Article Options
Categories


Search


Advanced Search



This service is provided on D[e]nt Publishing standard Terms and Conditions. Please read our Privacy Policy. To enquire about a licence to reproduce material from endodonticsjournal.com and/or JofER, click here.
This website is published by D[e]nt Publishing Ltd, Phoenix AZ, US.
D[e]nt Publishing is part of the specialist publishing group Oral Science & Business Media Inc.

Creative Commons License


Recent Articles RSS:
Subscribe to recent articles RSS
or Subscribe to Email.

Blog RSS:
Subscribe to blog RSS
or Subscribe to Email.


Azerbaycan Saytlari

 »  Home  »  Endodontic Articles 10  »  Evaluation of healing with use of an internal matrix to repair furcation perforations
Evaluation of healing with use of an internal matrix to repair furcation perforations
Introduction - Materials and methods.



M. Rafter,M. Baker, M. Alves, J. Daniel & N. Remeikis
University of Illinois at Chicago, Chicago, IL, USA.

Introduction.
Perforations are a relatively common cause of endodontic failure. When left untreated, perforation of the pulpal £floor results in an inflammatory response in the supporting tissues, with epithelial proliferation and eventual periodontal pocket formation (Lantz & Persson 1967, Bhasker & Rappaport 1971, ElDeeb et al. 1982, Jew et al. 1982).
Furcation perforations may be treated using either an internal or external (surgical) approach. Regardless of the approach used, the success rate is low (Seltzer et al. 1970, Sinai et al. 1989). Factors affecting the prognosis include location (Lantz & Persson 1970, Seltzer et al. 1970, Jew et al. 1982), adequacy of seal (Seltzer et al. 1970), degree of contamination (Nicholls 1962) and the material used to seal the perforation (ElDeeb et al. 1982, Jew et al. 1982, Himel et al. 1985, Sinai et al. 1989, Balla et al.1991, Lee et al.1993, Moloney et al.1993). Clinically, the outcome of treatment is affected by any superimposed infection. As this is not a compounding factor in the experimental situation, the healing responses observed experimentally may be different from the clinical situation. Another important factor appears to be the ability of the repair material to seal the defect. Many materials have been advocated (Lantz & Persson 1970, Seltzer et al. 1970, Bhasker & Rappaport 1971, ElDeeb et al.1982, Jew et al.1982, Himel et al.1985, Beavers et al. 1986, Sinai et al.1989,Balla et al.1991,Alhadainy&Himel 1993, Lee et al. 1993, Moloney et al. 1993, Torabinejad et al. 1995, Chau et al. 1997, Sluyk et al. 1998, Jantarat et al.1999). Given the wide variety of restorative materials used, it is evident that the nature of the material is not the only factor that limits success.
Unintentional extrusion of the sealing material into the alveolar bone may preclude success regardless of the material used. This produces additional inflammation and a foreign body reaction (Alhadainy & Himel 1993, Lee et al.1993).Attempts have been made to control this extrusion using biocompatible matrices (Auslander & Weinberg 1969, Lemon 1992, Jantarat et al. 1999). Lemon (1992) suggested that hydroxyapatite (HA 500, LifecoreBiomedical, Chaska, MN, USA) would be a highly biocompatible choice. This material fulfills many of the requirements for an internal matrix material (Jarcho et al.1977, Kenney et al.1986). However, the hydroxyapatite particles tend to migrate from the site before bony regrowth secures them (Kent et al.1983). If the material were combined with a binder, this may prevent migration of particles (Terry et al. 1989). A number of binders have been considered, resulting in the development of a commercial product, HAPSET (Lifecore Biomedical, Chaska, MN, USA), composed of 65% non-resorbable hydroxyapatite and 35% medical-grade plaster of paris as a resorbable binder (Ricci et al.1986,Terry et al.1989).
The aim of this study was to compare the healing responses following repair of furcation perforations with and without an internal matrix and to evaluate the efficacy of two matrix materials – HAPSET and hydroxyapatite.

Materials and methods.
A protocol for this study was reviewed and approved in accordance with the Animal Care and Use Policies of the University of Illinois. Four adult female baboons (Papio anubis) served as experimental animals. Two premolars and three molars in each animal yielded a total of 80 teeth (20 teeth per monkey). The animals were anaesthetized with 7-10 mg kg_1 ketamine hydrochloride and 0.5-1 mg kg_1 Xylazine (Rompun) intramuscularly. Maintenance doses were administered intramuscularly as required. The gingival and periodontal condition of each animal was assessed clinically and radiographs were taken. Each animal received full mouth scaling and root planing. Four weeks later the animals were once again anaesthetized. Local anaesthesia was achieved with a local infiltration technique, using lidocaine 2% and epinephrine 1:100 000. All experimental procedures were carried out under rubber- dam isolation.
Access to the pulp chamber of all premolar and molar teeth was made through the occlusal surface, using a crosscut ¢fissure bur in the high-speed handpiece. Once the pulp was exposed, the chamber was unroofed with a safe-ended bur and the coronal pulp removed to the level of the entrance to the root canals. Cotton pellets, soaked in a solution of lidocaine (2%) and epinephrine (1: 50 000) were applied, with pressure, to the radicular pulp stumps to achieve haemostasis. Once bleeding was controlled, the pulp stumps were capped with hard-setting calcium hydroxide (Dycal, LD Caulk Company, Tulsa, OK, USA). The teeth were then randomly assigned to one of the five groups: three experimental plus positive and negative controls.
In all but the negative control group, a perforation was made through the £floor of the pulp chamber and into the subjacent alveolar bone. A number 4 round bur was used to standardize the size of the opening. A relatively large perforation was made to create a‘worst case scenario’, in an effort to more effectively discriminate between different procedures. The defects were repaired in the following ways (Fig.1):
  • Positive control group (n=16): Unsealed.
  • Negative control group (n=16): No furcation perforation was prepared.
  • Experimental group 1 (n=16): HAPSET matrix and amalgam sealing material. Both HAPSET and amalgam were placed using small amalgam carriers and condensed with both endodontic (Schilder-type) and amalgam pluggers.
  • Experimental group 2 (n=16): Hydroxyapatite matrix and amalgam sealing material.
  • Experimental group 3 (n=16): No internal matrix used; amalgam sealing material (Table 1).

Figure 1. Use of an internal matrix. Hydroxyapatite in the furcal defect prevents extrusion of the sealing material - amalgam - into the underlying bone.

Use of an internal matrix

Table 1. Experimental procedures.

Experimental procedures

Following repair of the perforation, the floor of the pulp chamber was sealed with heat-softened guttapercha and the occlusal access cavity was restored with amalgam. The animals were sacrificed 1 week, 1 month, 3 months and 7 months after the procedures. Prior to sacrifice, the animals were anaesthetized, and the periodontal status of the teeth was evaluated clinically and radiographically. Each animal, under general anaesthesia, was perfused with a10% aqueous solution of buffered formalin. Mandibles and maxillae were immersed in 10% buffered formalin for additional fixation for 24 h at room temperature. The specimens were decalcified in formic acid-sodium citrate (Evans & Krajion 1930). The tissues were embedded in parafin and sectioned longitudinally in a mesio-distal plane at a thickness of 6 mm. Sections at 0.3-mm intervals were saved until the defect was reached, at which point serial sections were made and stained with haematoxylin and eosin. Sections were analyzed under the light microscope by four investigators who were not aware of the source of the specimens. Each section was evaluated for:
  1. Epithelial reaction – Epithelium was graded as being either present or absent from the furcation region.
  2. 2.    Inflammation – Inflammation was scored as follows: None: no inflammatory cells present. Mild: a few scattered inflammatory cells. Moderate: considerable number of inflammatory cells present but tissue detail still clear. Severe: heavy infiltrate of inflammatory cells, which mask tissue detail (Fig. 2).
  3. Connective tissue reaction - Giant cell reaction (Fig. 3a):
    • A multinucleated giant cell reaction was graded as being either present or absent. Encapsulation of material (Fig. 3b):
    • Absent: no evidence of fibrous encapsulation.
    • Diffuse: fibrous capsule present, but poorly defined or incomplete.
    • Organized: well-defined and organized fibrous capsule.
  4. Bony reaction Osteoclastic activity- Osteoclastic activity was graded as follows:
    • Control: osteoclastic activity limited to bone in the region of the periodontal ligament.
    • Evident: osteoclasts scattered in areas other than the periodontal ligament.
    • Marked: considerable numbers of osteoclasts present in areas other than the periodontal ligament (Fig. 4a).

Figure 2. A severe inflammatory reaction in association with the amalgam group, in which nomatrix was placed (haematoxylin and eosin; original magnification x160).

A severe inflammatory reaction in association with the amalgam group, in which nomatrix was placed

Figure 3. Connective tissue response to HAPSET. (a) Giant cell reaction (haematoxylin and eosin; original magnification x400). (b) Giant cells and well-oriented collagen fibres in association with hydroxyapatite (haematoxylin and eosin; original magnification x160).

Connective tissue response to HAPSET

Figure 4. Bony reaction. (a) Osteoclastic activity seen in all groups in the early time periods (haematoxylin and eosin; original magnification x_400). (b) New bone formation - osteoblasts become embedded in the new bone giving rise to osteocytes (haematoxylin and eosin; original magnification x160).

Osteoclastic activity seen in all groups in the early time periods

Figure 5. Deposition of bone around and between the matrix (HAPSET) particles (haematoxylin and eosin; original magnification x400).

Deposition of bone around and between the matrix (HAPSET) particles

Evidence of new bone formation - Evaluated according to the level of osteoblastic activity. The presence of multiple layers of osteoblasts on the periosteal or endosteal surface and of large osteocytes being trapped in lacunae was considered to be indicative of new bone formation. This was graded as being either present or absent (Fig. 4b).
Bone depositionin direct contact with the foreign material (Fig. 5) - The formation of bone in direct contact with the foreign material was graded as being either present or absent.