Effect of Defective Collagen Synthesis on Epithelial Implant Interface: Lathyritic Model in Dogs. An Experimental Preliminary Study
Peri-implant mucosa is composed of 2 compartments: a marginal junctional epithelium and a zone of connective tissue attachment. Both structures consist mainly of collagen. Lathyrism is characterized by defective collagen synthesis due to inhibition of lysyl oxidase, an enzyme that is essential for interfibrillar collagen cross-linking. The lathyritic agent beta-aminoproprionitrile (β-APN) is considered a suitable agent to disrupt the connective tissue metabolism. Therefore, the purpose of this study was to assess the effect of defective connective tissue metabolism on epithelial implant interface by using β-APN created chronic lathyrism in the canine model. Two 1-year-old male dogs were included in this study. A β-APN dosage of 5 mg/0.4 mL/volume 100 g/body weight was given to the test dog for 10 months, until lathyritic symptoms developed. After this, the mandibular premolar teeth (p2, p3, p4) of both dogs were atraumatically extracted, and the investigators waited 3 months before implants were placed. In the test dog, 3 implants were placed in the left mandible, and 2 implants were placed in the right mandible. In the control dog, 2 implants were placed in the left mandibular premolar site. The dogs were sacrificed 10 months after healing. Peri-implant tissues obtained from the dogs were examined histomorphologically and histopathologically. Bone to implant contact (BIC) values and bone volumes (BV) were lower in the lathyritic group compared to the control group; however, no statistical significance was found. Significant histologic and histomorphometric changes were observed in peri-implant bone, connective tissue, and peri-implant mucosal width between test and control implants. Defective collagen metabolism such as lathyrism may negatively influence the interface between implant and surrounding soft tissue attachment.
(a) Control group: mesiodistal sectioning, magnification ×8. Adequate cortical bone width was seen. Old bone (light purple) and new bone (dark purple) around implant could be easily seen. A well-adapted peri-implant mucosa and implant surface were seen with no pathologic gap in between. (b) Beta-aminoproprionitrile treated experimental group, magnification ×25. Significant inflammatory cell infiltration and absence of collagen fibrils in connective tissue were observed. A gap between peri-implant mucosa and a bent (black arrow) in the sulcular epithelium at the neck of implant were noted. Active bone resorption and Howship's lacunae were visible (red arrow).
Beta-aminoproprionitrile treated experimental group. (a) Toluidine blue basic fuchsin, magnification ×8. Active bone resorption (blue arrow) and gap were visible at the neck of implant. Fatty cells or adipose tissues were seen at connective tissue region (red arrow). (b) Buccolingual section, magnification ×8. Pathologic gaps were observed (black arrows). (c) Buccolingual section, (toluidine blue basic fuchsin, magnification ×8). Active bone resorption was visible in lingual region. Pathologic gap between peri-implant mucosa and implant surface was seen (black arrows). Inadequate collagen fiber orientation was visible at peri-implant mucosa. (d) Magnification ×25. A pathologic gap was visible between implant surface and peri-implant mucosa. Collagen fibril network was not seen in peri-implant connective tissue mucosa. Good bone-to-implant contact was observed. Inside newly formed (dark purple) bone, osteons were visible (red arrows). No inflammatory reactions were seen in subepithelial connective tissue around implant.
(a) Beta-aminoproprionitrile treated experimental group, magnification ×25. A pathologic gap was visible between implant surface and peri-implant mucosa. Collagen fibril network was not seen in peri-implant connective tissue mucosa. (b) Control group, magnification ×25. Well-organized collagen fibril network was seen. Pathologic gap was not seen in this image.
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