Personal risk factors for generalized periodontitis.

Periodontitis is generally considered to be a consequence of an unfavourable host-parasite interaction in which bacteria are the determinants of disease. An intense search continues for the bacteria, specific or non-specific, that are responsible for periodontitis and various forms of the periodontal diseases have been associated with, and are widely believed to be caused by, specific bacterial groups. However, the distribution of periodontopathic bacteria is far wider than the distribution of periodontitis, indicating that the association between bacteria and periodontitis is weak. This paper proposes a paradigm for the etiology of generalized periodontitis in which 'host' factors are not only those triggered by bacteria (the agent) but are also those personal factors that influence the outcome of the host/parasite relationship. The personal factors that diminish the efficiency of host defense may include psycho-social stress from the social environment, factors from the lifestyle such as diet, smoking and alcoholism and systemic factors such as intercurrent disease or deficiencies within the immune/inflammatory system. A model is described in which the interaction of personal factors with the social environment provides the potential for the initiation of periodontitis. Biological variation is significant and the combination of factors that cause generalized periodontitis or any other chronic disease in one individual may not result in dental or any other chronic disease in another.

Importance of bicarbonate/CO2 for fertilization of pig oocytes in vitro, and synergism with caffeine.

Fertilization of pig oocytes was performed in vitro in modified Tyrode's media in which either HEPES or bicarbonate/CO2, or both, were included as buffer systems; caffeine (2 mM) was also included in some of the media because it is a reported stimulant of fertilization. The composition of the bicarbonate-containing media was designed so as to maintain the same pH and osmolality as bicarbonate-free media. The inclusion of bicarbonate during gamete co-incubation in caffeine-containing medium led to high levels of fertilization (66% of 238 mature oocytes were fertilized). However, essentially no fertilization occurred if bicarbonate was replaced with HEPES (0.7% of 146 oocytes were fertilized; significantly different, P < 0.001). Inclusion of HEPES in bicarbonate-containing medium during gamete co-incubation did not affect fertilization, showing that HEPES did not exert an inhibitory effect. Omission of bicarbonate during sperm preincubation also did not affect fertilization. If caffeine was included in bicarbonate-containing medium, 73% of 311 oocytes were fertilized whereas if caffeine was omitted only 14% of 326 oocytes were fertilized (significantly different, P < 0.001). In the absence of bicarbonate, when fertilization was very low, caffeine had no stimulatory effect. The results indicate that bicarbonate is essential for pig fertilization in vitro, but that caffeine exerts a synergistic stimulatory effect.

Pulpal disease and bursts of periodontal attachment loss.

Progression of periodontitis is currently thought to occur during bursts of activity, followed by periods of remission, when healing may occur. This concept contrasts with the older hypothesis that periodontitis was continuously, but slowly, progressive throughout life. At present, there is no proof of the conventional (microbiological) hypothesis which gives a major role to site-specific bacteria in the initiation of bursts of attachment loss. An alternative hypothesis is presented in this paper which accounts for periodontal attachment loss by pathways that are independent of plaque. Severe lesions of the periodontium caused by pulpal pathoses (apical and retrograde periodontitis) are known to form at any level of the periodontium, not only at the root apex. When these lesions cause destruction of the periodontal tissues at the alveolar crest, and when plaque, calculus and gingivitis are also present, an endodontic origin is rarely suspected. Three pathways are proposed to account for the development of localized periodontal attachment loss consequent to pulpal disease. This hypothesis accounts for the sudden deterioration of periodontal sites under regular review, the strict localization of alveolar defects with normal alveolar bone immediately adjacent, the presence of site-specific bacteria (secondary colonizers of deep pockets) which cannot cause disease when transferred to healthy sites, and the antibody responses directed against them.

Two critical confounding factors in periodontal epidemiology.

The prevalence and severity of periodontitis is considerably lower than was previously estimated. The available epidemiological methods are based on the premise that loss of periodontal attachment is a unique sign of periodontitis. However, additional factors resulting in loss of periodontal attachment confound data obtained from modern studies. The physiological process of continuous tooth eruption results in loss of periodontal attachment over a lifetime, at an approximate rate of 0.1 mm/year. Anthropological and clinical evidence for continuous tooth eruption is reviewed. The position of the alveolar crest appears to be stable; loss of periodontal attachment occurs as the teeth erupt and less of the root is embedded in bone. Retrograde periodontitis caused by pulpal disease is a known cause of severe, localised destruction of periodontal tissues. Its signs and symptoms include periodontal pocket formation, purulent inflammatory exudates, angular bone loss, swelling and bleeding of the gingival tissues and increased tooth mobility. Anthropological, experimental and clinical evidence for retrograde periodontitis is discussed. Misdiagnosis of angular (hemiseptal), furcal and other forms of localised periodontal damage as periodontitis has probably resulted because of the inability to determine the quality of pulpal health and the assumption of a gingivitis-periodontitis continuum. New epidemiological methods need to be developed in which physiological and all pathological conditions which affect the periodontal attachment are recognised and appropriately categorised.

Tooth dislocation: the relationship with tooth wear and dental abscesses.

Tooth dislocation (tilting) was recorded in 1,200 skulls from 34 museum collections. The findings of dislocation by tooth type, tooth wear, and abscess location are presented. A model for dislocation based upon the progressive loss of tooth support provides a rational explanation for the phenomenon. Physiological continuous tooth eruption was considered to account for a component of the progressive loss of tooth attachment. The process of attrition, pulp perforation, and dental abscess cavity formation resulted in further, more severe loss of tooth support. Heavy functional forces, in association with greatly reduced bone support, tilted the crown lingually and root buccally. When the tooth had tilted to such an extent that the root apices protruded from the bone and, presumably (in life) through the gingival/mucosal tissues, the infected root canals were effectively isolated from the internal environment. The tooth continued to function. The more typical consequence of severe attrition and dental abscess formation was tooth loss; it also isolated an infected tooth from living tissue, but without the benefit of retaining function.

Continuous tooth eruption in Australian aboriginal skulls.

Increases in the distance from the cemento-enamel junction to the alveolar crest (CEJ-AC) have often been attributed to senile atrophy of the bone or to the effects of periodontitis, without reference to the condition of the alveolar crest. This study investigated the relationship between CEJ-AC distance, tooth wear, gender, site of the CEJ-AC measurements, and age in 161 pre-white-contact Australian aboriginal skulls. Individual teeth were included in the study when there was no evidence of dehiscence, periodontitis, or abscess cavity formation in the supporting alveolar bone. The CEJ-AC distances increased as the severity of attrition increased; in male skulls, CEJ-AC distances were greater than in female skulls for all categories of tooth wear. In general, CEJ-AC distances measured on the mesial aspects of teeth were greater than those recorded distally; lingual distances generally exceeded buccal recordings. The best explanation of these findings and similar reports in the anthropological literature is that continuous tooth eruption occurred without the concomitant coronal movement of alveolar bone. This conclusion has significant ramifications for anthropological, epidemiological, and clinical studies which use the CEJ and AC as reference points when measuring periodontal attachment loss (periodontitis).

Periodontal defects of pulpal origin: evidence in early man.

False assumptions have led to the widespread opinion that periodontitis of gingival origin is a ubiquitous disease and a common cause of tooth loss among ancient populations. Evaluation of dry skulls reveals that horizontal loss of crestal alveolar bone was unusual and of minor severity. Localized vertical bone defects of pulpal etiology were common and severe, often resulting in tooth mortality. The present paper identifies a number of factors that have contributed to the development of some important misconceptions about the nature of periodontal disease, its incidence, and its etiology.

Periodontitis and angular alveolar lesions: a critical distinction.

Modern anthropologic and epidemiologic studies reveal that the incidence of periodontitis is low in both ancient and modern populations. The distribution of plaque and gingivitis has little or no correlation with the distribution of pathologic alveolar bone loss or with periodontitis. The assumption that a distance from cementoenamel junction to alveolar crest (CEJ-AC distance) greater than 2 mm equates with disease overlooks the interrelationship between the CEJ-AC distance and continuous eruption in compensation for tooth wear and growth of the lower face height. Anatomic, physiologic, and pathologic factors increasing CEJ-AC distances are reviewed. Where horizontal periodontitis does result from gingivitis, it is usually of minimal significance and probably occurs when the host defenses have been diminished by environmental factors commonly associated with other chronic diseases. A pulpal-alveolar explanation for localized angular alveolar lesions better fits the clinical features of this form of periodontal bone loss than does the conventional hypothesis of primary periodontal infection by specific oral bacteria.

Differential diagnosis of severe periodontal lesions.

In current clinical practice, a differential diagnosis of severe localized periodontal lesions is rarely made; such lesions are considered to be manifestations of periodontitis caused by specific microbes from the commensal oral flora. However, deep seated lesions of the periodontium which are in communication with the alveolar crest, are well documented periodontal consequences of pulpal pathoses and can mimic the signs and symptoms of 'periodontitis'. The very low incidence of tooth-threatening periodontal disease in ancient and modern man is revealed when differential diagnoses are used in the examination of alveolar defects in anthropological materials and when epidemiological studies use more appropriate indices. However, no periodontal index to date has incorporated a differential diagnosis between gingival and pulpal causes of alveolar bone loss. The gingival and periodontal signs of severe localized periodontal lesions are reviewed and the imprecise nature of current clinical diagnostic tests (radiography, 'pulp testing', darkfield microscopy, bleeding on probing, periodontal probing) is discussed. None of these tests is able to detect disease activity and cannot be used to predict future patterns of disease behaviour. However, the commonly held belief that the tests are accurate has resulted in most severe periodontal lesions being falsely labelled as periodontitis. Failure to carry out differential diagnosis of severe periodontal lesions has resulted in the instigation of periodontal therapy for many lesions of non-gingival origin. Whenever severe localized lesions of the periodontium are detected, the differential diagnosis between pulpal and periodontal origins should be made. The results of diagnostic tests in current use should be interpreted with extreme caution; clinicians are left to exercise their judgment based on consideration of all the available evidence.

Infection and periodontal diseases.

Contemporary hypotheses that consider the severe forms of periodontal disease to be infections caused by site-specific microbes fail to satisfactorily explain the epidemiologic, anthropologic, and clinical features of periodontal diseases. The microbes that have been designated as periodontopathogens are commensal bacteria present in periodontal health and disease. Association of specific bacteria with various disease forms has been established, but association is confused with causation. None of the periodontal diseases can be transmitted between individuals or between diseased and healthy sites of a susceptible person. Past and present concepts of the etiology of the periodontal diseases are reviewed, and the deficiencies of contemporary periodontal theory are outlined. Host factors rather than bacteria determine whether gingivitis extends to horizontal periodontitis. Angular alveolar lesions, the severe form of periodontal bone loss, are hypothesized to be caused by the spread of pulpal inflammation to the adjacent periodontal tissues. When the resultant dental abscess becomes contiguous with the alveolar crest and gingival sulcus, secondary colonization of deep pockets by site-specific oral bacteria-selected for by the complex conditions of the site-can occur. This explanation accounts for the distribution of periodontopathogens, the localization of angular alveolar lesions, and the bursts of activity by which the disease progresses.

Endodontic effects of root planing in humans.

Although the deliberate removal of cementum by root planing remains part of periodontal therapy, its scientific basis is under challenge. A potentially harmful effect of root planing is the exposure of dentinal tubules to the oral environment; this study investigated the short-term endodontic effects of root planing in humans. Ten teeth with significant loss of periodontal attachment had one proximal surface root planed; the other proximal surface was not root planed. After 10-14 days, the teeth were extracted and processed for light microscopic and SEM examination. Hypersensitivity to thermal stimuli was reported by 4 subjects after root planing. Chronic pulpitis was found in 3 pulps adjacent to the area of root planing. Bacterial penetration of dentin was observed, although the depth of penetration was less than reported by others. The results indicated that previous perceptions of the beneficial role of root planing in periodontal therapy require reconsideration.

Pulpal pathosis and severe alveolar lesions: a clinical study.

Gingivitis is widely believed to be the precursor of crestal alveolar bone destruction (periodontitis) in some individuals. However, there is no correlation between gingivitis and severe localized lesions of alveolar bone. Specific 'periodontopathogens' of the indigenous oral flora are hypothesized to be the cause of localized lesions but the evidence to date is one of association only. Acute and chronic pulpal inflammation are known causes of irritation to the periodontal ligament and alveolar bone; retrograde pockets may subsequently form. Contamination by indigenous organisms best adapted to the special environment of the deep pocket could be expected to follow the establishment of the new conditions. This study was undertaken to examine the clinical and histological status of the pulps of teeth affected by severe localized alveolar lesions. A total of 153 teeth in 90 subjects were studied; full periodontic and endodontic assessments were made. Seventy-seven teeth responded in the normal range to pulp testing, but 52% of these had no recoverable tissue from their root canal systems on endodontic opening. The findings indicated that pulpal pathosis was not clinically detectable in the majority of teeth studied when conventional endodontic diagnostic tests were applied. Rather, the presence of localized severe alveolar defects was a more accurate predictor of pulpal pathosis.

Molecular cloning of Clostridium thermocellum DNA and the expression of further novel endo-beta-1,4-glucanase genes in Escherichia coli.

Sau3A fragments of Clostridium thermocellum (NCIB 10682) DNA were ligated into the BamHI site of pBR322 and expressed in Escherichia coli HB101 and a Lac- mutant thereof. Twenty-eight clones with carboxymethylcellulase (CMCase) activity were selected from two libraries by means of the Congo Red plate assay. Restriction enzyme analysis indicated that the CMCase+ clones contained a total of 13 unique DNA inserts. Hybridization of recombinant plasmids with chromosomal DNA confirmed the physical maps in all but one case and was further used to demonstrate the absence of homology between the HindIII restriction fragments of similar size which occurred in many of the clones. Without exception, CMCase+ E. coli clones expressed endoglucanase activity, but differed with respect to the amount and nature of the enzyme activity produced; additionally, some clones had exoglucanase activity which, in at least one case, was not attributable to the production of a second enzyme. For a few selected clones, the partially purified CMCase was analysed by electrophoresis. A temperature profile characteristic of a thermostable enzyme was demonstrated for the endoglucanase of one of the most active clones. Based on the evidence presented here, it is probable that the 13 unique DNA fragments described do not contain any of the C. thermocellum endoglucanase genes previously cloned.

Radiographic and visual assessment of alveolar pathology of first molars in dry skulls.

There are many reports in the literature relating to the dental pathology of ancient peoples. In most instances only visual observations of alveolar lesions have been made, precluding assessment of covert dental lesions. The present paper was undertaken to compare the incidence of alveolar dental lesions determined by both visual and radiographic methods in a group of Australian aboriginal skulls. First molars of the right side were used for the comparison: approximately ten percent more lesions were found by the radiographic method. The data demonstrated the limitation of either technique alone. The strong association between pulp exposure and furcal, angular, and apical lesions suggests that pulpal lesions provoke periodontal changes that have traditionally been assigned to a gingival etiology. The location of the lesions within the periodontium would appear to be determined by the location of the pulpal pathology and the pathways through dentin between that location and the periodontal ligament.

Juvenile periodontitis--a new perspective.

Juvenile periodontitis (JP) is a severe disease of the periodontium in adolescents. It is usually localized to the first permanent molars and (less commonly) the central incisors. The bacteria Actinobacillus actinomycetemcomitans (Aa) is currently implicated in the aetiology of JP since its numbers are high in JP pockets and low in subjects with healthy periodontal conditions or with adult periodontitis. However, Aa harvested from JP pockets and transferred to healthy sites in the same mouth are unable to colonize these areas or initiate disease (17). The conflicting evidence implicating intrinsic or induced impairment of host defence is reviewed. It is hypothesised that JP lesions are primarily of endodontic origin. By-products of an inflammatory process in the pulp enter the periodontium via dentinal tubules, lateral or furcation canals and drain through the periodontium into the mouth. The environmental conditions of the sinus select for bacteria such as Aa which secondarily infect the site and exacerbate the clinical situation by their potent virulence factors. Localized deep defects involving only one side of an interproximal space in an otherwise periodontally healthy mouth result. Studies of the pulpal status of JP teeth are indicated.

Periodontal disease in ancient populations.

Recent clinical and anthropological findings indicate that the conventional concept of the pathogenesis of periodontal disease requires review. The periodontal lesion has been defined as a generalised horizontal loss of crestal bone resulting from host immune and inflammatory responses triggered by the action of commensal bacteria, and the extension of gingivitis into the deeper periodontium to become periodontitis has been assumed to occur slowly but steadily over many years. Anthropological and clinical investigations reveal that the widespread loss of crestal tissue is relatively unusual and that lesions of the alveolus are commonly localised and severe. Longitudinal studies have shown that the disease progresses in bursts and is stable in both the gingivitis and periodontal modes in between the burst activity. The findings of the present study demonstrate that generalized horizontal periodontitis has been unusual and has not been responsible for tooth loss. Other factors responsible for deficient alveolar margins in dry bones have been overlooked in most studies, leading to overassessment of the incidence of periodontal disease in postmortem materials; the same assumptions have led to overassessment of periodontal disease in clinical studies and practice.

The internship--a prospective investigation of emotions and attitudes.

In a prospective survey for changes in emotions and attitudes of all medical interns of The Oregon Health Sciences University (N = 22) at six intervals during the 1982-1983 academic year, both positive and negative emotional changes were noted. Satisfaction with the decision to become a physician decreased during the period, a change that correlated directly with depression and fatigue and inversely with excitement and importance.

Distribution of nocturnal bruxing patterns in man.

The distribution of nocturnal bruxing patterns in nine subjects was recorded and interpreted in accordance with current concepts of sleep physiology. Few bruxing events were seen in the first 2 h of sleep but peak periods were identified during the night. The findings suggested that bruxism and REM sleep were closely associated and pointed towards a central aetiology for bruxing activity.

Bruxing patterns in man during sleep.

Nocturnal clenching was monitored using a dedicated microprocessor, appropriate EMG amplification and digitisation. The hardware was located at the subject's bedside and the software provided for the real time recording of clenching bruxism, duration of the episode and the severity in electronic values. Forced clenches before retiring and on arousing provided maximal baseline data against which to compare the severity of sleeping clenches. All ten subjects tested were found to brux and two used intensities of effort while asleep that exceeded their maximal conscious clenches.