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Rationale of the conference on inflammation
n fereq.ee
On Cln lamntatio L Rationale
of the Conference
The Conference on Inflammation w a s held in Monterey, Calif, on Sept 9-12, 1976. Authors, educators, a n d clinicians a s s e m b l e d to participate ir~ a forum for the synthesis of current concepts a n d controversies relative to the subject of inflammation. Six introductory p a p e r s are in this issue, a n d s e v e n p a p e r s will a p p e a r in forthcomincj issues.
on Inflammation
Henry J. Van Hassel, DDSo MSD, Phi), Seattle
It is altogether fitting and proper that the Endowment and Memorial Foundation of the American Association of Endodontists should sponsor an international conference on inflammation. A stated purpose of the foundation is the dissemination of information on subjects that are particularly relevant to the health care needs of the general public whom endodontists serve. No more relevant or important topic than inflammation can be identified. Consider the triad of symptom, disease mechanism, and healing process with which the endodontist deals. The overriding presenting symptom arising from pulpal pathosis is pain. The psychological experience that we call pain is engendered when a suitable pattern of impulses impinges on the central nervous system. In the trigeminal system, this volley of impulses reaches the CNS along the central processes of nerve ceils located in the gasserian ganglion. In the instance of pulpal pain, the afferent discharge to these cells is carried by peripheral processes that terminate in the dental pulp. The adequate stimuli that depolarize pulpal receptors likely inelude, as a principal factor, mechanical pressure. All dentists have at some
time opened a painfully throbbing tooth and observed the release of inflammation-induced fluids under pressure and the associated relief of pain. The association between inflammation and pain--the principal symptom of the pathosis that endodontists treat-need not therefore be belabored. It is a fact of clinical experience. Similarly, but perhaps less obviously, the basic mechanism that leads to pulpal death is also intrinsic to the inflammatory process. The tendency toward fluid accumulation in the tissues following injury is perhaps beneficial in most integumental structures because it leads to dilution of toxic material and can cushion injured tissue from further mechanical contact with the environment. The tooth pulp, however, is rigidly encased; thus, tendencies toward even small volume increases due to inflammatory extravasation of fluids are translated into large pressure increases. Elevated circumvascular tissue pressure may lead to circulatory collapse and pulpal death. Thus, both the symptom and the mechanism of pulpal disease ,are inflammation-induced. Finally, the universally accepted hallmark of successful endodontic therapy is the healing of a periapical
lesion. Yet this lesion constitutes nothing more than the effect on bone of the cellular processes, which arises from the inflammatory response to foreign substances and which reaches the periapical bone by way of a diseased pulp. The endodontist's expectations of reossification following removal of the original irritant must be grounded in his understanding of the progression of inflammation to healing. In summary, the need for the endodontist's services arises from the symptoms of pulpal inflammation, and the treatment he renders might be viewed as nothing more than the arranging of conditions so that the inflammatory process may be resolved. Clearly, inflammation is an appropriate subject for this first major conference sponsored by the foundation.
Dr. Van Hassel is associate professor in the departments of physiology, biophysics, and endodontics, University of Washington, Seattle. He is also affiliated with the United States Public Health Service Hospital in Seattle. Requests for reprints should be directed to Dr. Henry J. Van Hassel, Department of Endodontics, School of Dentistry, University of Washington, Seattle, 98195.
207
On Cln lamntatio L Rationale
of the Conference
The Conference on Inflammation w a s held in Monterey, Calif, on Sept 9-12, 1976. Authors, educators, a n d clinicians a s s e m b l e d to participate ir~ a forum for the synthesis of current concepts a n d controversies relative to the subject of inflammation. Six introductory p a p e r s are in this issue, a n d s e v e n p a p e r s will a p p e a r in forthcomincj issues.
on Inflammation
Henry J. Van Hassel, DDSo MSD, Phi), Seattle
It is altogether fitting and proper that the Endowment and Memorial Foundation of the American Association of Endodontists should sponsor an international conference on inflammation. A stated purpose of the foundation is the dissemination of information on subjects that are particularly relevant to the health care needs of the general public whom endodontists serve. No more relevant or important topic than inflammation can be identified. Consider the triad of symptom, disease mechanism, and healing process with which the endodontist deals. The overriding presenting symptom arising from pulpal pathosis is pain. The psychological experience that we call pain is engendered when a suitable pattern of impulses impinges on the central nervous system. In the trigeminal system, this volley of impulses reaches the CNS along the central processes of nerve ceils located in the gasserian ganglion. In the instance of pulpal pain, the afferent discharge to these cells is carried by peripheral processes that terminate in the dental pulp. The adequate stimuli that depolarize pulpal receptors likely inelude, as a principal factor, mechanical pressure. All dentists have at some
time opened a painfully throbbing tooth and observed the release of inflammation-induced fluids under pressure and the associated relief of pain. The association between inflammation and pain--the principal symptom of the pathosis that endodontists treat-need not therefore be belabored. It is a fact of clinical experience. Similarly, but perhaps less obviously, the basic mechanism that leads to pulpal death is also intrinsic to the inflammatory process. The tendency toward fluid accumulation in the tissues following injury is perhaps beneficial in most integumental structures because it leads to dilution of toxic material and can cushion injured tissue from further mechanical contact with the environment. The tooth pulp, however, is rigidly encased; thus, tendencies toward even small volume increases due to inflammatory extravasation of fluids are translated into large pressure increases. Elevated circumvascular tissue pressure may lead to circulatory collapse and pulpal death. Thus, both the symptom and the mechanism of pulpal disease ,are inflammation-induced. Finally, the universally accepted hallmark of successful endodontic therapy is the healing of a periapical
lesion. Yet this lesion constitutes nothing more than the effect on bone of the cellular processes, which arises from the inflammatory response to foreign substances and which reaches the periapical bone by way of a diseased pulp. The endodontist's expectations of reossification following removal of the original irritant must be grounded in his understanding of the progression of inflammation to healing. In summary, the need for the endodontist's services arises from the symptoms of pulpal inflammation, and the treatment he renders might be viewed as nothing more than the arranging of conditions so that the inflammatory process may be resolved. Clearly, inflammation is an appropriate subject for this first major conference sponsored by the foundation.
Dr. Van Hassel is associate professor in the departments of physiology, biophysics, and endodontics, University of Washington, Seattle. He is also affiliated with the United States Public Health Service Hospital in Seattle. Requests for reprints should be directed to Dr. Henry J. Van Hassel, Department of Endodontics, School of Dentistry, University of Washington, Seattle, 98195.
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