Histologic features of apical periodontitis in human biopsies

Ricucci, Domenico; Bergenholtz, Gunnar

doi:10.1111/j.1601-1546.2004.00097.x

Cited by 25 publications

(12 citation statements)

References 68 publications

(113 reference statements)

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“…Correlation between the presence of microorganisms in the cementum portion of root canal and the development of periapical lesions 2,7,10,13,14 suggests the need for including instrumentation of this segment of the canal during endodontic therapy. 16 Apical patency consists of the passive use of a small size file through the apical constriction without enlarging it 3 and it is believed to promote cleaning of cemental canal.…”

Section: Introductionmentioning

confidence: 99%

Location of the apical foramen and its relationship with foraminal file size

Araújo¹,

Pinto²,

Djalma³

2011

Dental Press Endod.

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Aim: This article analyzed the location of the apical foramen and its relationship with foraminal file size in maxillary central incisors. Methods: Eighty four human maxillary central incisors were used in this study. K-files of progressively increasing diameters were inserted into the root canal until it got snugly fit and the tip was visible at the apical foramen. The files were removed and teeth were crosssectioned 10 mm from the root apex. The files were then reinserted, fixed with a cyanoacrylate-based adhesive, and sectioned at the same level as the root. The root apices were examined using a scanning electron microscope set at 140x magnification, the images were captured digitally and the results were subjected to Chi-square test. Results: It was observed that 63 (75%) of the apical foramen emerged laterally to the root apex and 21 (25%) coincided with the apex. The results presented statistically significant differences ‫ג(‬ 2 =22.1; p=0.00). Conclusions: Lateral emergence of the apical foramen is more common than coincidence of the foramen with the apex in maxillary central incisors. This anatomical characteristic may have influence on determination of the foraminal file size.

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Section: Introductionmentioning

confidence: 99%

Location of the apical foramen and its relationship with foraminal file size

Araújo¹,

Pinto²,

Djalma³

2011

Dental Press Endod.

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“…An AP lesion may be histologically classified as an apical abscess, periapical granuloma or radicular cyst, with a variety of transition stages between these forms (Ricucci & Bergenholtz 2004). An apical abscess has pus in a cavity formed by tissue liquefaction and is characterized by an accumulation of polymorphonuclear neutrophils (PMNs), with or without epithelial strands (Ricucci & Siqueira 2013).…”

mentioning

confidence: 99%

Potential role of TP63 in apical periodontitis development

et al. 2019

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Aim To investigate the expression of TP63 in apical periodontitis (AP) tissues and the association of single nucleotide polymorphisms (SNPs) in the TP63 gene with AP using a case‐control dataset. Methodology Expression of TP63 in human AP lesions (apical abscess, radicular cyst, periapical granuloma) was evaluated using immunohistochemistry. A case‐control association study was performed to assess the association of TP63 polymorphisms in individuals having AP with or without associated pain. Cases were defined as subjects with deep caries and AP (n = 151) and subjects with symptomatic apical periodontitis or acute apical abscess (n = 124). Subjects without AP (n = 169) and asymptomatic (n = 196) were used as controls, respectively. Saliva samples were collected as source of genomic DNA. Twelve SNPs in the TP63 gene were selected for genotyping using Taqman chemistry in real‐time PCR. Data analysis was performed using PLINK software. The Bonferroni method was applied to correct for multiple testing; α ≤ 0.004 indicates significant differences between groups. Results TP63 expression was evident in apical abscesses and radicular cysts, while weaker expression was observed in periapical granulomas. Positive expression was observed in mononuclear cells in the granulation tissues of all AP lesions. Regarding the presence of AP, a trend for allelic association was observed for rs16864812 and rs9810322 (P = 0.04) and rs9810322 genotypes were also nominally associated with AP under a dominant model (P = 0.04). When considering the presence of periapical pain, a trend for allelic and genotypic association was observed for rs10155037 (P = 0.03). Haplotypes were also associated with AP and periapical pain (P ≤ 0.05). Conclusions Apical periodontitis is a complex multifactorial condition and it is likely that multiple genes and environmental effects may influence its susceptibility, progression or both. TP63 variants may play a role in AP pathogenesis and susceptibility, individually or interactively with other genes. Additional studies in other populations and functional studies are needed to improve understanding of the role of TP63 in AP.

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“…There are probably two main routes of infection resulting in root surface biofilms: one is continuous expansion of microbial growth through the apical foramen or through lateral canals, and the second alternative is through dentinal tubules in an area where root surface cementum has been resorbed away (57,58). The presence of a long-standing sinus tract may also play a role in allowing bacterial penetration from the oral cavity (75,81). Irrespective of the pathway of infection, when actinomycosis-like colonies in the tissue or root surface biofilm have developed, surgical treatment including apicoectomy and removal of the infected hard and soft tissue has been shown to be effective with an excellent long-term prognosis (65,(82)(83)(84).…”

Section: Extraradicular Microbesmentioning

confidence: 99%

“…Periapical biofilm colonies, like biofilms in general, are assumed to be resistant to systemic antibiotic treatment (62,63). In addition to such biofilms inside the periapical tissue, there are several reports of bacteria growing in biofilms on the root surface close to the apex (75,(79)(80)(81). There are probably two main routes of infection resulting in root surface biofilms: one is continuous expansion of microbial growth through the apical foramen or through lateral canals, and the second alternative is through dentinal tubules in an area where root surface cementum has been resorbed away (57,58).…”

Section: Extraradicular Microbesmentioning

confidence: 99%

Reasons for persistent and emerging post‐treatment endodontic disease

Haapasalo¹,

Shen²,

Ricucci³

2008

Endodontic Topics

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This article is a critical review of the reasons for persistent and emerging post‐treatment endodontic disease (PTED). While there is a strong consensus that micro‐organisms, mainly bacteria, are practically the only cause of primary apical periodontitis, the reasons for persistent apical periodontitis lesions have been more a matter of debate. The authors of this review focus on the role of micro‐organisms in PTED, and while secondary developments such as cholesterol crystals or foreign material in the periapical area of a tooth with apical periodontitis may contribute to additional irritation and/or an inflammatory reaction, a detailed analysis of the available data suggests that evidence supporting a primary role for such secondary factors without the continued presence of bacteria is lacking. Therefore, even in PTED, elimination of micro‐organisms residing within the tooth structure, root surface, or periapical tissues remains the goal of treatment and the key to long‐term success.

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Histologic features of apical periodontitis in human biopsies

Cited by 25 publications

References 68 publications

Location of the apical foramen and its relationship with foraminal file size

Location of the apical foramen and its relationship with foraminal file size

Potential role of TP63 in apical periodontitis development

Reasons for persistent and emerging post‐treatment endodontic disease

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