Published at the College of Dental Medicine, Medical University of South Carolina
Volume 4, Issue 2
Letter from the Editors
The National Institute of Dental Research sponsored a symposium entitled Scientific Frontiers in Clinical Dentistry from June 13 - 14, 1996 in Bethesda, Maryland. In the introduction to this symposium, Dr. Harold C. Slavkin (Director, National Institute of Dental Research) states "dental professionals will need to adapt to new health care arrangements and must be prepared to offer high-quality, cost-effective care that is consistent with rapidly evolving technologies" and that "to reach this goal we will need to embrace a paradigm that integrates research, education and practice - one that allows scientists, educators, and clinicians to work together to ensure improvements in oral, dental and craniofacial health for all". These statements elegantly summarize the goals of the American Association of Oral Biologists and the talks presented in this meeting presented a "state of the art" overview of current progress in the state of dental science.
There were 20 presentations during the two day symposium covering many facets of dentistry. Topics included periodontal disease, bone physiology and regeneration, HIV manifestations in the oral cavity, analgesics, chronic pain, tempormandibular disorder and gene therapy. In this edition of the AAOB Newsletter we have focused on two presentations which advocate conservative treatment of dental caries. Both Dr. John Featherstone and Dr. Kenneth J. Anusavice advocate for biological treatment (vs. surgical treatment) as the treatment of choice for dental caries. We would like to thank both Dr. Featherstone and Dr. Anusavice for their contributions to the Newsletter. We also would like to thank Dr. Harold C. Slavkin for providing us with his view of Dentistry in the 21st century. Abstracts of other talks given at the Symposium are contained at the NIDR Web Site which can be accessed through the AAOB Home Page.
As in the past, we have continued our tradition of highlighting Oral Biology programs in the Newsletter. In this issue, we have reported on the Oral Biology program at the University of Florida. Of particular interest to members is the integration of the Oral Biology graduate program faculty and coursework into a newly designed, interdepartmental graduate program which initiates at the University of Florida this fall. The Editors would like to thank Drs. Arnold S. Bleiweis and Thomas A. Brown for providing us with the information on the Oral Biology Graduate Program at the University of Florida.
The Editors welcome any letters or contributions from the membership for the next (Feb. 1997) issue of the AAOB Newsletter. We will also be glad to include announcements of interest in the Newsletter concerning openings in graduate Oral Biology programs and news items of interest on AAOB members, Oral Biology programs, or areas of concerns in Oral Biology education and research.
The AAOB Newsletter
Steven D. London, D.D.S., Ph.D., Editor
John G. Blackburn, Ph.D., Co-Editor
The AAOB Newsletter is published for the members of the American Association of Oral Biologists and individuals interested in the discipline of Oral Biology. Statements in this publication do not constitute an endorsement by the College of Dental Medicine or the Medical University of South Carolina. All correspondence should be directed to Dr. Steven D. London, Department of Microbiology and Immunology, Medical University of South Carolina, 171 Ashley Avenue, Charleston, South Carolina 29425 (E-Mail: LondonSD@MUSC.EDU).
Dentistry In The 21st Century
Harold C. Slavkin, D.D.S., Director, National Institute of Dental Research, Bethesda, Maryland.
What will clinical dentistry be like in the 21st century? During the 20th century, in no small measure due to the heroic efforts of the
1926 Gies Report and then World War II, American dental education evolved from free-standing and often proprietary schools to become integral
parts of research-intensive university professional education. This evolution provided dentistry with a formidable scientific basis for
diagnosis, therapeutics and disease prevention. The development of clinical skills coupled with advanced dental materials and therapeutics
has truly been remarkable. And now we approach the 21st Century as a nation of changing demographics. Consider the "social math"
of America. By 2010 nearly 40 million Americans will be 65 years of age and older. Expectations for "quality of life" now punctuate
American values. Whereas in 1900 the human lifespan was 45 years, today it approaches 80 years. While in 1900 the primary causes of mortality
and morbidity were acute infectious diseases, today our challenges include complex viral infections as well as neoplastic diseases and chronic
disabling diseases (e.g. chronic facial pain, skeletal-muscular degeneration, osteoporosis, osteoarthritis, cerebrovascular and coronary
diseases and disorders). In fact, one American dies every hour of oral cancer. The practice of clinical dentistry in the 21st century will
change — these changes will continue.
To integrate dental practice into comprehensive health care.
To become increasingly proactive for health promotion.
To represent an increased knowledge-base for diagnostics and therapeutics.
To utilize novel strategies for oral health care.
Remineralization: A Treatment Option for Caries
John D.B. Featherstone MSc, PhD, Department of Restorative Dentistry, University of California at San Francisco, San Francisco, California.
Clinically observable dental caries is the end product of an imbalance between demineralization and remineralization of tooth enamel and/or dentin. The acid challenge resulting from metabolism of carbohydrates by acidogenic oral bacteria is offset most of the time by calcium, phosphate and fluoride present in the saliva, in the plaque and inside carious lesions. Partially demineralized (decayed) regions of crowns or tooth roots can be arrested or remineralized by altering the balance between acid-induced dissolution of mineral and replacement of lost mineral by remineralization. We now have a clear picture of the various ways by which fluoride acts to inhibit or reverse the caries process. We are also at the stage where this information can and should be used in clinical practice as part of caries preventive or conservative restorative procedures. Our new understanding of the role of remineralization can be put directly to clinical use.
The caries process is simple in concept, if complicated in detail. Acids generated by plaque bacterial metabolism diffuse into the subsurface of the tooth and dissolve calcium phosphate from the mineral crystal surfaces. The mineral of teeth and bone consists of carbonated hydroxyapatite, which is much more soluble in acid than pure hydroxyapatite or fluorapatite. While the acid challenge continues calcium and phosphate dissolve and diffuse out into the plaque. If fluoride is present in the water phase surrounding the crystals it markedly inhibits the acid from dissolving the crystal surface sites. As saliva neutralizes the acid in the plaque calcium, phosphate and fluoride diffuse back into the tooth where remineralization can occur at the surfaces of the partially eroded crystals of carbonated apatite. Fluoride speeds up this remineralization process and combines with calcium and phosphate. The new (remineralized) crystal surfaces are now coated with a fluorapatite-like veneer that is several orders of magnitude less soluble than the original mineral crystals and strongly resistant to the next acid challenge.
Fluoride present at relatively low levels in saliva and plaque in the mouth therefore acts in at least two important ways:
Fluoride can also inhibit plaque bacteria if present at sufficient concentration in plaque during the production of acid. The major effects of fluoride on the caries process therefore occur by the topical presence of that ion in the mouth when needed.
Incorporation of fluoride during remineralization makes the mineral much more resistant to future acid attack. Remineralization can be effectively enhanced by the daily use of fluoride products such as dentifrices and mouthrinses. Fluoride in the drinking water works for the same reasons. Fluoride tablets are most effective if chewed and swished rather than simply swallowed. Antibacterial therapy coupled with fluoride enhancement of remineralization is an option for lesions not yet cavitated. Patients at high risk of caries should have antibacterial therapy to reduce the challenge, coupled with daily fluoride therapy to provide effective low levels of fluoride in the saliva continually.
"Treating" caries by simply placing restorations is no longer acceptable. The future resistance to caries must be enhanced. Conservation of tooth structure is extremely important. A planned conservative/preventive approach with remineralization as one of the treatment options for caries should be the norm rather than the exception.
Breaking from Tradition: Guidelines for Optimum Preventive and Restorative Care
Kenneth J. Anusavice, D.M.D., Ph.D., Department of Dental Biomaterials, College of Dentistry, University of Florida, Gainesville, Florida.
Traditional clinical dental education has been based primarily on empirical evidence and subjective opinions rather than on direct scientific evidence. Although caries prevalence has declined over the past several decades, the criteria for placement and replacement of restorations have not changed markedly when a surgical model of care is adopted compared with a disease-controlling model. When surgical intervention of demineralized enamel is chosen as the treatment of choice, teeth with lesions which can be seen radiographically to extend to the DEJ are often restored rather than remineralized even though scientific evidence indicates that approximately 60% of these lesions are not cavitated. If they are not cavitated, remineralization is the most conservative option.
Evidence that acid causes demineralization of enamel and that saliva can cause remineralization was demonstrated by Joseph Head in 1912. However, remineralization of enamel lesions is neither taught routinely in North American dental schools nor is it given credit as a requirement for graduation. In fact, the vast majority of procedures that are required for graduation are surgical or restorative in nature rather than preventive. This surgical tradition is subsequently upheld in private practices long after personal experience should have indicated that many of the decisions to restore and re-restore teeth may have been inappropriate. This tendency to surgically intervene is reinforced by tradition and the higher level of respect that is accorded our peers for their surgical skills compared with their preventive skills. These decisions to restore or to attempt remineralization are further supported by payment plans which do not provide adequate compensation for diagnosis of early lesions, for analyzing the caries activity status, or for monitoring these lesions radiographically and visually over time to determine whether remineralization efforts have been successful.
To challenge this traditional tendency to restore rather than to remineralize, we should redirect our attention to answering critical questions on the lesion status before a treatment option is chosen. For example, is radiographic evidence of enamel demineralization a good or bad scenario? Based on conventional practices, it would be considered a bad situation by dentists and by patients because an assumption is made that such lesions are likely to progress to a more advanced state. However, what would the answer be if it was determined that these lesions had been arrested for the past two years, five years, or 10 years? Such evidence of lesion arrest and tissue remineralization would suggest that these sites are highly resistant to further demineralization.
In spite of our best attempts to adopt a preventive practice philosophy, treatment outcomes are quite variable. These outcomes are affected by the poor sensitivity of diagnostic aids in positively identifying caries sites, the nonstandardized quality of radiographic films, the failure to identify the activity status of existing lesions, the variability of disease progression risk factors for individual patients and populations of patients, the poor compliance of patients to recommended oral hygiene practices, and the methods of payment for the preferred treatment options. Furthermore, because caries is a site-specific disease, generalized whole-mouth indicators of future risk for new lesions and progression of existing ones (such as DMFS scores, S. mutans concentrations, dietary factors, and saliva flow rate) are not useful for predicting whether a specific tooth surface will be highly susceptible to demineralization.
For teeth with defective restorations, replacement decisions are still based on traditional beliefs that the width of a marginal gap between an amalgam and the prepared tooth or the depth of stained marginal gap next to a resin-based composite are correlated with caries progression probabilities. Scientific data show that the relative longevity of amalgam and composite restorations decreases as they become replaced and as they increase in size. Restoration replacement leads to progressively larger restorations. Thus, replacement decisions should be delayed as long as possible unless evidence of caries progression exists.
Dentists are not adequately compensated by patients or by third-party payers for monitoring noncavitated enamel lesions to determine whether they are active or arrested, or to analyze the success of caries arrestment and remineralization procedures. Because of this failure to sufficiently compensate dentists for such complete preventive care, decisions to restore lesions that are radiographically determined to be at the DEJ or slightly beyond are viewed more favorably than decisions to arrest progression and effect remineralization.
Diagnosis and treatment of new lesions include the following procedural sequence: examination for evidence of cavitation, diagnosis of noncavitated lesions, recording of the depth of noncavitated lesions, assessing the caries risk level (high or low), monitoring caries activity over time (every three months for high risk and six months or longer for low risk patients), reassessing and modifying remineralization treatment if active caries exists, and restoring when lesions are one-third or more of the dentin thickness or are progressing rapidly through dentin despite previous preventive measures to arrest and remineralize the lesions. A simple flow chart of a typical treatment sequence follows this article.
Diagnosis and treatment of recurrent lesions include the following procedural sequence: examination for evidence of cavitation, differentiation between actual lesions and evidence of marginal gaps or marginal staining, assessing the caries risk level (high or low), monitoring caries activity over time (every three months for high risk and six months or longer for low risk patients), reassessing and modifying remineralization treatment if active caries exists, repairing or sealing when the caries risk is low, and restoring the tooth when lesions have progressed through one-third or more of the dentin thickness or are progressing rapidly through dentin despite previous preventive measures to arrest and remineralize the lesions.
Dentists with considerable levels of advanced education do not agree consistently with their peers on decisions of preventive and restorative treatment. In the United States, decisions to restore initial approximal lesions are based traditionally on detection of radiolucencies at the DEJ or slightly into dentin. However, this aggressive approach toward operative intervention is contrary to the recommendation of an international group of dentists and researchers for the initial placement of an initial restoration be delayed until the lesion is located "well into dentin" as determined from bitewing radiographs (Anusavice, 1989) since a significant percentage of teeth with such lesions are noncavitated and thus can be remineralized. Monitoring of early enamel lesions using bitewing radiographs every three to six months initially for one year and then once per year thereafter to determine evidence of remineralization is necessary to delay operative intervention as long as possible until the lesion has been detected to be "well into dentin" and conserve as much tooth structure as possible. However, even when attempts to effect remineralization of enamel lesions have not been successful during this monitoring period, the progression of proximal lesions into dentin should continue to be very slow (Shwartz et al., 1984) except for the highest risk patients.
Shwartz et al. (1984) reported mean progression time through enamel of 43 months for children and older adolescents in the U.S. and 85 months for Swedish children and adolescents. Since there is a relatively long period of time for incipient (noncavitated) lesions to progress into dentin, remineralization and monitoring efforts should be taken before a surgical intervention is implemented. Decisions to replace restorations because of faulty margins are complicated by the variable radiodensity of different restorative materials. The sensitivity of detecting caries under these restorations is poor. Based on radiographic examination of 6,285 restored teeth in 490 patients, Hewlett et al. (1993) found a nearly three-fold increase in the probability of radiographically-detected caries, but the proportion of defective restorations (with evidence of radiographic secondary caries) to defective restorations (with no evidence of radiographic secondary caries) ranged from 14% to 86%. Restorations were judged to be defective if any of the following conditions was present:
They concluded that, because of its low sensitivity of 28%, the use of defective margins alone as a criterion for replacement is inappropriate and this finding confirms the conclusion of Söderholm et al. (1989) that gap width is not strongly linked to recurrent caries. Although the high specificity of this criterion (88%) suggests that the intact status of restorations is a reliable indicator of the absence of radiographically-diagnosed caries, 71% of secondary caries was associated with restorations judged to be intact. This result indicates the need for radiographs and "intactness" observations to confirm the absence of secondary caries.
Secondary (recurrent) caries is cited as the major cause of amalgam replacement in many studies, but no study has yet validated whether these lesions represent:
One of the major deficiencies of these many studies is that the caries risk status of these patients was not monitored, thus clouding the interpretation of these data. Furthermore, recording of caries may or may not include white-spot noncavitated lesions, and secondary caries lesions is excluded when recording DMFS scores. It is clear, however, that amalgam, composite or glass ionomer restorations do not cure caries as clearly evidenced in many recent studies which identified secondary caries as the principal cause of restoration replacement. If caries originates in any one of the ways described above, a replacement restoration will not cure the disease process, although the excavation process will remove a large concentration of bacteria from the cavitated site. However, for a high-risk patient who has not been shifted to a low-risk status, the replacement restoration may correct the marginal gap discrepancy, but only for a limited time.
Concepts which support the foundation of ultraconservative preventive and restorative treatment include monitoring early lesions for caries activity, assessing the site specific risk for caries progression, analyzing possible decision outcomes relative to the effectiveness of remineralization treatment, delaying the initial placement of a restoration, performing exploratory surgery on high-risk patients prior to generalized surgical intervention of all teeth with lesions, and changing treatment protocols depending on the variations in risk status of the patient. Options for treating restored teeth include repair and sealing of defective restorations and alteration of the treatment plan as patient risk factors for future caries progression so dictate.
In summary, it is now possible to arrest caries and remineralize teeth with noncavitated enamel and to delay operative intervention until an accurate diagnosis of caries status is ensured. Only teeth with caries extending past the DEJ or teeth with cavitation are indicated for restorative treatment. Caries progression rates are much slower than previously believed and these rates are even slower for patients at a low caries risk. However, current fee-for-service systems and managed care options fail to provide adequate compensation for such preventive services. To overcome this obstacle to prevention of the 90s, the public must be educated on the value of modern prevention so that they will demand such prevention services in the future.
Acknowledgments: This work was supported in part by NIH-NIDR Grants DE09307 and DE06672.
Anusavice KJ. Summary statements. In: Anusavice KJ ed. Quality evaluation of dental restorations: criteria for placement and replacement. Chicago: Quintessence Publishing Co., 1989: 412-413.
Head J (1912). A study of saliva and its action on tooth enamel in reference to its hardening and softening. J Am Med Assoc 59(24):2118-2122.
Hewlett ER, Atchison KA, White SC, Flack V (1993). Radiographic secondary caries prevalence in teeth with clinically defective restorations. J Dent Res 72(12):1604-1608.
Pitts NB (1983). Monitoring of caries progression in permanent and primary posterior approximal enamel by bitewing radiography. Community Dent Oral Epidemiol 11:228-235.
Pitts NB, Rimmer PA (1992). An in vivo comparison of radiographic and directly assessed clinical caries status of posterior approximal surfaces in primary and permanent teeth. Caries Res;26:146-152.
Shwartz M, Gröndahl H-G, Pliskin JS, Boffa J (1984). A longitudinal analysis from bite-wing radiographs of the rate of progression of approximal carious lesions through human dental enamel. Arch Oral Biol 29(7):529-536.
Söderholm K-J, Antonsson DE, Fischlschweiger W. Correlation between marginal discrepancies at the amalgam/tooth interface and recurrent caries. In: Anusavice KJ ed. Quality evaluation of dental restorations: criteria for placement and replacement. Chicago: Quintessence Publishing Co., 1989: 95-108.
Simplified Flow Chart for Modern Management of Caries
The American Association of Oral Biologists World Wide Web Home Page
Since 1995 the AAOB has maintained an American Association of Oral Biologists Home Page on the World Wide Web. The AAOB Home Page has been updated several times since its introduction in 1995 and we suggest that members visit this site on a periodic basis. This site has had ~800 visitors during the five months of March - July, 1996. The AAOB Home Page contains links to other dental sites of interest to AAOB members and has important information on the AAOB and its activities (AAOB Bylaws, Curricular Guidelines for Oral Biology, past issues of AAOB Newsletters, abstracts of articles which appear in current and past issues of Critical Reviews in Oral Biology and Medicine , and AAOB Membership Application materials). The AAOB Home Page can be accessed at the following URL address via your favorite web browser (i.e. Netscape, Mosaic, or your particular favorite): http://www2.musc.edu/AAOB.html
1997 AAOB Business Meeting
This year, the American Association of Dental Schools Annual Meeting will precede the American and International Dental Research Meeting in Orlando, Florida. The AADS meeting will be from Saturday, March 15th to Wednesday, March 19. The IADR/AADR meeting will be from Wednesday, March 19th until Sunday March 23rd. Wednesday, March 19th will be the only day on which joint AADS/IADR meetings will occur. We will report on the specific times of the 1997 AAOB Business Meeting in the next edition of the AAOB Newsletter. As has been the custom in the past, the AAOB Business Meeting will be scheduled through the AADR and will be during the later part of the week in conjunction with the AADR meeting.
Report on the 1996 AAOB Joint Symposium
Last year, in San Francisco, the AAOB in collaboration with the AADS Sections on Biochemistry and Nutrition, Microbiology, Oral Biology, Pharmacology & Therapeutics, and Physiology co-sponsored a joint program/workshop entitled "Foundation Knowledge for Competencies: The Merging of Basic and Clinical Sciences" . This program was presented on Saturday, March 16, 1996 from 2:00 until 5:00 PM. Following introductory comments by Dr. Virginia Merchant, Moderator, and Ms. Carolyn Gray (Assistant Executive Director, Division of Educational Affairs, AADS), Dr. David Chambers (Univ. of Pacific) gave an overview of foundation knowledge as related to competencies. His comments were followed by a panel of individuals (Dr. William J. Babler (Baylor), Dr. Jose E. Torres (Puerto Rico), Dr. Les Felpel (San Antonio), and Dr. Larry Luke (UCLA) from schools who have worked with foundation knowledge in context of competencies and who discussed some of the lessons learned in their process. The workshop participants (totaling over 80) were divided into working groups to begin the process of relating foundation knowledge to competencies using selected competency statements from the drafted AADS Competencies for the New Dentist. Due to a time crunch, the hands-on aspect was abbreviated. The workshop closed with reactions from the facilitators, the panel, and Dr. Tom Kilgore (Boston University) to the afternoon's discussion.
Overall, the workshop seemed to have been well received. Time did not permit the working groups to become actively involved in the process, and many of the participants had difficulties with the competencies selected. There are still strong opinions regarding the issues of competencies vs. behavioral objectives, the interaction between basic science and clinical dentistry, and communication among disciplines. Although an effort was made to include clinicians in the discussions, there were a limited number of clinicians present. The workshop did establish the necessity for continued dialogue as interdisciplinary groups in the further development of competencies and supporting skills and foundation knowledge. Thanks to all who attended, and especially our distinguished speakers, who made this program possible.
Virginia A. Merchant, M.S., D.M.D.
Professor, Department of Biomedical Sciences
University of Detroit Mercy School of Dentistry
Minutes of the 1996 Annual AAOB Business Meeting
The 1996 Annual AAOB business meeting was held on Saturday, March 16, 1996 from 12:00 - 1:00 P.M. in Golden Gate Salon A3, San Francisco Marriott Hotel. Dr. Murray R. Robinovitch, AAOB president, opened the meeting and extended his appreciation to the AAOB officers for their input during the preceding year. He then set the agenda and lead the membership in their discussion of the following items of business.
Item 1: The minutes of the AAOB business meeting on Saturday, March 11, 1995 at the San Antonio Convention Center were accepted as presented in the February, 1996 issue (Volume 4, Issue 1) of the American Association of Oral Biologists Newsletter.
Item 2: Dr. Steven D. London, AAOB Secretary/Treasurer reported that the balance of Association funds as of March 12, 1996 was $5,998.06. There were 112 members in good standing for the 1995 calendar year. Dr. London reported that 1996 Dues will be $57.00 and include $12.00 AAOB Dues and $45.00 for the 1996 issues Critical Reviews in Oral Biology and Medicine . Subscription to Critical Reviews in Oral Biology and Medicine will remain optional for associate (student) and retired members. Dues Notices were sent out in February, 1996.
1995 marked the first year that all full association members were required to subscribe to Critical Reviews in Oral Biology and Medicine. Dr. London reported that he collected and forwarded $4,590.00 in subscription fees for Critical Reviews in Oral Biology and Medicine to the IADR/AADR. Dr. London reported that the transfer of money to the IADR for Journal subscriptions went smoothly and acknowledged Mr. Bobby Phipps (IADR Membership Dues Coordinator) for his help in the coordination of the Journal subscriptions for AAOB members.
Item 3: Dr. Kathleen Dobrosielski-Vergona reported that the results of the 1996 AAOB election were not yet available. It was agreed at the Annual Meeting that the 1996 AAOB officers would be listed in the next issue of the AAOB Newsletter and be included in the minutes of the 1996 Annual Meeting. The following members were elected or appointed officers for 1996-1997:
President: Frank Dowd – Creighton University
President-Elect: Frank Oppenheim – Boston University
Secretary/Treasurer: Steven D. London (1996-1999) – Medical University of South Carolina
Elected Directors: Mark Wolff (1995-1997) – SUNY, Stony Brook
Lorne Golub (1996-1998) – SUNY, Stony Brook
Appointed Directors: Firoz Rahemtulla (1996-1997) – University of Alabama
Andrew Spielman (1996-1997) – New York University
Program Officer: Beverly Dale-Crunk (1996-1998) – University of Washington
Past-President: Murray R. Robinovitch – University of Washington
Editor, CROBM Olav Alvares – Univ. of Texas, San Antonio
Item 4: Dr. Kenneth Etzel, 1996 Chair of the AADS Oral Biology Section reported that the section had approximately 180 members. However, he expressed the section's concern that the phase in of the one section per basic AADS membership rule would result in the decreased viability of the Oral Biology section. In response to this challenge, he reported that the section will continue its close relationship with the AAOB and would develop new programs to maintain the sections viability. Two programs that will be pursued in the following year include the development of a pool of problem based learning cases for oral biology as well as an examination test bank of oral biology questions. Dr. Etzel invited AAOB members to participate in the activities of the AADS Oral Biology section.
Item 5: Dr. Kathleen Dobrosielski-Vergona announced the 1995 winners of the AAOB Junior Scientist award program which was held on February 3, 1996 in Breidgeville, Pennsylvania. The purpose of the program is to promote oral biology and educate the public about the nature of oral biology. She reported that there was a large increase in the number of oral biology projects once this award was initiated at the Annual Pennsylvania Junior Academy of Sciences meeting and encouraged other members to initiate similar programs in their communities where Junior Academies of Sciences (or similar programs) exist.
Item 6: Dr. Olav Alvares, Editor of Critical Reviews in Oral Biology and Medicine , expressed his appreciation to the IADR/AADR for their excellent management of the Journal during the past year. He reported a healthy increase in the number of Journal subscriptions from ~180 when the IADR/AADR acquired the Journal in December 1994 to between 500 and 600 at the present time. He reported having 55 manuscripts in various stages of preparation and that the IADR is considering increasing the number of issues from the current rate of four/year to six issues in 1997. Dr. Alvares reported that the subscription rate for members of the AAOB and all IADR members in 1996 will remain at $45.00. Dr. Alvares expressed his appreciation for the support of the AAOB and its members. Dr. Dabbous expressed his and the membership's appreciation to Dr. Alvares for his efforts as the Journal's editor.
Item 7: Dr. Murray R. Robinovitch, AAOB President, initiated a discussion of a number of items of New Business. They included:
With no further business items to be discussed, the meeting was adjourned at 1:00 P.M.
Oral Biology at the University of Florida
The Department of Oral Biology had its origins as the Department of Basic Dental Sciences in 1972 when the College of Dentistry admitted its first class . Initially, the department's responsibilities included instruction in both biological and behavioral sciences to undergraduate dental students as well as the development of a research faculty in dental and oral facial diseases. By 1986 the department had focused on the biological sciences and research activities centered in the areas of microbiology, immunology, salivary gland physiology, and biochemistry related to dental and oral facial diseases. With the appointment of Dr. Arnold S. Bleiweis as Chairman in 1986, the department became the Department of Oral Biology. At the undergraduate level, the department teaches a number of basic and dental science courses. A Ph.D. tract in Oral Biology within the Medical Sciences degree program at the University of Florida was initiated in 1987. In 1990, a training grant for the graduate program in Oral Biology was obtained from the NIDR which has since been renewed until the year 2000. The department has graduated 8 Ph.D. students and 4 M.S. students. Currently, there are 7 students enrolled in the Oral Biology graduate program (all at the Ph.D. level).
Beginning this fall (1996), the Medical Sciences degree program at the University of Florida has been reorganized into an non-departmental interdisciplinary mode. Students enter the graduate program in one of six interdepartmental programs (IDP) including Microbiology/Immunology, Physiology/Pharmacology, Biochemistry, Neuroscience, Genetics, or Cell Biology. All students take a comprehensive core curriculum during the first year which includes instruction in aspects of biomedical sciences relevant to the five IDPs. During the first year, students also take a laboratory course in Molecular Biology and are instructed in the use of computers and library resources within the context of grant writing. Lab rotations during the spring and summer semesters guide the students choices concerning which particular laboratory they will do their thesis in and the second year of required advanced coursework within the IDP of their choice. The Oral Biology faculty is fully integrated into this interdepartmental structure and Oral Biology faculty teach in both the first year core curriculum as well as in advanced courses during the second year. Students interested in Oral Biology will receive a Ph.D. in Medical Sciences within the IDP of their choice with specialization in Oral Biology. Written and oral comprehensive examinations will be administered after the second year of classes and follow the format of the IDP selected by the student. After satisfactorily passing this examination, the student is allowed to officially begin research for the dissertation.
Candidates for the Ph.D. program who specialize in Oral Biology must demonstrate the ability to perform independent research and critically evaluate research data. The program requires submission of a dissertation and its approval by the graduate committee, and successful completion of an oral examination and defense of the dissertation. Upon successful completion of all requirements and recommendation by the candidate's committee, the candidate receives a Ph.D. in Medical Sciences with specialization in oral biology. (Students will not be admitted for studies towards an M.S. degree in this specialization.)
The program is designed, first, to provide a strong background in the basic biological principles relevant to the various subspecialties of oral biology; and second, to provide specialized training in the various aspects of diseases and disorders of the oral cavity. This specialized training may include the application of anatomical, physiological, molecular, microbiological and immunological concepts and technologies to answer critical questions about oral cavity development, function, and disease. The program will provide scholars well-versed and trained to take leadership roles in dental research.
The M.S. in Medical Sciences with specialization in Oral Biology will be awarded only in special cases where a student is unable to complete studies for the Ph.D. degree. The consent of the departmental faculty and of the dean of the College of Medicine will be required. Requirements for such a degree will include the necessary course credits, as determined by the graduate school, plus a thesis.
Oral Biology Faculty and Courses
Chairman: A. S. Bleiweis. Graduate Coordinator: W. P. McArthur. Graduate Research Professor: A. S. Bleiweis. Distinguished Service Professor: P. E. Mahan (Emeritus). Professors: W. Fischlschweiger (Emeritus); C. H. Gibbs; A. Hefti; J. B. Hillman; M. G. Humphreys-Beher; N. I. Magnusson; W. P. McArthur; A. Progulske-Fox; C. B. Walker; W. N. Williams. Associate Professors: T. A. Brown; Assistant Scientist: L. J. Brady.
Undergraduate Oral Biology Coursework:
DEN5230 - Nutrition
DEN5210 - Tooth Development
DEN5128 - Immunology
DEN6212 - Stomatognathics
DEN10100 - Introductory Elective in Oral Biology Research (open to freshmen dental students)
DEN10101 - Advanced Elective in Oral Biology Research (open to sophmore, junior and senior dental students)
Oral Biology Coursework for Postgraduate Dental Residents:
GMS 6160 - Introduction to Oral Biology I (2) Survey of anatomy and development of head and neck, oral histology and ultrastructure, salivary gland function,oral sensory function, and pathology of the periodontium and teeth.
GMS 6161 - Introduction to Oral Biology II (2) Survey of microbial and viral pathogens responsible for oral diseases, host defense mechanisms in oral cavity, and aspects of cell biology relevant to functions of oral soft tissues.
Graduate Oral Biology Coursework:
GMS 6170 - Immunology and Immunopathology of the Oral Cavity (2) Specific and nonspecific immune factors in saliva, with special emphasis on secretory IgA. Immunology and immunopathology of oral soft tissues.
GMS 6172 - Molecular Biology and Pathology of the Periodontium (2) Ultrastructure and biochemical composition of periodontal tissues, the microbial interrelations with the organic and inorganic components of periodontal tissues, the biochemical dynamics of gingival inflammation, and wound healing and the metabolic processes responsible for the composition and flow of the gingival crevicular fluid.
GMS 6173 - Stomatognathic System: Form and Function (2) Anatomy and function of head and neck muscles, temporomandibular joints, and salivary glands. Normal and abnormal mastication, deglutition, speech, and oral sensorimotor measures.
GMS 6174 - Oral Microbial Systems (2) Major bacterial pathogens of the oral cavity: their morphology, physiology, genetics, and ecologic associations. Roles of key organisms in oral diseases (e.g., caries and periodontitis) stressed.
GMS 6176 - Biology of Tooth Supporting Structures I (1) Organization, vasculature, and innervation of the periodontium; chemistry; biosynthesis, biophysics, and degradation of collagen; studies of other associated, unique proteins.
GMS 6177 - Biology of Tooth Supporting Structures II (1) Development and function of the periodontal ligament; organization, development, biophysics, and biochemistry of bone; calcification mechanisms and bone remodeling; effects of hormones and nutrients on bone.
GMS 6178 - Glycoproteins: Structure, Function, and Biosynthesis (3) Current findings on the structures of N- and O-linked oligosaccharides, biosynthetic enzymes, intracellular trafficking, and biological functions.
GMS 6193 - Research Conference in Oral Biology (1; max: 8) Critical discussion and appraisal of current research within department by students and faculty. S/U.
GMS 7179 - Journal Colloquy (1; max: 8) Required of graduate students in oral biology; open to others by permission of the department. Critical presentation and discussion of recent original articles in the oral biology literature.