Susceptibility of different mouse strains to peri‐implantitis

Background and Objective

Peri‐implantitis (PI) is an inflammatory condition that affects the tissues surrounding dental implants. Although the pathogenesis of PI is not fully understood, evidence suggests that the etiology is multifactorial and may include a genetic component. The aim of this study was to investigate the role of genetics in the development of peri‐implantitis.

Material and Methods

Four‐week‐old C57BL/6J, C3H/HeJ and A/J male mice had their left maxillary molars extracted. Implants were placed in the healed extraction sockets. Upon osseointegration, ligatures were placed around the implant head for 1 or 4 weeks to induce PI. Micro‐computed tomography scanning was used to measure volumetric bone loss. Histological analyses were also performed to evaluate collagen organization and the presence of neutrophils and osteoclasts.

Results

Radiographically, comparing the ligature‐treated mice, C57BL/6J displayed the greatest amount of bone loss, followed by C3H/HeJ and A/J mice at 1 and 4 weeks. Histologically, at 1 week, C57BL/6J mice presented with the highest numbers of neutrophils and osteoclasts. At 4 weeks, C57BL/6J mice presented with the most active bone remodeling compared with the other two strains.

Conclusion

There were significant differences in the severity of peri‐implantitis among the different mouse strains, suggesting that the genetic framework can affect implant survival and success. Future work is needed to dissect the genetic contribution to the development of peri‐implantitis.     

The effect of fibronectin and a bone xenograft on regenerative treatment: a feasibility study

The purpose of this study was to evaluate the ability of fibronectin to augment the regenerative effects of a bovine-derived xenograft in human periodontal defects. Using a parallel arm, randomized double-blind design, 24 patients with an intrabony defect or a Class II furcation defect were randomly assigned to either the experimental group (xenograft plus fibronectin) or the control group (xenograft without fibronectin). Probing attachment level, pocket depth, and gingival recession were measured at baseline and at 12 months after surgery. Both treatment modalities resulted in attachment gain and pocket depth reduction compared with baseline values. Changes in clinical attachment were not significantly different between the groups (gain of 1.5 mm +/- 1.1 mm in the experimental group and 1.3 mm +/- 1.4 mm in the control). Pocket depth reduction was greater in the control (2.3 mm +/- 1.2 mm) than in the experimental group (2.1 mm +/- 1.9 mm). Gingival recession also was greater in the control (0.9 mm +/- 0.6 mm) than in the experimental group (0.6 +/- 1.5 mm). Subtraction radiography revealed no significant differences between the groups when measuring changes in the distance between the cementoenamel junction and the crest of the bone or in the estimated gain in mineralized tissue mass. It was concluded that a significant difference between the regenerative treatment modalities could not be demonstrated within the limitations of the study. Fibronectin appears to have a stabilizing or proliferative effect on the gingival soft tissue by promoting less postoperative gingival recession.     

Periapical Disease and Bisphosphonates Induce Osteonecrosis of the Jaws in Mice

Osteonecrosis of the jaw (ONJ) is a well‐recognized complication of antiresorptive medications, such as bisphosphonates (BPs). Although ONJ is most common after tooth extractions in patients receiving high‐dose BPs, many patients do not experience oral trauma. Animal models using tooth extractions and high BP doses recapitulate several clinical, radiographic, and histologic findings of ONJ. We and others have reported on rat models of ONJ using experimental dental disease in the absence of tooth extraction. These models emphasize the importance of dental infection/inflammation for ONJ development. Here, we extend our original report in the rat, and present a mouse model of ONJ in the presence of dental disease. Mice were injected with high dose zoledronic acid and pulpal exposure of mandibular molars was performed to induce periapical disease. After 8 weeks, quantitative and qualitative radiographic and histologic analyses of mouse mandibles were done. Periapical lesions were larger in vehicle‐treated versus BP‐treated mice. Importantly, radiographic features resembling clinical ONJ, including thickening of the lamina dura, periosteal bone deposition, and increased trabecular density, were seen in the drilled site of BP‐treated animals. Histologically, osteonecrosis, periosteal thickening, periosteal bone apposition, epithelial migration, and bone exposure were present in the BP‐treated animals in the presence of periapical disease. No difference in tartrate‐resistant acid phosphatase (TRAP)+ cell numbers was observed, but round, detached, and removed from the bone surface cells were present in BP‐treated animals. Although 88% of the BP‐treated animals showed areas of osteonecrosis in the dental disease site, only 33% developed bone exposure, suggesting that osteonecrosis precedes bone exposure. Our data further emphasize the importance of dental disease in ONJ development, provide qualitative and quantitative measures of ONJ, and present a novel mouse ONJ model in the absence of tooth extraction that should be useful in further exploring ONJ pathophysiological mechanisms.