Diagnosing Periodontal Disease
To date, the most widely accepted method for diagnosing periodontal disease or peri-implant status is based on clinical judgement after inspection of the gingival inflammation by observing bleeding upon probing of the target tissues and measuring the pocket depth. However, emerging trends in oral and periodontal diagnostic research are moving toward methods by which risk can be identified and quantified by objective measures, such as biochemical markers of disease or inflammation. The inflammatory response plays a fundamental role in oral surgery, being an essential process for repairing traumatized or infected tissues. This response can also serve as an early and objective means for monitoring health, by quantifying the biochemical markers of inflammation, even before clinical signs and symptoms are measurable. The repair of injury, and in particular the repair of a bone lesion around a dental implant, is a sequentially organized and coordinated mechanism of the body, wherein the inflammatory response is directed to remove damaged tissue and prepare the site for either regeneration or repair. Dental clinics in Turkey offer the most convenient and reliable implant treatments and much more… Since dental implants emerge from the bone toward the septic oral environment, the interactions between bacteria and host cells in the peri-implant tissues result in the release of several cytokines, depending on the nature of the bacterium and idiosyncratic host immune response. Several authors have found a close relationship between the degree of inflammation in peri-implant tissues and the various components collected from the peri-implant sulcus fluid (PISF), such as interleukin-1β, prostaglandin E2, matrix metalloproteinases, myeloperoxidase (MPO) and products of nitric oxide metabolism. In addition, the level of MPO has been shown to be a good indicator of neutrophil activity in failed periimplant sites as compared to successful endosseous dental implant sites. Thus, MPO may be a good marker of the inflammatory process and of implant failure. Some authors have suggested that MPO production is not confined to the inflamed sites, but also extends to sites that otherwise appear healthy. The toothless patients leave Dental clinics in Turkey happy and comfortable after having successful and reliable implant operations by the specialist dental surgeons… It is analyzed that the inflammatory response of the soft tissues surrounding dental implants subjected to several unfavorable conditions (ie, nonsubmerged implants inserted into fresh sockets, previously confirmed by trephine, with circumferential bone defects and without using membranes, in beagle dogs not receiving any measure of oral hygiene or soft diet). The rationale for this experimental design was to increase implant failure
rates in order to obtain an adequate subsample size for comparing the level of three highly robust inflammatory
mediators (MPO, TNF- α, and SOA) within the sites where implants were osseointegrated and those that were not. Both crestal and paracrestal biopsies of the gingiva were collected in order to test whether the inflammatory response might extend to the soft tissue of nearby regions, as has been reported elsewhere. To better understand why higher levels of certain biomarkers (mainly MPO but also TNF-α) might be elevated at sites where the implant failed in comparison with those sites where the implant survived, the main factors underlying the high failure rate and the high
peri-implant pocket depth of the surviving implants observed here should be reviewed. First, an increase in bone resorption in immediate implants in beagle dog studies has been demonstrated. In addition, the peri- implant defects created in fresh sockets generate higher marginal bone resorption. The ensuing inflammatory response of this additional trauma, added to the damage generated by the trephination per se, may be considered an additional risk factor leading to bone loss and periimplant inflammation. Furthermore, the flap elevation performed to carry out the trephination impairs the vascular supply to the healing site, in the initial phase of regeneration, hampering initial wound healing and possibly having a long-lasting effect on the dimensional reduction of the supporting bone and the concomitant inflammatory response. It also should be taken into account that the primary stability of implants was only assured by 3 mm of the apical zone of the implant, with the rest of the implant body contained within the circumferential defect. This caused the implants to have less than optimal primary stability to absorb the indirect occlusal loading exerted toward the healing abutments. Although there is no convincing causal relation between compression and bone loss, a clear relationship between high-stressed bones and bone resorption has been found. The surgeons at Dental clinics in Istanbul are highly experienced about implant operations and use the most reliable implant treatments technique with very high percentage of success to the toothless patients.
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