Antibody-producing cells in human periapical granulomas and cysts

Stern, Michael H.; Dreizen, Samuel; Mackler, Bruce; Levy, Barnet M.

doi:10.1016/s0099-2399(81)80304-4

Cited by 56 publications

(33 citation statements)

References 14 publications

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“…The present findings are inconsistent with a previous immunohistochemical study which reported that K and X light chain-containing cells were equally distributed in periapical lesions (5), although this was a qualitative analysis. An explanation may be that the results obtained by in situ hybridization are not always in agreement with those obtained by immunohistochemistry (14)(15)(16).…”

Section: Discussioncontrasting

confidence: 99%

See 1 more Smart Citation

Analysis of immunoglobulin‐synthesizing cells in human dental periapical lesions by in situ hybridization and immunohistochemistry

Takahashi

MacDonald²,

Kinane³

1996

J Oral Pathology Medicine

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Immunoglobulin (Ig) kappa (kappa) and lambda (lambda) light chain mRNA-expressing cells were investigated by in situ hybridization (ISH) to assess the local humoral immune response in human dental periapical lesions. Twenty-seven biopsy samples (17 periapical granulomas and 10 radicular cysts) were examined. Both types of light chain mRNA-positive cells were detected in formalin-fixed/paraffin-embedded tissue sections in all samples. Plasma cells showed weak to strong cytoplasmic staining with both probes and background staining was negligible. The ISH methodology is specific and sensitive in detecting Ig light chain mRNAs and retains cell morphology well. kappa to lambda ratios showed moderate variability for both granulomas and cysts (mean = 1.66 +/- 0.85 SD, 1.47 +/- 0.51, respectively). There was no significant difference in light chain distribution between granulomas and cysts. Ig kappa and lambda light chain proteins were also studied by immunohistochemistry (IHC) but the results were disappointing due to excessive background staining. This study confirms that Ig is locally produced in periapical lesions and that the ISH method localises Ig light chain-containing cells better than IHC. The wide variability in kappa/lambda ratio may support the concept of non-specific multibacterial infection in these lesions.

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Section: Discussioncontrasting

confidence: 99%

“…as detected by immunofiuorescence techniques (4)(5)(6) or by immunoenzymatic methods with monoclonal or poiycional antibodies (7)(8)(9). B cells and plasma cells are predominant in these lesions and locally produce immu-noglobulin G (IgG).…”

mentioning

confidence: 99%

Analysis of immunoglobulin‐synthesizing cells in human dental periapical lesions by in situ hybridization and immunohistochemistry

Takahashi

MacDonald²,

Kinane³

1996

J Oral Pathology Medicine

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“…The concentration of IgG in apical periodontitis was found to be nearly five times that in non-inflamed oral mucosa (Greening and Schonfeld, 1980). Immunoglobulins have also been shown in plasma cells residing in the periapical cyst wall (Toller and Holborow, 1969;Pulver et al, 1978;Stern et al, 1981;Smith et al, 1987) and in the cyst fluid (Toller and Holborow, 1969;Selle, 1974;Skaug, 1974;Ylipaavalniemi, 1977). Their concentration in the cyst fluid was several times higher than that in blood (Selle, 1974;Skaug, 1974).…”

Section: (7) Antibodiesmentioning

confidence: 97%

Pathogenesis of Apical Periodontitis and the Causes of Endodontic Failures

Nair

2004

Critical Reviews in Oral Biology & Medicine

820

385

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Apical periodontitis is a sequel to endodontic infection and manifests itself as the host defense response to microbial challenge emanating from the root canal system. It is viewed as a dynamic encounter between microbial factors and host defenses at the interface between infected radicular pulp and periodontal ligament that results in local inflammation, resorption of hard tissues, destruction of other periapical tissues, and eventual formation of various histopathological categories of apical periodontitis, commonly referred to as periapical lesions. The treatment of apical periodontitis, as a disease of root canal infection, consists of eradicating microbes or substantially reducing the microbial load from the root canal and preventing re-infection by orthograde root filling. The treatment has a remarkably high degree of success. Nevertheless, endodontic treatment can fail. Most failures occur when treatment procedures, mostly of a technical nature, have not reached a satisfactory standard for the control and elimination of infection. Even when the highest standards and the most careful procedures are followed, failures still occur. This is because there are root canal regions that cannot be cleaned and obturated with existing equipments, materials, and techniques, and thus, infection can persist. In very rare cases, there are also factors located within the inflamed periapical tissue that can interfere with post-treatment healing of the lesion. The data on the biological causes of endodontic failures are recent and scattered in various journals. This communication is meant to provide a comprehensive overview of the etio-pathogenesis of apical periodontitis and the causes of failed endodontic treatments that can be visualized in radiographs as asymptomatic post-treatment periapical radiolucencies.

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“…The tissues, mainly fibrous connective tissue with varying degrees of inflammatory cells, trapped inside the epithelial ball mass will gradually degenerate because of a loss of blood supply, and a cyst cavity will be formed (Table 1). Consequently, inflammatory mediators, proinflammatory cytokines, growth factors, and immunoglobulins can be found in a cyst cavity (69,70). It has been speculated that apical cysts may expand after periapical osteoclastic bone resorption mediated by inflammatory mediators (prostagladins) and proinflammatory cytokines (IL-1, IL-6, and TNF) (35-40).…”

Section: Formation Of Radicular Cyst In Apical Periodontitismentioning

confidence: 99%