A New Concept of Periodontal Diseases
movements, (2) pain, (3) rearrangement of the occlusion by (unconsciously exerted) compensating movements after chewing, and (4) regeneration and adaptation of the periodontal tissues in periods of rest. Thus the chewing function may be said to be selfprotected and nontraumatic, apart from accidents. In searching for destructive forces in the masticatory sys tem, we should consider other activities of the system, such as bruxism, bruxomania, the Karolyi phenomenon, certain habits, tongue thrusting, and muscle spasms. A l l these activities beyond the chewing function may be called "parafunctions." Although there is some overlap ping, the parafunctions may be classified according to their cause into five categories.
by W A L T E R D R U M , DR. MED. DENT. Some of the opinions expressed in the following paper are contrary to much of our current thinking on the etiology of periodontal disease. However, it is felt that the reader would be interested in how authorities in another part of the world look at the problem of periodontal pathology and its treat ment.—The Editors
7
1. Psychically Motivated Parafunctions. More or less neurotic phenomena, including the Karolyi phenomenon, bruxism, bruxomania, clenching or grinding teeth at night, thumb sucking, nail biting, etc. 2. Stress-motivated Parafunctions. Non-neurotic phe nomena, reactions to stress, as by soldiers in combat, workers on high buildings, truck drivers, athletes, and persons in severe pain. 3. Habitual Parafunctions. Tailors, bootmakers, and upholsterers keeping pins between their teeth, writers chewing on pencils, drummers tapping their teeth to the rhythm of the music, etc. 4. Endogenous Parafunctions. Muscle spasms caused by diseases such as tetanus, meningitis, and epilepsy. 5. Hyper-compensating Parafunctions. Exaggerations of the normal compensating movements, triggered by occlusal interferences and other disturbances in the mouth. The parafunctions are very likely to be destructive forces, because all the protective mechanisms described above fail when parafunctions are exerted. The normal neuromuscular control is overruled by a feedback mecha nism of subcortical reflexes, the pain is diverted, the compensating movements are exaggerated and the regen erating and adapting processes are interrupted. The classification of parafunctions facilitates the choice of therapeutic means for eliminating them. Hypercompensating parafunctions can be eliminated by selec tive grinding or occlusal adjustment. Endogenous para functions disappear after treatment of the systemic disease by a physician. Habitual and stress-motivated parafunctions can be eliminated by patient education, whereas in psychically motivated parafunctions it may be helpful for the patient to consult a psychotherapist. Because a psychic component is always present in parafunctions, it is helpful to apply a Drum splint, which temporarily eliminates all parafunctions by the monitor effect. There is ample evidence concerning the exertion of parafunctions. The gnashing and grinding of teeth during sleep can often be heard. Sometimes contractions of the masseter muscles can be seen in persons who are unaware of their "habits." E i s m a n n has collected photographs
IT IS COMMONLY ACCEPTED that there are two types of periodontal diseases. The inflammatory type begins with a septic inflammatory process breaking the barrier of the gingival attachment and proceeding into the periodontal tissues and the alveolar bone. The nonin flammatory type begins with a dystrophic process involv ing the gingiva and the crest of the alveolar bone. Both types can be combined in different phases of the disease. 1-4
THE
N E W CONCEPT
In fact, however, both the inflammatory and nonin flammatory dystrophic types of periodontal diseases begin with a noninfectious traumatic destruction of alveolar bone, caused by traumatizing parafunctions and followed by changes in the gingiva. The latter may or may not be complicated by superimposed infectious inflammatory processes. A new concept to fit these facts is proposed : the concept that periodontal diseases are autodestructive processes in the masticatory system, with or without superimposed infectious inflammation. The theory of autodestruction is based on work by many investigators in many c o u n t r i e s . Ac ceptance of the proposed concept requires evidence that: (1) traumatizing forces exist in the masticatory system, (2) traumatic destruction of alveolar bone occurs, (3) changes in the gingiva follow destruction of alveolar bone, and (4) all persons afflicted by periodontal diseases exert parafunctions. Direct evidence is still lacking for certain details, because of the difficulty of direct observation and measurement. In such instances indirect but conclusive evidence will be presented, together with suggestions for obtaining direct evidence. 5
1 - 5 , 1 1 , 1 2 , 1 4
8
EVIDENCE FOR EXISTENCE OF TRAUMATIZING, DESTRUCTIVE FORCES IN T H E MASTICATORY
1
9
SYSTEM 1,6
It has been s h o w n that the masticatory system is protected against self-destruction during chewing by at least four protective biologic mechanisms: (1) highly sensitive neuromuscular control of the masticatory
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and motion pictures of children who demonstrate uncon scious exertion of various kinds of parafunctions. Statements of patients are reliable when they are positive. They are not reliable when they are negative, because most parafunctions are exerted unconsciously. Electromyography has been u s e d to show the contrac tions of the masticatory muscles. This method is valuable for detecting some, but not all, parafunctions. By con necting wires to the muscles and by installing bulky equipment, the psychic situation of the subject is altered. He may or may not exert his customary parafunctions; he may even exert "iatrogenic" parafunctions. Telemetry through miniaturized radiotransmitters in crowns or partial prostheses is perhaps the best method to gain information about all parafunctions. A t present, however, this method can be used only in research applications. 1,4
TRAUMATIZING POTENTIAL OF PARAFUNCTIONS
Although parafunctions might seem to be of a harm less, nontraumatizing nature, evidence will be presented that they have a high traumatizing potential and that they can cause pathologic signs and symptoms. By periodontometry, M ü h l e m a n n has shown that the mobility of teeth is increased when the patient has exerted parafunctions during the night. Ramfjord pre sented direct evidence for the traumatizing potential of parafunctions such as biting on a pipe stem (Fig. 1) or penholder (Fig. 2a and b). Fröhlich reported direct evidence for the traumatizing potential of the parafunction of tongue thrusting (Fig. 3). Lorenz treated two sisters, aged 8 and 14, at the same time. Both had the habit of nail biting. The younger girl preferred the left central and lateral incisors; she had a Stillman's cleft on the left mandibular incisor. Her sister preferred the right central and lateral incisors; she had a Stillman's cleft on a right mandibular incisor (Fig. 4a and b). This coincidence provides direct evidence for the 11
1
12
13
FIGURE 1. Traumatizing effects of the parafunction of biting on a pipe stem. Destruction of tooth substance.
FIGURE 2 . a . Parafunction of biting on a penholder; b . Trau matizing effect: destruction of bone and periodontal tissues.
cause and effect relationship between a traumatizing parafunction (nail biting) and a periodontal lesion (Still man's cleft). Indirect, but conclusive evidence for the traumatizing potential of parafunctions can be gained from the study of tooth abrasions. In the dentition of prehistoric and primitive populations, tooth abrasion was a consequence of mastication. In the dentition of recent, civilized populations very little abrasion is caused by abrasive particles in the food. Severe abrasions, as shown in Figure 5, are not caused from mastication but by parafunctional attrition by unconscious grinding of the teeth night and day. Therefore, it may be concluded that, when the traumatic potential of parafunctions is great enough to cause destruction of hard tooth enamel, it surely will be great enough to cause destruction of periodontal tissues. Whether traumatizing parafunctions lead to attrition
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horizontal forces are developed which traumatize the periodontal tissues. "Diagnosis ex juvantibus" means securing a diagnosis from the success of certain therapeutic methods. Selec tive grinding and insertion of splints are therapeutic techniques for eliminating or distributing occlusal trau matizing forces. When these are used commonly to influence periodontal lesions and disturbances of the temporomandibular joint, it may be concluded "ex juvantibus," that the lesions have been caused by occlusal forces, i.e., traumatizing parafunctions. FIGURE 3. Traumatizing effect of the paprafunction of tongue thrusting on the tongue: hyperkeratotic impressions.
EVIDENCE FOR TRAUMATIC DESTRUCTION OF ALVEOLAR
B O N E BY PARAFUNCTIONS
Destruction of alveolar bone is a well known event in the course of periodontal diseases. It is also well known that bone may be destroyed by a septic inflammatory process or by an aseptic, mechanically traumatic process. It is widely believed that in periodontal disease bone is destroyed by a septic inflammatory process (pocket formation), beginning at the gingival margin and spread ing irregularly through the periodontal tissues and alveo-
FIGURE 5. Severe abrasions. Not from mastication, but parafunctional attrition.
FIGURE 4.a and b. Traumatizing effect of the parafunction of nail biting. Stillmarfs clefts (arrows) on mandibular right and left incisors.
or to periodontal diseases depends on anatomical charac teristics of the dentition. Figure 6 shows two extremely different types of dentition. The Patagonian (left) has flat cusps and edge-to-edge bite. When he grinds his teeth, small horizontal forces are developed, the enamel will be abraded, but the periodontal tissues remain healthy. The Ethiopian (right) has steep cusps and deep overbite. When he grinds his teeth, few signs of abrasion are seen on the steep inclines of the teeth, but strong
FIGURE 6. Extremely different anatomical type of dentition. (Left) Patagonian. (Right) Ethiopean. For explanation see text.
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lar bone. Periodontists are aware that mechanical trau matizing forces, such as bruxism, also may play a role in bone destruction in periodontal diseases; however, they assume that this is a secondary role. Glickman and Smulow have suggested "co-destruction," meaning that septic and traumatic inflammatory processes may act simultaneously. In contrast to this view, parafunctional trauma may be seen as the primary source of bone destruction in periodontal diseases, with infectious proc esses occurring later and becoming superimposed upon existing traumatic lesions. Unfortunately, it is very difficult to present direct evidence for this theory, because small defects in the alveolar bone cannot be detected accurately on radiographs. The small bone lesions caused by the traumatizing effect of parafunctions are commonly stituated in the "pressure zones" created by a tilted tooth on the vestibular or oral side of the alveolus of this tooth. There, in radiographs, they are overshadowed by the opaque bulk of the root. Thus, even considerable defects cannot be seen on the radiograph. Reichborn-Kjennerud has shown a striking example (Fig. la and b). Although the labial surfaces of the roots of the incisors are completely denuded of bone, no defect is seen on the radiograph. One may hope that recent developments in medical diagnostic techniques (scintigraphy, echoencephalogra4
14
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phy, etc.) may presage similar developments in dentistry to permit early diagnosis of alveolar bone defects. With direct evidence lacking, indirect but conclusive evidence is gained from orthodontic studies. In order to move a tooth in the jaw, the orthodontist must destroy a certain amount of alveolar bone and have it rebuilt. He must apply traumatizing, bone-destroying forces on the teeth and he achieves his goal with very small, but continuously acting, forces. When a patient exerts parafunctions, e.g., uncon sciously grinding or clenching his teeth, he applies forces analogous to those effected by orthodontic appliances. These parafunctions have a high traumatizing potential, as seen in parafunctional attrition (Fig. 5). Therefore, alveolar bone is destroyed to a greater or lesser degree when parafunctions are exerted. EVIDENCE
FOR CHANGES
IN
GINGIVA
DESTRUCTION OF ALVEOLAR
FOLLOWING
BONE
The traumatizing forces of parafunctions act on the tooth, the root of the tooth, and the periodontal tissues. They do not act directly on the gingiva, because the gingival tissues are connected with the tooth in form of a cuff, which is firm, yet mobile, yielding to mechanical forces. However, when aseptic, traumatic inflammatory processes occur in the alveolus, the gingiva will be involved in various different ways. Inflammatory or noninflammatory changes in the gingiva will be seen, depending on the following factors: (1) force of the parafunctions; (2) direction of that force; (3) duration of the parafunctions; (4) intervals between periods of para functions, in which tissues may regenerate; (5) configura tion of the roots; (6) configuration of the alveolar bone; and (7) position of teeth. There have been no longitudinal studies to investigate the interdependence of these factors. But, tentatively accepting the idea that parafunctions cause minor, but cumulative destruction of the alveolar bone, it is not difficult to imagine several combinations and their results. RETRACTION
O F GINGIVA,
MCCALL
STILLMAN'S
FIGURE 7.a. Labial surfaces of the roots are completely denuded of bone; b. These defects cannot be seen on the radiograph.
FESTOONS, A N D
CLEFTS
It has long been supposed that M c C a l l festoons are of traumatic origin. Direct evidence connecting Stillman's clefts with parafunctional influences has been presented by Lorenz (see Fig. 1). The festoon form of gingival retraction may be explained in the following way. In these patients, bone destruction is quite evident and one sees part of the root denuded of bone. N o w there seems to be a distinct correlation between the configura tion of the alveolar bone and the configuration of the gingiva. When the alveolar ridge is resorbed after tooth extractions, the gingiva covering the ridge is also re sorbed. One could say that the gingiva follows the alveolar bone. So it is readily understood that the retracted gingiva assumes the form of a festoon, follow-
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ing the V-shaped defect in the alveolar bone. In nonin flammatory retraction of the gingiva with thin, sharp edges, the process may be enhanced by vigorous horizon tal brushing of the teeth and soft tissues. Often, wedgeshaped defects on the tooth necks (marks of the tooth brush) are found together with gingival retraction (Fig. 8). Retraction of the gingiva on the palatal surfaces of the roots of maxillary molars may be enhanced by parafunc tions of the tongue. In M c C a l l festoons the bulky roll of the gingival margins seems to reinforce the gingival cuff covering and protecting the epithelial attachment. In Stillman's cleft there seems to be a tearing effect of inserting muscles. This explanation of the phenomenon of noninflamma tory changes in the gingiva after destruction of alveolar bone seems more satisfactory than the assumption of a dystrophic type of periodontal disease of unknown origin. POCKET
FORMATION
When, how, and why pocket formation begins have always been the most critical questions in periodontology. Undoubtedly it is an infectious inflammatory process starting at the gingival margin. However, the gingival cuff normally protects the periodontal tissues against the invasion of microorganisms and their products. Even an inflamed gingival cuff is able to protect the periodontal tissues. Often we find gingivitis and much plaque and calculus, but no pocket formation, and again we find pocket formation in relatively clean mouths. Numerous investigations have been carried out to find a factor or factors which may lower the resistance of the gingival cuff in such a way that bacteria may penetrate the barrier of the epithelial attachment. If we tentatively accept the idea that periodontal diseases do not begin with pocket formation, but with lesions in the alveolar bone caused by traumatizing parafunctions, we have no difficulty at all in explaining pocket formation. The existence of aseptic traumatic inflammatory processes in
the alveolus is the factor which lowers the resistance of the gingival cuff, by impairing the blood supply of the epithelial attachment. The blood supply is impaired in two ways: (1) quantita tively, by temporary compression of the periodontal and osseal blood vessels in the pressure zones in the alveolus; and (2) qualitatively, by depriving the epithelial attach ment of blood-supplied components needed for repair of the inflammation in the alveolus. A s a consequence of inadequate nourishment, the resistance of the gingival cuff is lowered and sooner or later microorganisms are able to break the barrier of the epithelial attachment. O f course, it is not possible to present direct evidence for this succession of events, because periodontal diseases have never been observed from beginning to end, and. because small defects in the alveolar bone cannot be detected on radiographs. But some observations may be regarded as indirect evidence. There is, for example, no direct correlation between pocket depth and bone destruction. Relatively large amounts of bone destruction are often found near the root apex and near the alveolar crest, whereas pocket formation is shallow, not even reaching the alveolar crest. This phenomenon (Häupl's "Parodontics profun da") has been attributed to "distant effects" of inflam mation in the gingival cuff and to other causes. A more satisfying explanation seems to be that the bone has been destroyed by accumulated parafunctional trauma, before pocket formation began. Another observation is the correlation between pocket depth and tooth mobility. Often a combination is found of a relatively shallow pocket and relatively great mobility of a tooth. This is expecially true for maxillary molars with relatively parallel, conically shaped roots. This again may be regarded as indirect evidence that bone destruction, allowing mobility of the tooth, has been caused by parafunctional trauma before pocket forma tion began. Naturally, molars with cone-shaped roots are more readily tilted by parafunctional forces than molars with diverging roots which impede tooth movement. Many other supporting observations cannot be discussed in the limited space of this report. ANIMAL 1-3
FIGURE 8. Noninflammatory retraction of the gingiva, com bined with wedge-shaped defects in the tooth necks.
EXPERIMENTS
Periodontists have stated categorically that occlusal trauma (analogous to parafunctional trauma) never leads to pocket formation. They have based their opinion on animal experiments. This opinion must be challenged, because one of the factors listed above has been neglected in the animal experiments: intervals between periods of parafunctions, in which tissues may regenerate. Pocket formation is a slow process, beginning with the accumulation of minor traumatic defects in the alveolar bone, which impairs the blood supply of the gingival cuff and gradually weakens the resistance of the epithelial attachment against invasion of microorganisms.
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To cause pocket formation in animal experiments, this sequence must be simulated. However, the investigators have used appliances which have grossly and continu ously traumatized the periodontal tissues. That this was a mistake will be seen in the following example. Assume one wishes to show that the trauma of digging leads to callus formation on the hands. Give a man a spade and force him to dig vigorously and continuously. We know in advance that this investigator makes the mistake of omitting intervals—he will find various lesions on the hand of the digger, but no callus formation. Similarly, the animal experiments carried out heretofore are not evidence that parafunctional trauma does not lead to pocket formation. E V I D E N C E T H A T A L L P E R S O N S A F F L I C T E D BY P E R I O D O N T A L DISEASES E X E R T
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incidence of periodontal diseases is greater among the flight personnel than among the ground personnel. Periodontal diseases have been called diseases of modern civilization. This points to the increased stress of living in modern cities. In the therapy of periodontal diseases increasing importance is assigned to measures for adjusting the occlusion, meaning elimination of trigger factors for hyper-compensating parafunctions. This strongly sug gests that traumatizing parafunctions are an important factor in the etiology of periodontal diseases. Indeed, traumatizing parafunctions should be regarded as the main causal factor in periodontal diseases. In treating patients with periodontal disease, we must assume that recurrences are inevitable unless parafunctions have been eliminated.
PARAFUNCTIONS SUMMARY
The patient's own statements may be regarded as direct evidence of the exertion of parafunctions, and we have never failed to elicit such statements from patients. However, psychologic skill is required to elicit such statements. The patient is almost invariably unconscious of his oral habits and he may resent the dentist's questioning. Ask him to become conscious of the position of his teeth, when he picks up a telephone. Tell him that his lips should be together, but his teeth should be apart. Ask him to report deviations, and then point out the possible consequences. It should be kept in mind that a negative answer is not evidence that the patient does not exert parafunctions. It may take weeks, months, or even years, before the patient becomes aware of his oral habits. For the dentist, sure signs of the exertion of parafunctions are the following: (1) strong abrasion on all teeth; (2) grinding facets on several teeth; (3) pain or peculiar feelings in the masticatory muscles in the morning; (4) pain or disturbances in the temporomandibular joints; (5) masseter hypertrophy; (6) chronic gingival hyperemia, disappearing after insertion of a Drum splint; and (7) periodontal diseases with or without infection, which are not symptoms of systemic diseases. CONCLUSION
Many systemic factors play a certain role in the development of periodontal diseases. But "function" is a predominant factor in the fate of the entire alveolar process: it is resorbed when its function ceases after the loss of teeth. We can, therefore, rightly assume that exaggerated function, i.e., traumatizing parafunctions, plays a dominant role in the development of diseases in the alveolar process. Ramfjord has found increased bruxism (a parafunction) in students before an examination. Psychologic studies have shown that an increased incidence of periodontal disease is found in persons with emotional stress. In the U . S . A i r Force, it has been found that the 1
Both the inflammatory and noninflammatory types of periodontal diseases begin with an aseptic, traumatic destruction of alveolar bone, caused by traumatizing parafunctions and followed by changes in the gingiva. The latter may or may not have a superimposed infec tious inflammatory process. A new concept to fit these facts is proposed: periodontal diseases are autodestructive processes in the masticatory system, with or without superimposed septic inflammation. To confirm the theory of autodestruction, direct evidence as well as indirect but conclusive evidence is given for the existence of traumatizing forces in the masticatory system, for traumatic destruction of alveolar bone, for changes in the gingiva following destruction of alveolar bone, and for the parafunctions by all persons afflicted by periodontal disease. It is concluded that traumatizing parafunctions are the main factor in the etiology of periodontal diseases and that in therapy recurrences are inevitable unless para functions have been eliminated. REFERENCES
1. Ramfjord, S. P., and Ash, M . M . : Occlusion. Philadelphia, W. B. Saunders Co., 1966. 2. Grant, D. A., Stern, I. B., and Everett, F. G.: Orban s Parodontologie. Berlin, Quintessenz-Verlag, 1965. 3. Goldman, H. M . : Periodontia. St. Louis, C V. Mosby Co., 1953. 4. Glickman, I., and Smulow, J. B.: The combined effect of inflammation and trauma from occlusion in periodontics. Int Dent J 19: 393, 5.
Drum,
1969.
W.:
Parafunktionen
und
Autodestruktionsp-
rozesse. Berlin, Quintessenz-Verlag, 1969. 6. Drum, W.: Autodestruction of the masticatory system. Parodontologie
16: 155,
1962.
7. Drum, W.: Klassifikation von Parafunktionen. Dtsch ZahnaerztlZ
17: 411,
1963.
8. Schuyler, C. H.: Fundamental principles in the correction of occlusal disharmony. J Am Dent Assoc 22: 1193, 1935. 9. Drum, W.: The mechanism of splints according to Drum. Quintessence Int 1: 93,
1969.
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10. Eismann, D.: Über das Ausmass der Parafunktionen im allgemeinen Lebensvollzug des Kindes. Berlin, QuintessenzVerlag, 1961. 11. Mühlemann, H. R., Herzog, H., and Vogel, A.: Occlusal trauma and tooth mobility. Schweiz Monatsschr Zahnheilkd 66: 527, 1956.
12. Fröhlich, E.: Über Parafunktionen. Symptomatologie, Ätiologie und Therapie. Dtsch Zahnaerztl Z 21: 536, 1966. 13. Lorenz, G.: Wirkungen von Parafunktionen (Nägelbeißen) auf das Zahnbett. Berlin, Quintessenz-Verlag, 1968. 14. Reichborn-Kjennerud, J.: Tro og periodonti. Nor Tannlaegeforen Tid 73: 307, 1963.
Abstracts CYTOTOXIC EFFECTS OF SOLUBLE PLAQUE EXTRACT ON CELLS IN VITRO
ULTRASTRUCTURE OF THE GINGIVAL EPITHELIUM IN THE NEW BORN CAT—SOME CHARACTERISTICS OF THE INTERCELLULAR JUNCTIONS
Mlinek, A . , Buchner, A . , Hennig, S., and Begleiter, A . J Periodont Res 9: 342, N o . 6, 1974.
Mignon, M . L . , Malet, P., Perissel, B., and Geneix, A . J Dent Res 53: 1484, November-December, 1974.
Gingival inflammation is accompanied by exudation of gingival fluid into the crevice which results in a continuous bathing of the space between the adherent plaque and crevicular epithelium. It is therefore assumed that plaque products reaching the periodontal tissues are water soluble. The effects of this water soluble plaque extract on cultured cells when added at different phases of the normal growth curve were studied. Plaque was gathered from patients and pooled and a stock solution of 50 mg of plaque extract (P.E.) per 1 ml of Eagle's Basal Medium was made. Final concentrations of 0.5, 1.5 and 2.0 mg of P . E . per 1 m l of cell suspension were used. The cell culture was a fibroblast-like cell line ( B H K ) from a hamster kidney. The results showed an inhibition of cell growth in culture by the plaque extract. Higher doses of plaque extract resulted in increased inhibition. Cells treated with P . E . were fewer in number than the control, exhibited vacuolization and lysis of cytoplasm, nuclei appeared dark and pyknotic and intranuclear structures were not readily observed. Higher concentrations of P . E . resulted in faster and more intensive degenera tive signs. The damage was caused whether added before cells attached to the culture surface or after in the growth phase. This showed that P . E . is cytotoxic and that bacterial plaque products may cause damage to tissues on a cellular level. It can then be hypothesized that bacterial plaque damages both crevicular and attachment epithelium and initiates inflammatory reaction and pocket formation in vitro. Depart ment of Pathology, Sackler School of Medicine, School of Continuing Education, Dental Division, Tel-Aviv University, Ramat-Aviv, Israel
The electron microscope was used to study intercellular junctions in the gingival epithelium of new born cats. Gingival epithelia of 2 or 3 mm were taken from the incisive part of regions where odontogenesis was active, from the region of the future diastema between canines and molars, and skin. A comparison was then made of gingiva during odontogenesis, mucosa without dental organ, and skin. A total of twelve female and eight male kittens were used. They were sacrificed at intervals from 1 to 15 days. New born cat gingiva showed numerous hemidesmosomes and desmosomes in the stratum spinosum with tonofibril systems. Zonalae occludens were rare and mainly seen in the stratum spinosum. Other junctional types were not observed. It was found that the desmosomes were well defined. The tonofilament apparatus was especially developed in the stratum spinosum. Spaces between membrane leaflets increased with age, but desmosome length remained constant. The number and size of tight junctions in kittens were constant during the experimental period. Intercellular spaces were wide with extensive distensions in the stratum spinosum. A s deciduous teeth erupted the intercellular spaces widened. Skin desmosomes were more irregular and the tonofibrils shorter and more clustered than the gingiva. Intercellular spaces were narrower, junctional types less defined and tight junctions less numerous than epithelium of the gingiva. The epidermal tight junctions were also predominately located in the stratum spinosum. Laboratory of Histology and Embryology of UER Medicine, University of Clermont-Ferrand, BP 38, 63001 Clermont-Ferrand Cedex, France
CHEMICAL PREVENTION OF CALCULUS FORMATION IN THE RAT
A HLSTOCHEMICAL STUDY OF GLYCOSIDASES IN HYDANTOIN INDUCED HYPERPLASTIC, HEALTHY AND INFLAMED HUMAN GINGIVA
2 1
Stookey, G . K . , and M c D o n a l d , J . L . J Dent Res 53: 1334, November-December, 1974. The ability of an amidopolyphosphate, Victamide, to prevent calculus, was investigated by feeding rats a calculus-producing diet and treating them with either a solution or slurry of Victamide twice daily for three weeks. Application was done to each molar quadrant using cotton applicators. The rats were killed and the molar quadrants were removed surgically and examined for calculus under a binocular dissecting microscope. T w o studies were done. In the first, concentra tions of victamide ranging from 1 to 5% were applied topically. Significant reductions in calculus formation were observed after three weeks for concentrations between 2.5 and 5.0%. The use of the amidopolyphosphate as a dentifrice in the second study confirmed the inhibitory action by reducing calculus formation by 31.3%. Although the exact mechanism is unknown, the calculus inhibition properties of amidopolyphosphate might be a result of the formation of an insoluble complex with the nucleating template, or the chelation of available calcium ions. Oral Health Research Institute, Indiana University-Pur due University at Indianapolis, Indiana 46202 U.S.A.
Larmas, L . J Periodont Res 9: 374, N o . 6, 1974. Various azo dyes for ß - g l u c u r o n i d a s e , α - and ß-glucosidase, for ß-galactosidase and for N-acetylglucosaminidase were used in healthy and inflamed human gingiva and hydantoin induced hyperplasia. Strong ß-glucuronidase activity was observed in all types of the tissue of inflamed gingiva and hydantoin induced hyperplasia. The fibroblasts, inflammatory cells, polymorphonuclear leucocytes, and marcophages showed moderate ß-glucuronidase activity. In healthy gingiva only a few inflammatory cells and macrophages were observed and a low activity of ß-glucuronidase was noted, otherwise, the distribution of this enzyme was similar to what it was in the two other samples. There was weak activity of ß-galactosidase, N-acetylglucosaminidase and ßglucosidase in all of the samples. There was no ß-glucuronidase activity in stratum corneum of healthy tissue. The activity of this enzyme in stratum corneum of the other samples may be due to microbial enzyme which diffused to this layer. Institute of Dentistry, University of Turku, SF-20520, Turku 52 Finland
movements, (2) pain, (3) rearrangement of the occlusion by (unconsciously exerted) compensating movements after chewing, and (4) regeneration and adaptation of the periodontal tissues in periods of rest. Thus the chewing function may be said to be selfprotected and nontraumatic, apart from accidents. In searching for destructive forces in the masticatory sys tem, we should consider other activities of the system, such as bruxism, bruxomania, the Karolyi phenomenon, certain habits, tongue thrusting, and muscle spasms. A l l these activities beyond the chewing function may be called "parafunctions." Although there is some overlap ping, the parafunctions may be classified according to their cause into five categories.
by W A L T E R D R U M , DR. MED. DENT. Some of the opinions expressed in the following paper are contrary to much of our current thinking on the etiology of periodontal disease. However, it is felt that the reader would be interested in how authorities in another part of the world look at the problem of periodontal pathology and its treat ment.—The Editors
7
1. Psychically Motivated Parafunctions. More or less neurotic phenomena, including the Karolyi phenomenon, bruxism, bruxomania, clenching or grinding teeth at night, thumb sucking, nail biting, etc. 2. Stress-motivated Parafunctions. Non-neurotic phe nomena, reactions to stress, as by soldiers in combat, workers on high buildings, truck drivers, athletes, and persons in severe pain. 3. Habitual Parafunctions. Tailors, bootmakers, and upholsterers keeping pins between their teeth, writers chewing on pencils, drummers tapping their teeth to the rhythm of the music, etc. 4. Endogenous Parafunctions. Muscle spasms caused by diseases such as tetanus, meningitis, and epilepsy. 5. Hyper-compensating Parafunctions. Exaggerations of the normal compensating movements, triggered by occlusal interferences and other disturbances in the mouth. The parafunctions are very likely to be destructive forces, because all the protective mechanisms described above fail when parafunctions are exerted. The normal neuromuscular control is overruled by a feedback mecha nism of subcortical reflexes, the pain is diverted, the compensating movements are exaggerated and the regen erating and adapting processes are interrupted. The classification of parafunctions facilitates the choice of therapeutic means for eliminating them. Hypercompensating parafunctions can be eliminated by selec tive grinding or occlusal adjustment. Endogenous para functions disappear after treatment of the systemic disease by a physician. Habitual and stress-motivated parafunctions can be eliminated by patient education, whereas in psychically motivated parafunctions it may be helpful for the patient to consult a psychotherapist. Because a psychic component is always present in parafunctions, it is helpful to apply a Drum splint, which temporarily eliminates all parafunctions by the monitor effect. There is ample evidence concerning the exertion of parafunctions. The gnashing and grinding of teeth during sleep can often be heard. Sometimes contractions of the masseter muscles can be seen in persons who are unaware of their "habits." E i s m a n n has collected photographs
IT IS COMMONLY ACCEPTED that there are two types of periodontal diseases. The inflammatory type begins with a septic inflammatory process breaking the barrier of the gingival attachment and proceeding into the periodontal tissues and the alveolar bone. The nonin flammatory type begins with a dystrophic process involv ing the gingiva and the crest of the alveolar bone. Both types can be combined in different phases of the disease. 1-4
THE
N E W CONCEPT
In fact, however, both the inflammatory and nonin flammatory dystrophic types of periodontal diseases begin with a noninfectious traumatic destruction of alveolar bone, caused by traumatizing parafunctions and followed by changes in the gingiva. The latter may or may not be complicated by superimposed infectious inflammatory processes. A new concept to fit these facts is proposed : the concept that periodontal diseases are autodestructive processes in the masticatory system, with or without superimposed infectious inflammation. The theory of autodestruction is based on work by many investigators in many c o u n t r i e s . Ac ceptance of the proposed concept requires evidence that: (1) traumatizing forces exist in the masticatory system, (2) traumatic destruction of alveolar bone occurs, (3) changes in the gingiva follow destruction of alveolar bone, and (4) all persons afflicted by periodontal diseases exert parafunctions. Direct evidence is still lacking for certain details, because of the difficulty of direct observation and measurement. In such instances indirect but conclusive evidence will be presented, together with suggestions for obtaining direct evidence. 5
1 - 5 , 1 1 , 1 2 , 1 4
8
EVIDENCE FOR EXISTENCE OF TRAUMATIZING, DESTRUCTIVE FORCES IN T H E MASTICATORY
1
9
SYSTEM 1,6
It has been s h o w n that the masticatory system is protected against self-destruction during chewing by at least four protective biologic mechanisms: (1) highly sensitive neuromuscular control of the masticatory
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and motion pictures of children who demonstrate uncon scious exertion of various kinds of parafunctions. Statements of patients are reliable when they are positive. They are not reliable when they are negative, because most parafunctions are exerted unconsciously. Electromyography has been u s e d to show the contrac tions of the masticatory muscles. This method is valuable for detecting some, but not all, parafunctions. By con necting wires to the muscles and by installing bulky equipment, the psychic situation of the subject is altered. He may or may not exert his customary parafunctions; he may even exert "iatrogenic" parafunctions. Telemetry through miniaturized radiotransmitters in crowns or partial prostheses is perhaps the best method to gain information about all parafunctions. A t present, however, this method can be used only in research applications. 1,4
TRAUMATIZING POTENTIAL OF PARAFUNCTIONS
Although parafunctions might seem to be of a harm less, nontraumatizing nature, evidence will be presented that they have a high traumatizing potential and that they can cause pathologic signs and symptoms. By periodontometry, M ü h l e m a n n has shown that the mobility of teeth is increased when the patient has exerted parafunctions during the night. Ramfjord pre sented direct evidence for the traumatizing potential of parafunctions such as biting on a pipe stem (Fig. 1) or penholder (Fig. 2a and b). Fröhlich reported direct evidence for the traumatizing potential of the parafunction of tongue thrusting (Fig. 3). Lorenz treated two sisters, aged 8 and 14, at the same time. Both had the habit of nail biting. The younger girl preferred the left central and lateral incisors; she had a Stillman's cleft on the left mandibular incisor. Her sister preferred the right central and lateral incisors; she had a Stillman's cleft on a right mandibular incisor (Fig. 4a and b). This coincidence provides direct evidence for the 11
1
12
13
FIGURE 1. Traumatizing effects of the parafunction of biting on a pipe stem. Destruction of tooth substance.
FIGURE 2 . a . Parafunction of biting on a penholder; b . Trau matizing effect: destruction of bone and periodontal tissues.
cause and effect relationship between a traumatizing parafunction (nail biting) and a periodontal lesion (Still man's cleft). Indirect, but conclusive evidence for the traumatizing potential of parafunctions can be gained from the study of tooth abrasions. In the dentition of prehistoric and primitive populations, tooth abrasion was a consequence of mastication. In the dentition of recent, civilized populations very little abrasion is caused by abrasive particles in the food. Severe abrasions, as shown in Figure 5, are not caused from mastication but by parafunctional attrition by unconscious grinding of the teeth night and day. Therefore, it may be concluded that, when the traumatic potential of parafunctions is great enough to cause destruction of hard tooth enamel, it surely will be great enough to cause destruction of periodontal tissues. Whether traumatizing parafunctions lead to attrition
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horizontal forces are developed which traumatize the periodontal tissues. "Diagnosis ex juvantibus" means securing a diagnosis from the success of certain therapeutic methods. Selec tive grinding and insertion of splints are therapeutic techniques for eliminating or distributing occlusal trau matizing forces. When these are used commonly to influence periodontal lesions and disturbances of the temporomandibular joint, it may be concluded "ex juvantibus," that the lesions have been caused by occlusal forces, i.e., traumatizing parafunctions. FIGURE 3. Traumatizing effect of the paprafunction of tongue thrusting on the tongue: hyperkeratotic impressions.
EVIDENCE FOR TRAUMATIC DESTRUCTION OF ALVEOLAR
B O N E BY PARAFUNCTIONS
Destruction of alveolar bone is a well known event in the course of periodontal diseases. It is also well known that bone may be destroyed by a septic inflammatory process or by an aseptic, mechanically traumatic process. It is widely believed that in periodontal disease bone is destroyed by a septic inflammatory process (pocket formation), beginning at the gingival margin and spread ing irregularly through the periodontal tissues and alveo-
FIGURE 5. Severe abrasions. Not from mastication, but parafunctional attrition.
FIGURE 4.a and b. Traumatizing effect of the parafunction of nail biting. Stillmarfs clefts (arrows) on mandibular right and left incisors.
or to periodontal diseases depends on anatomical charac teristics of the dentition. Figure 6 shows two extremely different types of dentition. The Patagonian (left) has flat cusps and edge-to-edge bite. When he grinds his teeth, small horizontal forces are developed, the enamel will be abraded, but the periodontal tissues remain healthy. The Ethiopian (right) has steep cusps and deep overbite. When he grinds his teeth, few signs of abrasion are seen on the steep inclines of the teeth, but strong
FIGURE 6. Extremely different anatomical type of dentition. (Left) Patagonian. (Right) Ethiopean. For explanation see text.
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lar bone. Periodontists are aware that mechanical trau matizing forces, such as bruxism, also may play a role in bone destruction in periodontal diseases; however, they assume that this is a secondary role. Glickman and Smulow have suggested "co-destruction," meaning that septic and traumatic inflammatory processes may act simultaneously. In contrast to this view, parafunctional trauma may be seen as the primary source of bone destruction in periodontal diseases, with infectious proc esses occurring later and becoming superimposed upon existing traumatic lesions. Unfortunately, it is very difficult to present direct evidence for this theory, because small defects in the alveolar bone cannot be detected accurately on radiographs. The small bone lesions caused by the traumatizing effect of parafunctions are commonly stituated in the "pressure zones" created by a tilted tooth on the vestibular or oral side of the alveolus of this tooth. There, in radiographs, they are overshadowed by the opaque bulk of the root. Thus, even considerable defects cannot be seen on the radiograph. Reichborn-Kjennerud has shown a striking example (Fig. la and b). Although the labial surfaces of the roots of the incisors are completely denuded of bone, no defect is seen on the radiograph. One may hope that recent developments in medical diagnostic techniques (scintigraphy, echoencephalogra4
14
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phy, etc.) may presage similar developments in dentistry to permit early diagnosis of alveolar bone defects. With direct evidence lacking, indirect but conclusive evidence is gained from orthodontic studies. In order to move a tooth in the jaw, the orthodontist must destroy a certain amount of alveolar bone and have it rebuilt. He must apply traumatizing, bone-destroying forces on the teeth and he achieves his goal with very small, but continuously acting, forces. When a patient exerts parafunctions, e.g., uncon sciously grinding or clenching his teeth, he applies forces analogous to those effected by orthodontic appliances. These parafunctions have a high traumatizing potential, as seen in parafunctional attrition (Fig. 5). Therefore, alveolar bone is destroyed to a greater or lesser degree when parafunctions are exerted. EVIDENCE
FOR CHANGES
IN
GINGIVA
DESTRUCTION OF ALVEOLAR
FOLLOWING
BONE
The traumatizing forces of parafunctions act on the tooth, the root of the tooth, and the periodontal tissues. They do not act directly on the gingiva, because the gingival tissues are connected with the tooth in form of a cuff, which is firm, yet mobile, yielding to mechanical forces. However, when aseptic, traumatic inflammatory processes occur in the alveolus, the gingiva will be involved in various different ways. Inflammatory or noninflammatory changes in the gingiva will be seen, depending on the following factors: (1) force of the parafunctions; (2) direction of that force; (3) duration of the parafunctions; (4) intervals between periods of para functions, in which tissues may regenerate; (5) configura tion of the roots; (6) configuration of the alveolar bone; and (7) position of teeth. There have been no longitudinal studies to investigate the interdependence of these factors. But, tentatively accepting the idea that parafunctions cause minor, but cumulative destruction of the alveolar bone, it is not difficult to imagine several combinations and their results. RETRACTION
O F GINGIVA,
MCCALL
STILLMAN'S
FIGURE 7.a. Labial surfaces of the roots are completely denuded of bone; b. These defects cannot be seen on the radiograph.
FESTOONS, A N D
CLEFTS
It has long been supposed that M c C a l l festoons are of traumatic origin. Direct evidence connecting Stillman's clefts with parafunctional influences has been presented by Lorenz (see Fig. 1). The festoon form of gingival retraction may be explained in the following way. In these patients, bone destruction is quite evident and one sees part of the root denuded of bone. N o w there seems to be a distinct correlation between the configura tion of the alveolar bone and the configuration of the gingiva. When the alveolar ridge is resorbed after tooth extractions, the gingiva covering the ridge is also re sorbed. One could say that the gingiva follows the alveolar bone. So it is readily understood that the retracted gingiva assumes the form of a festoon, follow-
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ing the V-shaped defect in the alveolar bone. In nonin flammatory retraction of the gingiva with thin, sharp edges, the process may be enhanced by vigorous horizon tal brushing of the teeth and soft tissues. Often, wedgeshaped defects on the tooth necks (marks of the tooth brush) are found together with gingival retraction (Fig. 8). Retraction of the gingiva on the palatal surfaces of the roots of maxillary molars may be enhanced by parafunc tions of the tongue. In M c C a l l festoons the bulky roll of the gingival margins seems to reinforce the gingival cuff covering and protecting the epithelial attachment. In Stillman's cleft there seems to be a tearing effect of inserting muscles. This explanation of the phenomenon of noninflamma tory changes in the gingiva after destruction of alveolar bone seems more satisfactory than the assumption of a dystrophic type of periodontal disease of unknown origin. POCKET
FORMATION
When, how, and why pocket formation begins have always been the most critical questions in periodontology. Undoubtedly it is an infectious inflammatory process starting at the gingival margin. However, the gingival cuff normally protects the periodontal tissues against the invasion of microorganisms and their products. Even an inflamed gingival cuff is able to protect the periodontal tissues. Often we find gingivitis and much plaque and calculus, but no pocket formation, and again we find pocket formation in relatively clean mouths. Numerous investigations have been carried out to find a factor or factors which may lower the resistance of the gingival cuff in such a way that bacteria may penetrate the barrier of the epithelial attachment. If we tentatively accept the idea that periodontal diseases do not begin with pocket formation, but with lesions in the alveolar bone caused by traumatizing parafunctions, we have no difficulty at all in explaining pocket formation. The existence of aseptic traumatic inflammatory processes in
the alveolus is the factor which lowers the resistance of the gingival cuff, by impairing the blood supply of the epithelial attachment. The blood supply is impaired in two ways: (1) quantita tively, by temporary compression of the periodontal and osseal blood vessels in the pressure zones in the alveolus; and (2) qualitatively, by depriving the epithelial attach ment of blood-supplied components needed for repair of the inflammation in the alveolus. A s a consequence of inadequate nourishment, the resistance of the gingival cuff is lowered and sooner or later microorganisms are able to break the barrier of the epithelial attachment. O f course, it is not possible to present direct evidence for this succession of events, because periodontal diseases have never been observed from beginning to end, and. because small defects in the alveolar bone cannot be detected on radiographs. But some observations may be regarded as indirect evidence. There is, for example, no direct correlation between pocket depth and bone destruction. Relatively large amounts of bone destruction are often found near the root apex and near the alveolar crest, whereas pocket formation is shallow, not even reaching the alveolar crest. This phenomenon (Häupl's "Parodontics profun da") has been attributed to "distant effects" of inflam mation in the gingival cuff and to other causes. A more satisfying explanation seems to be that the bone has been destroyed by accumulated parafunctional trauma, before pocket formation began. Another observation is the correlation between pocket depth and tooth mobility. Often a combination is found of a relatively shallow pocket and relatively great mobility of a tooth. This is expecially true for maxillary molars with relatively parallel, conically shaped roots. This again may be regarded as indirect evidence that bone destruction, allowing mobility of the tooth, has been caused by parafunctional trauma before pocket forma tion began. Naturally, molars with cone-shaped roots are more readily tilted by parafunctional forces than molars with diverging roots which impede tooth movement. Many other supporting observations cannot be discussed in the limited space of this report. ANIMAL 1-3
FIGURE 8. Noninflammatory retraction of the gingiva, com bined with wedge-shaped defects in the tooth necks.
EXPERIMENTS
Periodontists have stated categorically that occlusal trauma (analogous to parafunctional trauma) never leads to pocket formation. They have based their opinion on animal experiments. This opinion must be challenged, because one of the factors listed above has been neglected in the animal experiments: intervals between periods of parafunctions, in which tissues may regenerate. Pocket formation is a slow process, beginning with the accumulation of minor traumatic defects in the alveolar bone, which impairs the blood supply of the gingival cuff and gradually weakens the resistance of the epithelial attachment against invasion of microorganisms.
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To cause pocket formation in animal experiments, this sequence must be simulated. However, the investigators have used appliances which have grossly and continu ously traumatized the periodontal tissues. That this was a mistake will be seen in the following example. Assume one wishes to show that the trauma of digging leads to callus formation on the hands. Give a man a spade and force him to dig vigorously and continuously. We know in advance that this investigator makes the mistake of omitting intervals—he will find various lesions on the hand of the digger, but no callus formation. Similarly, the animal experiments carried out heretofore are not evidence that parafunctional trauma does not lead to pocket formation. E V I D E N C E T H A T A L L P E R S O N S A F F L I C T E D BY P E R I O D O N T A L DISEASES E X E R T
509
incidence of periodontal diseases is greater among the flight personnel than among the ground personnel. Periodontal diseases have been called diseases of modern civilization. This points to the increased stress of living in modern cities. In the therapy of periodontal diseases increasing importance is assigned to measures for adjusting the occlusion, meaning elimination of trigger factors for hyper-compensating parafunctions. This strongly sug gests that traumatizing parafunctions are an important factor in the etiology of periodontal diseases. Indeed, traumatizing parafunctions should be regarded as the main causal factor in periodontal diseases. In treating patients with periodontal disease, we must assume that recurrences are inevitable unless parafunctions have been eliminated.
PARAFUNCTIONS SUMMARY
The patient's own statements may be regarded as direct evidence of the exertion of parafunctions, and we have never failed to elicit such statements from patients. However, psychologic skill is required to elicit such statements. The patient is almost invariably unconscious of his oral habits and he may resent the dentist's questioning. Ask him to become conscious of the position of his teeth, when he picks up a telephone. Tell him that his lips should be together, but his teeth should be apart. Ask him to report deviations, and then point out the possible consequences. It should be kept in mind that a negative answer is not evidence that the patient does not exert parafunctions. It may take weeks, months, or even years, before the patient becomes aware of his oral habits. For the dentist, sure signs of the exertion of parafunctions are the following: (1) strong abrasion on all teeth; (2) grinding facets on several teeth; (3) pain or peculiar feelings in the masticatory muscles in the morning; (4) pain or disturbances in the temporomandibular joints; (5) masseter hypertrophy; (6) chronic gingival hyperemia, disappearing after insertion of a Drum splint; and (7) periodontal diseases with or without infection, which are not symptoms of systemic diseases. CONCLUSION
Many systemic factors play a certain role in the development of periodontal diseases. But "function" is a predominant factor in the fate of the entire alveolar process: it is resorbed when its function ceases after the loss of teeth. We can, therefore, rightly assume that exaggerated function, i.e., traumatizing parafunctions, plays a dominant role in the development of diseases in the alveolar process. Ramfjord has found increased bruxism (a parafunction) in students before an examination. Psychologic studies have shown that an increased incidence of periodontal disease is found in persons with emotional stress. In the U . S . A i r Force, it has been found that the 1
Both the inflammatory and noninflammatory types of periodontal diseases begin with an aseptic, traumatic destruction of alveolar bone, caused by traumatizing parafunctions and followed by changes in the gingiva. The latter may or may not have a superimposed infec tious inflammatory process. A new concept to fit these facts is proposed: periodontal diseases are autodestructive processes in the masticatory system, with or without superimposed septic inflammation. To confirm the theory of autodestruction, direct evidence as well as indirect but conclusive evidence is given for the existence of traumatizing forces in the masticatory system, for traumatic destruction of alveolar bone, for changes in the gingiva following destruction of alveolar bone, and for the parafunctions by all persons afflicted by periodontal disease. It is concluded that traumatizing parafunctions are the main factor in the etiology of periodontal diseases and that in therapy recurrences are inevitable unless para functions have been eliminated. REFERENCES
1. Ramfjord, S. P., and Ash, M . M . : Occlusion. Philadelphia, W. B. Saunders Co., 1966. 2. Grant, D. A., Stern, I. B., and Everett, F. G.: Orban s Parodontologie. Berlin, Quintessenz-Verlag, 1965. 3. Goldman, H. M . : Periodontia. St. Louis, C V. Mosby Co., 1953. 4. Glickman, I., and Smulow, J. B.: The combined effect of inflammation and trauma from occlusion in periodontics. Int Dent J 19: 393, 5.
Drum,
1969.
W.:
Parafunktionen
und
Autodestruktionsp-
rozesse. Berlin, Quintessenz-Verlag, 1969. 6. Drum, W.: Autodestruction of the masticatory system. Parodontologie
16: 155,
1962.
7. Drum, W.: Klassifikation von Parafunktionen. Dtsch ZahnaerztlZ
17: 411,
1963.
8. Schuyler, C. H.: Fundamental principles in the correction of occlusal disharmony. J Am Dent Assoc 22: 1193, 1935. 9. Drum, W.: The mechanism of splints according to Drum. Quintessence Int 1: 93,
1969.
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10. Eismann, D.: Über das Ausmass der Parafunktionen im allgemeinen Lebensvollzug des Kindes. Berlin, QuintessenzVerlag, 1961. 11. Mühlemann, H. R., Herzog, H., and Vogel, A.: Occlusal trauma and tooth mobility. Schweiz Monatsschr Zahnheilkd 66: 527, 1956.
12. Fröhlich, E.: Über Parafunktionen. Symptomatologie, Ätiologie und Therapie. Dtsch Zahnaerztl Z 21: 536, 1966. 13. Lorenz, G.: Wirkungen von Parafunktionen (Nägelbeißen) auf das Zahnbett. Berlin, Quintessenz-Verlag, 1968. 14. Reichborn-Kjennerud, J.: Tro og periodonti. Nor Tannlaegeforen Tid 73: 307, 1963.
Abstracts CYTOTOXIC EFFECTS OF SOLUBLE PLAQUE EXTRACT ON CELLS IN VITRO
ULTRASTRUCTURE OF THE GINGIVAL EPITHELIUM IN THE NEW BORN CAT—SOME CHARACTERISTICS OF THE INTERCELLULAR JUNCTIONS
Mlinek, A . , Buchner, A . , Hennig, S., and Begleiter, A . J Periodont Res 9: 342, N o . 6, 1974.
Mignon, M . L . , Malet, P., Perissel, B., and Geneix, A . J Dent Res 53: 1484, November-December, 1974.
Gingival inflammation is accompanied by exudation of gingival fluid into the crevice which results in a continuous bathing of the space between the adherent plaque and crevicular epithelium. It is therefore assumed that plaque products reaching the periodontal tissues are water soluble. The effects of this water soluble plaque extract on cultured cells when added at different phases of the normal growth curve were studied. Plaque was gathered from patients and pooled and a stock solution of 50 mg of plaque extract (P.E.) per 1 ml of Eagle's Basal Medium was made. Final concentrations of 0.5, 1.5 and 2.0 mg of P . E . per 1 m l of cell suspension were used. The cell culture was a fibroblast-like cell line ( B H K ) from a hamster kidney. The results showed an inhibition of cell growth in culture by the plaque extract. Higher doses of plaque extract resulted in increased inhibition. Cells treated with P . E . were fewer in number than the control, exhibited vacuolization and lysis of cytoplasm, nuclei appeared dark and pyknotic and intranuclear structures were not readily observed. Higher concentrations of P . E . resulted in faster and more intensive degenera tive signs. The damage was caused whether added before cells attached to the culture surface or after in the growth phase. This showed that P . E . is cytotoxic and that bacterial plaque products may cause damage to tissues on a cellular level. It can then be hypothesized that bacterial plaque damages both crevicular and attachment epithelium and initiates inflammatory reaction and pocket formation in vitro. Depart ment of Pathology, Sackler School of Medicine, School of Continuing Education, Dental Division, Tel-Aviv University, Ramat-Aviv, Israel
The electron microscope was used to study intercellular junctions in the gingival epithelium of new born cats. Gingival epithelia of 2 or 3 mm were taken from the incisive part of regions where odontogenesis was active, from the region of the future diastema between canines and molars, and skin. A comparison was then made of gingiva during odontogenesis, mucosa without dental organ, and skin. A total of twelve female and eight male kittens were used. They were sacrificed at intervals from 1 to 15 days. New born cat gingiva showed numerous hemidesmosomes and desmosomes in the stratum spinosum with tonofibril systems. Zonalae occludens were rare and mainly seen in the stratum spinosum. Other junctional types were not observed. It was found that the desmosomes were well defined. The tonofilament apparatus was especially developed in the stratum spinosum. Spaces between membrane leaflets increased with age, but desmosome length remained constant. The number and size of tight junctions in kittens were constant during the experimental period. Intercellular spaces were wide with extensive distensions in the stratum spinosum. A s deciduous teeth erupted the intercellular spaces widened. Skin desmosomes were more irregular and the tonofibrils shorter and more clustered than the gingiva. Intercellular spaces were narrower, junctional types less defined and tight junctions less numerous than epithelium of the gingiva. The epidermal tight junctions were also predominately located in the stratum spinosum. Laboratory of Histology and Embryology of UER Medicine, University of Clermont-Ferrand, BP 38, 63001 Clermont-Ferrand Cedex, France
CHEMICAL PREVENTION OF CALCULUS FORMATION IN THE RAT
A HLSTOCHEMICAL STUDY OF GLYCOSIDASES IN HYDANTOIN INDUCED HYPERPLASTIC, HEALTHY AND INFLAMED HUMAN GINGIVA
2 1
Stookey, G . K . , and M c D o n a l d , J . L . J Dent Res 53: 1334, November-December, 1974. The ability of an amidopolyphosphate, Victamide, to prevent calculus, was investigated by feeding rats a calculus-producing diet and treating them with either a solution or slurry of Victamide twice daily for three weeks. Application was done to each molar quadrant using cotton applicators. The rats were killed and the molar quadrants were removed surgically and examined for calculus under a binocular dissecting microscope. T w o studies were done. In the first, concentra tions of victamide ranging from 1 to 5% were applied topically. Significant reductions in calculus formation were observed after three weeks for concentrations between 2.5 and 5.0%. The use of the amidopolyphosphate as a dentifrice in the second study confirmed the inhibitory action by reducing calculus formation by 31.3%. Although the exact mechanism is unknown, the calculus inhibition properties of amidopolyphosphate might be a result of the formation of an insoluble complex with the nucleating template, or the chelation of available calcium ions. Oral Health Research Institute, Indiana University-Pur due University at Indianapolis, Indiana 46202 U.S.A.
Larmas, L . J Periodont Res 9: 374, N o . 6, 1974. Various azo dyes for ß - g l u c u r o n i d a s e , α - and ß-glucosidase, for ß-galactosidase and for N-acetylglucosaminidase were used in healthy and inflamed human gingiva and hydantoin induced hyperplasia. Strong ß-glucuronidase activity was observed in all types of the tissue of inflamed gingiva and hydantoin induced hyperplasia. The fibroblasts, inflammatory cells, polymorphonuclear leucocytes, and marcophages showed moderate ß-glucuronidase activity. In healthy gingiva only a few inflammatory cells and macrophages were observed and a low activity of ß-glucuronidase was noted, otherwise, the distribution of this enzyme was similar to what it was in the two other samples. There was weak activity of ß-galactosidase, N-acetylglucosaminidase and ßglucosidase in all of the samples. There was no ß-glucuronidase activity in stratum corneum of healthy tissue. The activity of this enzyme in stratum corneum of the other samples may be due to microbial enzyme which diffused to this layer. Institute of Dentistry, University of Turku, SF-20520, Turku 52 Finland
