Internal apical resorption and its correlation with the type of apical lesion

Int Endod J. 2004 Nov;37(11):730-7. doi: 10.1111/j.1365-2591.2004.00830.x.

Abstract

Aim: To determine the presence of various periapical pathologies and their association with the presence and extent of internal apical inflammatory root resorption in human teeth.

Methodology: A total of 75 root apices from extracted teeth with periapical lesions were examined. Semi-serial sections of soft tissue lesions were stained with HE. The lesions were classified as non-cystic or cystic, and according to the degree of abscess severity: 0, 1, 2 or 3. The apices were reduced to 3 mm in length and longitudinally cut so that the internal aspect could be analyzed under scanning electron microscopy (SEM). Internal root resorption was also classified as 0, 1, 2 or 3 according to the extent of the resorbed area. Additionally, six vital teeth were used as a control.

Results: Non-cystic lesions with severe abscesses were the most common finding (70.7%), while 20% of the lesions were cystic (4% little or no abscess; 16% severe abscesses). Non-cystic lesions with little or no abscess comprised 9.3% of the sample. Of the root canals containing periapical lesions, 48% had internal apical resorption in more than half of the area, while 25.3% of the sample had no internal resorption. Resorption degree 1 was identified in 12% of the cases, and 14.7% showed resorption degree 2. The control group displayed significantly less internal resorption than the test groups.

Conclusions: Most periapical lesions (86.7%), whether cystic (16.0%) or non-cystic (70.7%), showed large collections of acute inflammatory cells. Apical internal resorption was present in 74.7% of roots and was associated with periapical lesions. There was no correlation between internal apical resorption and the histological diagnosis of the lesions.

MeSH terms

  • Analysis of Variance
  • Humans
  • Periapical Periodontitis / complications*
  • Radicular Cyst / complications*
  • Root Resorption / etiology*