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. 2017 Jun;47(3):143-153.
doi: 10.5051/jpis.2017.47.3.143. Epub 2017 Jun 28.

Periodontal and Endodontic Pathology Delays Extraction Socket Healing in a Canine Model

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Free PMC article

Periodontal and Endodontic Pathology Delays Extraction Socket Healing in a Canine Model

Jung-Hoon Kim et al. J Periodontal Implant Sci. .
Free PMC article

Abstract

Purpose: The aim of the present exploratory study was to evaluate extraction socket healing at sites with a history of periodontal and endodontic pathology.

Methods: The mandibular 4th premolar teeth in 5 adult beagle dogs served as experimental units. Periodontal and endodontic lesions were induced in 1 premolar site in each animal using wire ligatures and pulpal exposure over 3 months (diseased sites). The contralateral premolar sites served as healthy controls. The mandibular 4th premolar teeth were then extracted with minimal trauma, followed by careful wound debridement. The animals were sacrificed at days 1, 7, 30, 60, and 90 post-extraction for analysis, and the healing patterns at the healthy and diseased extraction sites were compared using radiography, scanning electron microscopy, histology, and histometry.

Results: During the first 7 days of healing, a significant presence of inflammatory granulation tissue was noted at the diseased sites (day 1), along with a slightly accelerated rate of fibrin clot resolution on day 7. On day 30, the diseased extraction sites showed a greater percentage of persistent fibrous connective tissue, and an absence of bone marrow formation. In contrast, healthy sites showed initial signs of bone marrow formation on day 30, and subsequently a significantly greater proportion of mature bone marrow formation on both days 60 and 90. Radiographs exhibited sclerotic changes adjoining apical endodontic lesions, with scanning electron microscopy showing collapsed Volkmann canals protruding from these regions in the diseased sites. Furthermore, periodontal ligament fibers exhibited a parallel orientation to the alveolar walls of the diseased sites, in contrast to a perpendicular arrangement in the healthy sites.

Conclusions: Within the limitations of this study, it appears that a history of periodontal and endodontic pathology may critically affect bone formation and maturation, leading to delayed and compromised extraction socket healing.

Keywords: Biological models; Bone marrow; Histology; Wound healing.

Conflict of interest statement

Conflict of Interest: The authors declare no conflict of interest related to this study. The opinions expressed in this article do not represent the views of the US Department of Defense, the Department of the Army, or the US Army Dental Corps. Use of any commercial products in this project does not imply endorsement by the US Government.

Figures

Figure 1
Figure 1
Outline of study: unilateral mandibular 4th premolar teeth in 5 dogs served as experimental units subject to induction of periodontal/endodontic pathology following pulp exposure and ligature enhanced plaque accumulation prior to extraction and subsequent healing (diseased extraction sites). Contralateral 4th premolar teeth served as healthy controls (fresh extraction sites). Block biopsies of the experimental and control sites were obtained at days 1, 7, 30, 60, and 90 post-extraction.
Figure 2
Figure 2
Clinical and radiographic view at induction of periodontal/endodontic pathology (A, B), and at 1 month (C) and 3 months (D) following induction. Note sclerotic changes near the margin of the periapical lesions (blue arrows).
Figure 3
Figure 3
Scanning electron microscopy observation of the apical portion of the alveolar socket walls immediately after extraction of diseased (B) and non-diseased extraction sockets (A). Evidence of Volkmann canals closure in diseased sites suggest deterioration of vascular supply in the infected areas possibly affecting bone remodeling.
Figure 4
Figure 4
Overview of fresh (A) and diseased (C) extraction sites day 1. Note large inflammatory cell infiltration coronally and apically in the diseased site (C). Also, note severed periodontal ligament in both groups (B, D). The periodontal ligament aligned perpendicular to the bundle bone in the fresh extraction sites (B: white arrow) whereas alignment appeared parallel to the extraction socket wall (D: white arrow) in the diseased sites. Osteoclast-like cell activity (blue arrows). H&E, original magnification ×16 and ×200. I-cells: inflammatory cells, CLOT: fibrin clot, PDL: periodontal ligament, BB: bundle bone, H&E: hematoxylin and eosin.
Figure 5
Figure 5
Overview of fresh (A) and diseased (C) extraction sites day 7. Note resorption of the socket wall in the diseased site (C). Also, note mineral deposition (white arrows) and pronounced osteoclast-like cells (blue arrows) in fresh (B) and diseased (D) sites at a higher magnification. H&E, original magnification ×16 and ×200. CLOT: fibrin clot, FT: fibrous connective tissue, BB: bundle bone, H&E: hematoxylin and eosin.
Figure 6
Figure 6
Overview of fresh extraction sites day 30 (A) and 60 (C) and diseased extraction sites day 30 (B) and 60 (D). Note fibrous connective tissue remaining in the central part of the diseased site day 30 (B) and larger portion of bone trabeculae remaining in the central part of the diseased site day 60 (D). H&E, original magnification ×16. H&E: hematoxylin and eosin.
Figure 7
Figure 7
Overview of fresh (A) and diseased (C) extraction sites day 90. Note the greater quantity of mature bone marrow formation at (A) vs. delayed healing and retained bone trabeculae at (C). Also, note cortical bone bridge at fresh (B) and diseased (D) extraction sites day 90. Note reversal line between pristine and new bone (white arrows). H&E, original magnification ×16 and ×200. H&E: hematoxylin and eosin.

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