Interrelationships between pulpal and periodontal diseases have been both confirmed and denied for over 100 years.[1–10] Both academicians and clinicians have attempted to categorize and pigeonhole each case into a preconceived and often arbitrary classification that may or may not have provided guidance to the clinician as to the nature of the problem and a reasonable course of treatment.[11–13] Coupled with a significant lack of agreement in terminology and thorough understanding of the disease processes as opposed to treatment procedures, these interrelationships have posed significant diagnostic and treatment dilemmas for all concerned.[14–17] Only too often the treatment rendered resulted in tooth extraction and replacement with fixed/removable partial dentures or currently with implants.
In 1896, Dr. M. L. Rhein, both an M. D and D. D. S, published an exposé on the alveolar abscess and its prevention and curative treatment. He recognized the unique relationship of pyorrhea and alterations in pulp tissue, using his diagnostic acumen and appropriate testing, especially the application of cold. His diagnostic and treatment approaches were especially revolutionary during an area of wholesale tooth extraction in favor of prosthetic replacement, and this occurred prior to the conflagrations of Focal Infection that came to bear on both the dental profession and the public at large 15 years later.[20,21]
“It might well to devote a little attention to the question of the number of alveolar abscesses that are occasioned by attempting to conserve pulps with exposed or diseased. At the present time we do not hear nearly so much about the conservative treatment of the pulps of teeth,-a subject which ten years ago was worn threadbare at our dental sessions. The majority of observant practitioners have learned to radically modify their practice in this respect; at the same time, very few of them have had the courage to present to the profession the results of their modified course of treatment. In order to prevent this possibility of an alveolar abscess in well-formed adult teeth, it has become almost an invariable rule with me to remove a pulp if it be at all exposed. There is another class which requires such treatment, and which we meet especially in the large cities among the highly-strung, nervous organizations which produce so many pathological conditions. All of us occasionally come across alveolar abscesses due to the death of the pulp in a tooth which has never been attacked by caries. The percentage of such teeth among the active brain-workers in a city like New York is very large, and it is our duty to look out for such cases, especially in patients subject to attacks of pyorrhea alveolaris. The pulps in these teeth do not die rapidly, but is generally a slow and gradual cessation of vitality due to either a lack of nutritive substance, or, in some cases, to the extraordinary irritation produced by acute pericemental attacks. It has been a long-standing rule with me, in the treatment of severe cases of pyorrhea alveolaris, to diagnose as carefully as possible the amount of vitality in the pulps of the individual teeth which are badly affected. This is accompanied by placing the rubber-dam over each of such teeth in turn, and testing it with a spray of chloride of methyl. Any other intense cold or heat will answer the same purpose. In most cases, illumination with the electric light is of very little value. As soon as one of these teeth shows a lack of appreciation intense cold, it has become my practice to enter the pulp-chamber and thoroughly remove the contents of the canal, and treat in the manner I have outlined above. A large number of these cases, if operated upon at the right time, will show the pulp-contents to be devoid of any vitality up to within a short distance of the end of the root.
The result of leaving such pulp-tissue undisturbed for a longer period of time means the eventual loss of life of the remaining small portion of the pulp, followed generally by an alveolar abscess which in many cases many not even be diagnosed, as they frequently open into the pyorrheal pockets that are present in such mouths, instead of burrowing through the alveolar plate, as is the common result in acute alveolar abscess in normal teeth.
There is also another class in this category, where the life of the pulp at its entrance into the tooth is destroyed, while some vitality remains in the canal proper, nourished for the time being through the pericemental circulation. The removal of the pulps of such teeth is not only essentially necessary to the proper local treatment of existing pyorrhea, but is generally preventive of subsequent attacks of alveolar abscess.”
In the early 1900s, Dr. S. B. Luckie from Chester, PA, discussed the relationship of the pulpal tissues to the periodontium in its development, form, and function, and addressed the changes that occur in the dental pulp relative to the apical region in the presence of disease.“The relation of the pulp to the apical region is thus evident in the normal function of organic beings. It is no less interesting when modification of function and change of structure caused by disease are brought to our notice.”
He specifically addressed the changes that may occur in the size of the pulpal space in the presence of periodontal disease, an issue that has been controversial for decades.
“In pyorrhea alveolaris tubular calcification is augmented; the pulp and its dwelling-house are reduced in size. Whether this be a result of diathesis or local abnormality of function, the exalted circulation in the periapical tissue may be the excitation for the accompanying dental calcification.”
Luckie also addressed multiple ways in which bacteria from periodontal disease may gain access to an apparent intact dental pulp, yet the impact of these observations may have gone unheeded for decades.
First… “A suggestion has been made that they (bacteria) may work their way to the pulp through the cementum and dentin at the neck of the tooth. It is a doubtful manner for them to gain entrance, but it must not be considered settled until disposed of by microscopic examination and further knowledge of osmotic action in the cementum and dentin.” Today we know this is one of the main pathways for disease interchange between the pulp and periodontium.[23–26] Second, bacterial ingress via the circulation… “Another very possible way for them (bacteria) to find a favorable point is by the circulation.” In making this statement, Luckie even alludes to the possibility of bacteria coming from a distant site; ironically, the theory of “anachoresis,” which attempts to explain this phenomenon, was really not promulgated until 1941 by Robinson and Boling.
Luckie explains his take on the issue as follows: “Bacteria enter the circulation by wounds and other means, and find in distant parts of the body centers of low vital resistance and here deposit themselves and produce inflammation, while at the point of introduction but little reaction will occur.”
Within today’s understanding of these concepts, the most intimate and demonstrable relationship of the communication of inflammation between the pulp and periodontium is via the vascular system[28–31] as demonstrated anatomically at the root apex and accessory/aberrant canals in the presence of periodontal disease.[3,32–35]
At the height of the Focal Infection, following the impact of Hunter and Billings on the massive and wholesale extraction of teeth, Turner and Drew performed experiments to demonstrate the range of bacteriology present in pyorrhea, searching for the presence of microorganisms in the following tissues:
- The presence and occurrence of bacteria in living dental pulps
- The presence and nature of the bacteria in the pulp cavities and dentinal tubules of dead teeth
- The presence of organisms in cementum
- The presence of organisms in the periodontal membrane
- The presence of organisms in the gum
- The presence of organisms in granulomata attached to dead or pyorrhetic teeth
- The presence of organisms in the bone in cases of periodontal disease.
While they found organisms in all tissues of the pulp and periodontium, a cause-and-effect relationship could not be established microscopically. However, the fact remained that even if bacteria were present (for which we tend to say “infection” and which does not necessarily indicate virulence and invasiveness), their activity in the disease process if any could not be established. Of particular interest was their finding of bacteria in cementum. They postulated that “The cementum frequently becomes infected, and we may distinguish three routes of infection-viz., (i) via the pulp cavity and tubules; (ii) through the periodontal membrane; and (iii) from surface caries. This section seems to show that cementum can be infected from a living, but infected, periodontal membrane. There were no sections, however, showing the actual invasion of cementum by bacteria by way of the dentinal tubules.” This concept that was speculated by Luckie, has been shown to be a potential major pathway today, especially in the cervical region and in the presence of periodontal disease and following trauma.
In Marshall’s text, DiseasesoftheTeeth:DiagnosisandTreatment, he indicated that pulpal disturbances were frequently seen in long-standing pyorrhetic cases. Therefore, in 1926, there was already an indication that periodontal disease caused pulpal changes. Further evidence for this relationship and potential outcome was registered by Dr. Lester Cahn in 1927.
“I believe that such pulps become involved, either via the apical periodontium, or through a lateral channel, and that infection once established within the pulp, a constant periapical infection was maintained; and that although the lateral lesions were apparently healed the periapical tissue remained involved until the offending pulp was removed.”
Cahn indicated further that he had never found pulp tissue that had been removed from a pyorrhetic tooth to be normal; and where a pathological pulp was present, a pyorrhetic condition could not be cured by treatment applied exclusively to the external surface of the root, with no treatment of the pulp itself. Yet many of these findings and concepts promulgated in the early 1900s, were disavowed by publications in the 1960s and 1970s, which somewhat muddied the waters in this controversy by indicating that no direct impact was found on the pulp in the presence of periodontal disease.
Based on difficulties in diagnosis and management of teeth in the presence of pulpal and periodontal diseases, a number of articles promulgated various aspects of endodontic-periodontic lesion interrelationships, resulting in numerous classifications surfacing in the last 50–60 years. These multiple classification systems have been made in an attempt to clarify the confusion as it relates to endodontic-periodontic lesions [Table 1].
From a historical perspective, most of these classifications were made for clinical convenience to enhance rapid diagnoses and to proceed with treatment as opposed to elucidating the nature and cause of the disease processes and how they did or did not interact. To appreciate the historical relevance and to reflect on its integration of historical findings, the most popularly used classification among the profession in the last 50 years will be addressed relative to historical information presented above, that is, the Simon, Glick, and Frank Classification (SGF), a classification that has received contemporary revival in the current literature, while perpetuating some inaccuracies that were clearly clarified and obvious in historical writings.
The five classifications they provided were as follows: (1) primary pulpal lesions; (2) primary pulpal lesions with secondary imposition of periodontal disease; (3) primary periodontal lesions; (4) primary periodontal lesions with secondary imposition of pulpal disease; and finally, (5) combined pulpal-periodontal lesions in which independent disease processes in both tissues have joined or coalesced in the periradicular tissues. A distinct, sixth classification was later proffered by other authors for clarity as an addition to the SGF classification; concomitant pulpal-periodontal lesions in which the disease processes exist independently of each other and treatment from both perspectives will be necessary. Anticipated outcomes will depend on the specific treatments rendered both endodontically and periodontally for which outcomes of each are independent of the other. From these classifications, more accurate diagnoses of disease processes arose, but still, there was little known with regard to the relationship between the two tissue environments. In fact, one of the classifications, the combined lesion, was identified as rare to nonexistent.
Historical dilemmas that have confused diagnostic schemes or classifications lie in the inadequacies of pulp testing and their interpretation. This is true of both electric pulp testing and cold testing, the two most used tests.[52–56] While studies may support the validity of the tests, to some extent, there are no tests to demonstrate that vitality is accurate regarding the histological status or health or sickness of the pulp, as even current research will attest. The same is true for cold testing. The assumption that a pulp is nonvital when a cold test yields no response would be erroneous for several reasons, including but not limited to insulating aspects of reparative/irritational dentin and the presence of residual, persistent neural fibers in the pulp tissue[59,60] this is true even when a discernible periapical lesion is present. Furthermore, the percussion test that was historically identified as being related to the status of the periodontium has been erroneously used to determine pulp vitality. Moreover, to further confuse the issue, the wide range of radiographic assessments and interpretation found can often result in failure to identify the presence of degenerative changes in the pulp due to the long-term presence of periodontal disease or restorative factors. For example, the presence of pulp stones in the coronal and radicular pulp; the reduction in the size of the coronal pulp or the narrowing of the pulp canals; or even the presence of chronic focal sclerosing osteitis,[61–63] are all indicative of pulpal demise regardless of the pulp testing results. These concepts were in the mind and clinical observations of both Rhein in the late 1800s and Cahn in the 1920s for which they expressed their opinions in the literature.
If the SGF classification or one similarly presented by all the authors cited is used, the terms vital and nonvital are dubious as to identifying a correlation of periodontal disease’s impact on the pulp. To paraphrase a recent publication in this regard, “There is agreement between endodontists and periodontists that pulpal disease can impact on the periodontium…yet there is conflicting evidence as to whether periodontal disease can cause pulpal disease.” Based on historical evidence. the previous empirical statement by Dunlap et al. can be challenged as to both its accuracy and application in the diagnosis of pulpal-periodontal lesions.
Clinically, the ability to determine with any degree of accuracy the pulpal status has always been difficult. This was especially true since most of the diagnostic schemes used up until the 1970s focused on histologic classifications, until a more clinically relevant diagnostic scheme was proposed in 1977. These distinctions have been replaced with a myriad of terms that reflect clinical determinations and outcomes, such as sensibility testing, responsive, nonresponsive, and abnormal responsiveness. This explains why most clinicians, if they do sensibility testing (thermal, electric pulp test), in the presence of periodontal disease and get a response that is perceived as normal, will identify the tooth as vital (instead of focusing on the pulp tissue); hence, no further attention is paid to the variability of findings in the in the diagnosis or treatment plan. Here, the use of the term “vital” may be a misnomer as it does not convey the concept of sickness or health of the pulp, a concept that appears to have been better understood by our astute predecessors.
The facts as we know them from over 100 years ago are solid and meaningful and are just as applicable today as they were for our forefathers. While classifications are convenient, impressive on paper, fit into today’s way of thinking, and provide the clinician with a rapid decision tree, they may not afford an accurate, cognizant assessment of the true disease process that may be occurring between the two tissues of concern. Often, the challenges and dilemmas encountered in the “tissue-to-tissue” (pulp-to-periodontal) relationship are due to the pooling of all factors that involve the clinical science, treatment planning, and treatment procedures in “endodontics” and “periodontics.” Here again, this pooling can muddy the waters of the diagnostic relationship of disease processes, inflammatory communications, and tissue responses. The decision process in both the pulp-periodontal tissue and endodontic-periodontic interactions requires focused attention on specific findings and what they mean, as opposed to placing each case into a preconceived, arbitrary category, especially when the clinician is confused and cannot rapidly ascertain an acceptable diagnosis. In this regard, greater attention must be placed on the thorough assessment of the tissues in question along with an integrated analysis and synthesis of historic and current data obtained that may result in a repair-predictive, treatment-oriented diagnosis. Failure to do so often results in needless, inappropriate treatment, or just a wholesale extraction of teeth in favor of implants. Rest assured that when extraction occurs, little if any assessment of the causative agents ever crosses the clinician’s inquisitiveness, as opposed to the cognizant pursuit of knowledge, and intuitive evaluations as seen and documented by our forefathers. This is the key to the dilemma and focus of this historical assessment and which raises a plea for the incorporation of meaningful historical data into contemporary thought and application.
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