Pathological and immunological differences of arterial thrombi and wall caused by three different periodontal bacterial injections in rat models and proposals on the pathogeneses of vascular diseases

Abstract

Objectives: Periodontal bacteria that have been studied show a strong connection to various vascular diseases. Among the many kinds of periodontal bacteria, Porphyromonas gingivalis (Pg) is well examined in the general aspects and in a rat model. However, whether other periodontal bacteria work or react differently is not studied well. Material and methods:We chose Aggregatibacter actinomycetemcomitans (Aa) and Prevotella intermedia (Pi) as different types of periodontal bacteria. Low-density and high-density bacterial solutions were injected in the small artery of rats' groins using our rat model. Eighteen limbs of 9 SD male rats (500-650 g) were used. After 7 days, 14-18 days, and 28 days, the rats were sacrificed. A pathological and an immunohistochemical study was conducted and reported on the low-density group with 12 limbs because the Pi group lacked a high-density study. Immuno-histochemical staining of live Pg was performed on three limbs of three rats at 1 h, 3 h, and 1 week after injection. Results:The appearances from the acute, at 7 days, to chronic phases, at 28 days, were observed. The differences of the species were certainly observed in the internal elastic lamina (IEL), and immuno-histochemical reactions. The inflammatory reactions, such as cellular distribution or intra-thrombus materials, were similar in all. One week later, we could not see any living bacteria in the specimen or immunological observation. Conclusions:The three species were essentially the same, except for Aa's stronger disruption of IEL, and more CD3 (Pan T cell) in Pi and more CD79a (Pan B cell) in Pg.We propose a new concept of a possible mechanism of vascular diseases, in which the work of LPS (lipopolysaccharides) and a toll-like receptor (TLR) is emphasized.

Buerger Disease: Pathological Changes in Elderly Patients

“…9 shows the developmental process of Buergerʼs disease and atherosclerosis, which was cited from a recently published paper. 6) Furthermore, Fig. 10 shows the hypothesis (partially modified) of the development of Buergerʼs disease and atherosclerosis presented by Professor Kenzo Tanaka in 1998.…”

“…5) It is believed that the success of the experimental study satisfied Kochʼs three postulates, and further immunological studies proved that it was innate immunity, thus satisfying Kochʼs four postulates. 6) If this developmental process is correctly recognized, atherosclerosis should develop newly in addition to the vascular changes in Buergerʼs disease if the patients with Buergerʼs disease are affected by the factors promoting atherosclerosis and aging. 6,9) As evidence of this, the three cases introduced here were able to show pathological specimens in two cases and typical echo findings in one case.…”

“…6) If this developmental process is correctly recognized, atherosclerosis should develop newly in addition to the vascular changes in Buergerʼs disease if the patients with Buergerʼs disease are affected by the factors promoting atherosclerosis and aging. 6,9) As evidence of this, the three cases introduced here were able to show pathological specimens in two cases and typical echo findings in one case. On the other hand, we examined 7 patients with Buergerʼs disease (all males) who did not develop atherosclerosis risk factors even after they were over 50 years old and in their 70s, but there was no evidence of complications of atherosclerosis with clear atheroma.…”

“…9 Iwai s proposal of pathogenesis in Buerger disease and athrosclerosis. 6) that do not match with the criteria for the diagnoses of Buergerʼs disease will increase. At present, Buergerʼs disease is properly named if the patient is under the age of 30, but when even one risk factor is added after that, it will no longer be "true" Buergerʼs disease and it will not match the diagnostic criteria and will be regarded as a "subtype of Buergerʼs disease" or called as atherosclerosis.…”

“…Furthermore, from the results of our research, we believe that smoking cessation and the spread of oral care are largely involved in the changes. 5,6) We encountered 34 new patients with Buergerʼs disease in 11 years. 7) This time, we examined three patients with Buergerʼs disease (2 males, 71 and 82 years of age; 1 female, 74 years of age) who were not treated despite additional atherosclerosis-risk factors after the age of 50.…”