Abstract
Aim and objectives: It is well known that the transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and functions as a pivotal mediator of inflammatory responses. In the present study, we evaluated the trauma generated (inflammatory reaction) after osteotomy bone surgical procedures and placement of implants in the femoral cortical bone of Wistar rats. Surgical stress was evaluated measuring the release and activation of the NF-κB factor. Materials and Methods: Rats were divided into four groups (n = 10) and submitted to different surgical treatments: Control Group (G1 group), only bone perforation was performed without irrigation; Implant Group (G2 group), a titanium implant was inserted after bone perforation without irrigation; Irrigated Group (G3 group) perforations were performed with intense irrigation; and Vitaminic Compound Group (G4 group) surgical perforation was performed without irrigation and a vitaminic compound containing the principal ions present in the natural bone structure was used to fill the bone defect. All animals were euthanized six hours after the surgical procedure and NF-κB levels were determined through immunohistochemical stain followed by direct counting of labeled and unlabeled osteocytes. Results: Among different treated groups, the overall mean of the NF-κB positive cell count in all positions were higher for G1 group (33.4 ± 2.45 cells). NF-κB values were lower in the G2 group (28.9 ± 2.70 cells), whereas in the G3 group (24.3 ± 2.72 cells) as well as in G4 group still lesser NF-κB positive cells were counted (26.5 ± 2.60 cells). Conclusions: The results here presented suggest that maneuvers performed during osteotomy procedures can significantly affect inflammation levels. The NF-κB activation during the surgical procedures can be minimized and/or controlled thought the adequate irrigation or application of adequate substances.
Highlights
During surgical procedures for the fixation of endosteal screws or implants, the drilling management may cause stress by the friction generated by surgical drills in the bone, hampering the proper healing of the tissue [1,2,3]
The first is a transcription factor expressed under hypoxia [15,16], and the second is a widely studied dimeric, redox-sensitive, transcription factor involved in the regulation of a large number of genes controlling various aspects of the immune and inflammatory response [17] that has been associated with several cellular functions, including stress-induced responses and survival [10,16,18,19]
On the basis of the hypothesis that transcription factor NF-κB could be considered as a sensor of cellular and tissue stress, in the present study, NF-κB was selected as a stress marker and the presence of this protein as well as its peak of activation were evaluated through a specific technique developed by our group in different bone trauma situations [36,37]
Summary
During surgical procedures for the fixation of endosteal screws or implants, the drilling management may cause stress by the friction generated by surgical drills in the bone, hampering the proper healing of the tissue [1,2,3]. The first is a transcription factor expressed under hypoxia [15,16], and the second is a widely studied dimeric, redox-sensitive, transcription factor involved in the regulation of a large number of genes controlling various aspects of the immune and inflammatory response [17] that has been associated with several cellular functions, including stress-induced responses and survival [10,16,18,19]. This transcription factor participates in bone remodeling processes by inducing increased osteoclast formation and activity participating in certain aspects in osteoblast and chondroblast activities [20]. NF-κB has been considered by many authors [21,22,23,24] as an important marker of cellular and tissue damage and it has been proposed to be a sensor for oxidative stress [25]
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