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.

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.