bacteremic potential of topical Chlorhexidine and its selection of resistant microorganisms. Bender et al.1 cautioned that the subgingival application of Chlorhexidine by irrigation may itself induce a bacteremia (as acknowledged by the AHA2), thereby necessitating prior systemic antibiotic prophylaxis. MacFarlane et al.3 demonstrated that 16/20 patients receiving a saline irrigation of the gingival sulcus prior to dental extractions experienced a bacteremia. The issue then appears settled that active gingival irrigation with antiseptic fluids requires prior antibiotic prophylaxis for patients at high risk from bacteremia. Dr. Lang's concerns appear more directed towards the prolonged use of Chlorhexidine in patients at-risk from oral bacteremias. Unfortunately, the current AHA recommendations in this regard are vague: "Individuals who are at risk for developing bacterial endocarditis should establish and maintain the best oral health to reduce potential sources of bacterial seeding. Dentists should make every attempt to reduce gingival inflammation in patients who are at risk by means of brushing, flossing, fluoride rinse, Chlorhexidine gluconate mouth rinse, and professional cleaning before proceeding with routine dental procedures. Chlorhexidine that is painted on isolated and dried gingiva 3 to 5 minutes prior to tooth extraction has been shown to reduce postoperative bacteremia." These statements could be interpreted to endorse the prolonged use of Chlorhexidine or to primarily advocate its use immediately before dental treatment.
Authors' Response: We thank Drs. Pollock and Lang for their interest in our article and welcome the opportunity to address their concerns.
There is little doubt that good oral hygiene may reduce the incidence and magnitude of orally-induced bacteremias. It is also very likely Chlorhexidine can aid in this regard.
Volume 62 Number 10
647
However, several questions remain. If Chlorhexidine or any
other liquid is employed in a vigorous manner, this might be analagous to gingival irrigation. Whether gentle supragingival rinsing with oral liquids induces a bacteremia is open to speculation since, to our knowledge, no controlled clinical studies have been performed. Of possibly greater concern is the potential for Chlorhexidine, while suppressing many viridans streptococci, to allow for the greater dominance of other bacteremic microorganisms. Such potential would likely increase with prolonged use. If Chlorhexidine does not alter the microbial ratio and composition of the targeted indigenous flora, it would be unique among antimicrobials. In 1975, Johansen et al.4 demonstrated that prolonged Chlorhexidine use (beyond 6 months) has little plaque and gingivitis-reducing effect probably due to growth of resistant organisms. Chlorhexidine rinses seem unable to suppress various enteric species, pseudomonads and enterococci in the human mouth5 8 and may even cause overgrowth of enteric rods in beagle dogs9 and certain compromised
patients.10-11
These above organisms can induce infective endocarditis and in such cases are associated with higher endocarditis mortality rates than viridans streptococci.12'13 The issue then appears to be the benefit of reducing major oral organisms
responsible for infective endocarditis (viridans streptococci) versus the potential for selection of possibly more lethal bacteremic organisms (pseudomonads, enterococci, and enteric species). Until the patient risk-benefit ratio is fully addressed in large study populations, since infective endocarditis is such
event, it appears best to stay within the confines of generally accepted principles of antibiotic prophylaxis. The guidelines for antibiotic prophylaxis to prevent infective endocarditis are much the same as for antimicrobial therapy of active infections: high doses for as short a time as possible to achieve optimum antibiotic activity during the period of patient risk and to reduce toxicity, allergy, and the selection of drug-resistant microorganisms. It is our opinion that the rules of antibiotic endocarditis prophylaxis are the same whether the antimicrobials are used systemically or topically. Individuals who favor some other protocol should gather laboratory and clinical evidence to substantiate their thesis that such rules do not apply to Chlorhexidine under the experimental and clinical conditions that surround infective endocarditis. Until such data become available, we caution against a prolonged use of Chlorhexidine or any other antimicrobial agent in infective endocarditis prophylaxis.—Thomas J. Pallasch, Jorgen Slots, University of Southern California.
docarditis: Recommendations by the American Heart Association. J Amer Med Assn 1990;264:2919-2922. 3. MacFarlane TW, Ferguson MM, Mulgrew CJ. Post-extraction bacteremia: Role of antiseptics and antibiotics. Brit Dent] 1984;156:179184. 4. Johansen JR, Gjermo P, Eriksen HM. Effect of 2-year's use of chlorhexidine-containing dentifrices on plaque, gingivitis and caries. Scand J Dent Res 1975;83:288-292. 5. Emilson CG, Fornell J. Effect of toothbrushing with Chlorhexidine gel on salivary microflora, oral hygiene and caries. Scand J Dent Res
1976;84:308-319. TE, Babalola OO, Slots J. Subgingival occurrence of enteric rods, yeasts and staphylococci after systemic doxycycline therapy. Oral Microbio! Immunol 1990;5:166-168. 7. Spijkervet FKL, van Saene HKF, Panders AK, et al. Effect of Chlor6. Rams
hexidine rinsing on the oropharngeal ecology in patients with head and neck cancer who have irradiation mucositis. Oral Surg Oral Med OralPathol 1989;67:154-161. 8. Wahlin YB, Holm -K. Changes in the oral microflora in patients with acute leukemia and related disorders during the period of induction therapy. Oral Surg Oral Med Oral Pathol 1988;65:411^117. 9. Hamp S-E, Emilson CG. Some effects of Chlorhexidine on the plaque flora of the Beagle dog. / Periodont Res 1973: 8(Suppl 12):28-35. 10. Ferretti GA, Ash RC, Brown AT, et al. Control of oral mucositis and candidiasis in marrow transplantation: A prospective, double blind trial of Chlorhexidine gluconate oral rinse. Bone Marrow Transp
1988;3:483-494.
11. Ferretti GA, Raybould TP, Brown AT, et al. Chlorhexidine prophylaxis for chemotherapy- and radiotherapy-induced stomatitis: A randomized double-blind trial. Oral Surg Oral Med Oral Pathol
1990;69:331-338. 12. Weinstein L. Infective endocarditis. In: Heart Disease: A Textbook of Cardiovascular Medicine, 2nd ed. Braunwald E, ed. Philadelphia: W.B. Saunders, 1984. 13. Durack DT. Infective and noninfective endocarditis. In: The Heart, 7th ed. Hurst JW, Schlant RC, Rackley CE, Sonnenblick EH, Wenger NK, eds. New York: McGraw-Hill, 1990.
a rare
References 1. Bender IB, Naidorf IJ, and Garvey GJ. Bacterial endocarditis:
A
consideration for physicians and dentists. / Amer Dent Assn 1984; 109:415^120. 2. Dajani AS, Bisno AL, Chung KJ, et al: Prevention of bacterial en-
To the Editor: re:
Guest Editorial: Diabetes and Periodontal Disease
(J Periodontol 1991;62:161-163) Dr. Robert Gottsegen's recent editorial on the role of diabetes mellitus in periodontal disease raises some interesting
questions.
As a member of two ADA's, the American Diabetes Association and the American Dental Association, I know that both groups are aware of the interconnection between the oral cavity and the rest of the body. But this awareness is marginal, at best. In the 1990 1991 Clinical Practice Recommendations the Diabetes American Association, no mention of the of of oral health be found. The position statecan importance ments range from somewhat general to quite specific. There is a position statement on the use of non-caloric sweeteners, but not on the need for dental check-ups. In no way can the blame for this be placed on the American Diabetes Association. It has done an excellent job of formulating and updating this information. Clinicians and researchers have input. Unfortunately, dentists do not join in any great number. The American Dental Association appears to be unaware of any need for input and dialogue. —
648
J Periodontol October 1991
LETTERS TO THE EDITOR
The recommendations and guidelines should be formulated by a committee of dentists familiar with the diabetic's problems. We are aware that diabetics may need more intensive dental treatment to maintain oral health and comfort. There may be times when treatment should be deferred. There are many questions to be addressed. These guidelines should be updated as needed. In diabetic individuals with infection, blood sugar rises. The higher the blood sugar, the more difficult it is to control infection. The destabilized insulin-blood sugar balance makes the goals of treatment-normoglycemia even more difficult to achieve. We, as dentists, treat Periodontitis, a disease of the oral tissues intimately connected with the infective process. It is a disease afflicting diabetic individuals with greater frequency, earlier in life, and with more destructiveness, than the general population. I see occasional review articles but little new research is being done in this area. The research which is done usually investigates (and confirms) the statistical significance of the relation between diabetes and periodontal disease. The other side of the coin is being neglected. We need to quantify the degree to which elimination of oral infection improves diabetic control and reduces insulin requirements. For instance, back in 1960 (!) Williams and Mahan reported their findings in the Journal of the American Medical Association. They found, after treatment for Periodontitis, 7 of 9 patients had reduced insulin needs. As far as I am aware, little has been published since then. Further, as pointed out in the Guest Editorial the level of standardization of the research leads to confusion. The 2 studies Dr. Gottsegen referred to may appear somewhat
conflicting.
Now, many of the problems inherent in periodontal recan be dealt with adequately and easily. In addition,
search
technological
advances have improved the ability of the researcher to monitor blood glucose levels. Home blood glucose monitoring units which can easily record and store the time and result of a test are more readily available. The memory chip can be retrieved and replaced by the research team. We should foster awareness in the dental profession of the requirement for greater awareness of diabetic needs and more research into dental infection and its relation to glycémie control. Research teams should be led by dentists. There should be greater communication by the dentist with the treating endocrinologist and with the diabetic educators. I would like to see the diabetic community better served by my fellow professionals and more meaningful input by
dentists into the daily lives of diabetic individuals.—Joanne Eisen, Old Bethpage, NY.
D.
To the Editor: re: Treatment of Periodontal Defects With an Absorbable Membrane (Polyglactin 910) With and Without Osseous Grafting (J Periodontol 1991; 276-
283)
Some
questions need to be raised about the 12 clinical case
reports published in the above article by Gager and Schultz.
There is considerable documentation in the literature and
experience indicating that the type of periodontal lesion described by the authors heal quite routinely and completely following debridement and curettage of the osseous defects. One need not go further than to refer to the early work of
Prichard and other clinicians who achieved considerable repair and regeneration in similar lesions with simple "clean out" procedures. While guided tissue regeneration may be considered by some a viable approach to treatment of periodontal lesions such as furcation involvements which continue to remain a challenge in periodontal therapy, the concept of using barrier membranes and/or grafts for treatment of lesions that heal spontaneously following simple curettage remains enigmatic to vat.—Bernard S. Moskow, Columbia University School of Dental and Oral Surgery.
Authors' Response: As Dr. Moskow has pointed out, some periodontal lesions do heal partially with techniques other than guided tissue regeneration. As clinicians we have observed this in isolated cases, and our patients have benefited. However, we could disagree with Dr. Moskow's impression that lesions such as we have treated heal "routinely and completely" following curettage alone. One need go no further than the carefully controlled reports in the literature comparing various regenerative methods. The control sites are often treated with flap debridement alone, and they do not heal "completely." Indeed, if curettage (open or closed) were such a predictable procedure, Periodontitis might not be the leading cause of tooth loss which it is. Much needs to be learned about GTR, and hopefully in the future we will have even better methods. However its current use is hardly enigmatic. The preponderance of the literature and clinical practice indicate that GTR is the best we have at this time.—Arthur H. Gager, Wells, ME and Allen J. Schultz, Mission Viejo, CA.
