| BackgroundThe term―osseintegration‖is defined as the process whereby dentalimplants and bone are joined in a rigid, clinically asymptomatic fixation that ismaintained during functional loading~[1]. Several factors, such as implantlength/diameter, smoking, and infection, have been linked to the failure toachieve osseointegration~[2-3]. In the first report of the relationship betweensmoking and the loss of endosseous dental implants, Jones and Triplett (1992)found that five of15patients undergoing intraoral bone grafting andsimultaneous implant placement experienced impaired wound healing (definedas loss of bone and/or implants)~[4]. Bain and Moy (1993)~[5]further assessedvarious predispositions to implant failure in a group of540patients receiving2,194implants between1984and1990and found that smoking was the mostsignificant factor in implant failure:4.76%of implants failed in non-smokers,whereas11.28%failed in smokers. A recent meta-analysis of19appropriatelyselected studies reported that when smokers were compared with non-smokers, the odds ratio of implant failure was significantly elevated (OR=2.17,95%confidence intervals1.67–2.83)~[6]. These retrospective studies indicate thatsmoking has a negative influence on the osseointegration of implants leading tomore significant implant failure among smokers than non-smokers.Smoking has been implicated as a risk factor for various diseases such asosteoporosis, oral cancer, and periodontal disease (Greer and Poulson,1983;Qandil et al.,1997)~[7-8]. Cigarettes contain a large number of toxic compounds,including nicotine, which causes addiction. Many of the undesirable healtheffects of smoking have been attributed to nicotine. Several studies haveexamined the in vitro effects of nicotine on cell proliferation, attachment, andosteoblast differentiation in various cell types. For example, the production ofcollagen and non-collagenous proteins in fibroblasts is reported to decrease afternicotine treatment[9]. In addition, nicotine inhibits cellular growth and stimulatesalkaline phosphatase (ALP) activity in rat osteoblast-like cells~[10]. Thesemajorities of animal in vivo studies and cytological experiments have illustratednegative impacts of nicotine on osseointegration and osteoblast differentiation.Nonetheless, the clinical data describing this impairment are still lack.In recent years, resonance frequency analysis (RFA) has been introduced toprovide non-invasive and objective assessments of implant stability and tomonitor stability over time[11-24]. RFA is believed to be a potentially usefulclinical instrument for the detection of implant tissue disintegration. Becauseresonance frequency has been postulated to reflect the bone anchorage of theimplant, RFA may be applicable in the prevention, diagnosis and prediction ofimplant failures~[25-26]. It has been speculated that higher ISQ values indicategreater implant stability and presumably more extensive osseointegration~[27]. Tovalidate this statement, monitoring of resonance frequency should reveal the events during early healing. Although the use of individual measurements ofimplant stability quotient (ISQ) as a measure of osseointegration is contentious,the longitudinal increment of implant stability expressed by a series of ISQvalues over time can reflect the course of the bone healing process.Materials and MethodsThirty-two consecutive partially edentulous adult males were recruited andassigned either to the smoking (n=16) and non-smoking (n=16) group accordingto the inclusion and exclusion criteria. A total of45Straumann dental implantswere placed and one implant (4.8×10mm) per participant was randomly selectedfor analysis, a total of16implants per group. The stability of these implants wasmeasured by resonance frequency analysis at implant insertion and at1,2,3,4,6,8and12weeks post-operatively. In these patients, peri-implant soft tissueconditions and radiographic marginal bone changes were evaluated12monthafter loading.ResultsAll implants achieved osseointegration without complications within the12-week investigation period. The implant stability quotient (ISQ) in bothgroups decreased within the first2weeks, but increased thereafter until week12.In this secondary stability phase, the rate of ISQ increase in non-smokers wasstatistically higher than in smokers (P<0.05), reaching a plateau at8weeks.Nonetheless, the ISQ values of the smoking group increased slowly from the3week to the12week point with a significant difference among the times of8to12weeks (P<0.05). At12weeks post-operatively, no significant difference inISQ values could be found between the groups. There were significantdifference in the PD and MBL (**P<0.01), no significant difference in the mSBIand mPLM between smoking group and nonsmoking group. Marginal bone loss and PD in smokers was significantly higher than in the non-smoking group at12month after loading (**p<0.01).ConclusionIt was demonstrated from this clinical study that smoking impairs theimplant healing process of osseointegration. And, we recommend thatStraumann implants be allowed three months to heal in smokers rather than theusual six weeks in non-smokers. |
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