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melanocortin receptor Introduction br Root resorption Root resorption

Introduction

Root resorption
Root resorption is common during orthodontic tooth movement (Krishnan, 2005). Limited root resorption, involving a number of teeth, can be considered a consequence of orthodontic treatment (Ketcham, 1927). If the patient develops additional pathosis, such as periodontal disease, this may further compromise the support of the tooth and the patient can eventually loose that tooth (Ketcham, 1927). However, no reports in the literature have documented tooth loss caused by root resorption. A long-term case report documented a follow-up of a case of severe root resorption that occurred for 33years, and the affected teeth were found to be functional (Parker, 1997). However, lack of reports in the literature on tooth loss due to root resorption does not exclude this as a potential risk.
The problem of root resorption as a consequence of orthodontic treatment was first discussed by Ketcham (1927). He was also the first to indicate other factors, such as hormonal disturbance and dietary deficiency in addition to orthodontic treatment variables, which may be contributing factors in root resorption (Davidovitch et al., 1996). The etiology of root resorption still remains unclear and is complex, including genetic predisposition and environmental factors (Al-Qawasmi et al., 2003; Abass and Hartsfield, 2007). The genetic predisposition makes root resorption associated with orthodontic treatment more predictable (Abass and Hartsfield, 2007).
The best approach toward root resorption is to consider the risk factors, discuss the identified factors with the patient seeking orthodontic treatment, and include these factors in the treatment consent form. These risk factors include the duration of treatment. The risk for root resorption increases with the length of treatment (Krishnan, 2005; Brezniek and Wasserstein, 1993; Baumrind, 1996). Treatment of impacted canines can extend treatment time or the movement of these canines may lead to an increase in the risk for root resorption (Krishnan, 2005). Thin, tapered, and dilacerated root morphology, results in melanocortin receptor that are more prone to resorption (Mirabella and Artun, 1995; Levander et al., 1998; Killiany, 1999; Sameshima and Sinclair, 2001). Additionally, history of trauma associated with the anterior teeth increases the risk for root resorption (Malmgren et al., 1982). Therefore, documentation of the condition through pre-treatment periapical radiographs of the maxillary and mandibular incisors is necessary. Potential extraction of maxillary and mandibular first or second premolars as well as the use of intermaxillary elastics during treatment should also be considered (Mirabella and Artun, 1995; Sameshima and Sinclair, 2001). Root resorption from previous orthodontic treatment is a risk that may result in further root shortening (Brezniak and Wasserstein, 2002). Orthodontic re-treatment of such cases should be performed with caution and treatment objectives should be limited. Some habits, such as thumb sucking, occlusal trauma, or history of chronic bruxism, may increase the risk for root resorption (Linge and Linge, 1991; Harris, 2000).
Assessment of the condition through a progress radiograph at 6–12months after the initiation of orthodontic treatment is recommended. These could be either periapical or panoramic radiographs. The patient must be informed that if root resorption is observed, then active treatment must be stopped for at least 3months (Levander et al., 1994). The reparative process of root resorption begins two weeks after active treatment is stopped (Krishnan, 2005). At this stage, an alternative treatment plan should be considered and treatment should be discontinued when severe root resorption is observed.

Pain associated with orthodontic treatment
Pain and discomfort is a common adverse effect associated with orthodontic treatment (Pollat, 2007). Previous studies have shown that 70–95% of orthodontic patients experience pain (Lew, 1993; Scheurer et al., 1996; Firestone et al., 1999). This pain could be a reason for discontinuing treatment; previous studies have indicated that 8% and even upto 30% of orthodontic patients discontinue treatment because of pain (Pollat, 2007). The pain and discomfort associated with orthodontic treatment is characterized by pressure, tension, or soreness of the teeth (Ngan et al., 1989). Pain in the anterior teeth is greater than the posterior teeth (Scheurer et al., 1996). Pain has been reported to begin 4h after the placement of separators or orthodontic wire, and the worst pain was found to occur on the second day of treatment (Ngan et al., 1989; Lew, 1993; Scheurer et al., 1996; Firestone et al., 1999). Usually, pain lasts for seven days (Ngan et al., 1989). Clinical anticipation of the need to use fixed appliances makes the risk for pain and discomfort greater (Stewart et al., 1997; Sergl et al., 1998). Management of pain should include informing the patient of the possibility of experiencing pain to reduce anxiety. Furthermore, the clinician can ask the patient to chew on plastic wafers or chewing gums containing aspirin (White et al., 1984; Hwang et al., 1994; Ngan et al., 1994). Chewing on plastic wafers theoretically increases the circulation in the periodontal ligament, which reduces the pain and discomfort. Additionally, clinicians are recommended to prescribe Ibuprofen or acetaminophen analgesics preoperatively and for a short duration after the placement of separators and initial wires (Ngan et al., 1994; Law et al., 2000; Polat and Karaman, 2005).

Fig Induction of E http www alkyne phosphoramidite terminal

Fig. 2. Induction of EGFP expression from the hTERT and CEA promoters mediated by PRV IE180 and HSV-1 ICP4 proteins. Panel A. The influence of PRV IE180 or HSV-1 ICP4 on the activation of the hTERT promoter (plasmid pZTERGF, 2 渭g) was studied in Hela Tet-Off melanocortin receptor by co-transfection with the plasmid pAZT180 (2 渭g), which expresses IE180, or with ptetICP4lac (2 渭g), which expresses ICP4. Plasmid pZTERGF expresses EGFP under the control of the hTERT promoter. EGFP protein expression was determined by flow cytometry 24 h posttransfection. Each value represents the mean and standard deviation (error bars) from three independent experiments. Panel B. The influence of PRV IE180 or HSV-1 ICP4 on the activation of the CEA promoter (plasmid pACEA-FG (2 渭g) was studied in Hela Tet-Off cells by co-transfection with the plasmid pAZT180 (2 渭g), which expresses IE180, or with ptetICP4lac (2 渭g), which expresses ICP4. Plasmid pACEA-FG expresses EGFP under the control of CEA promoter. EGFP protein expression was determined by flow cytometry 24 h posttransfection. Each value represents the mean and standard deviation (error bars) from three independent experiments.Figure optionsDownload full-size imageDownload high-quality image (123 K)Download as PowerPoint slide
Fig. 3. Induction of EGFP expression from the hTERT promoter mediated by PRV IE180. The influence of PRV IE180, expressed under the control its own promoter (plasmid pRIE180), on the activation of the hTERT promoter (plasmid pZTERGF, 2 渭g), PRV gG promoter (plasmid pZGF-SD4) and DNA polymerase (UL30) promoter (plasmid p30GF, 2 渭g) was evaluated by co-transfection of pRIE180 (2 渭g) with pZTERGF (2 渭g) or pZGF-SD4 (2 渭g) plasmids in Hela Tet-Off cells. EGFP protein expression was determined by flow cytometry 24 h posttransfection. Each value represents the mean and standard deviation (error bars) from three independent experiments.Figure optionsDownload full-size imageDownload high-quality image (124 K)Download as PowerPoint slide
Expression of PRV IE180 under the control of hTERT and CEA tumor promoters in recombinant pseudorabies viruses
We next assessed the replication of recombinant PRV viruses in which the hTERT or CEA human tumor promoters were used to drive IE180 expression in lieu of its endogenous viral promoter. The transfection of PBAC90 with the hTERT-IE180 cassette of pOTER180-N or the CEA-IE180 cassette of pOCEA180-N into U2OS cells resulted in the production of PRV-TER and PRV-CEA viruses, respectively. Replacement of the PRV IE180 promoter with the hTERT or CEA promoters in the PRV recombinants was confirmed by PCR characterization of packaged viral DNA from PRV-TER, PRV-CEA, the parental virus vBecker2 and PBAC90 (Fig. 4, panel A and B). Specific primers for each promoter P180-S (PIE180), TERT-2D (PhTERT), CEA-S (PCEA) and 180-AS (coding sequence of IE180 gene) were used for amplification (Table 1). The specificity of the amplification products was confirmed by DNA size resolution on a 1% agarose gel: 1201 bp for PIE180-IE180, 710 bp for PhTERT-IE180 and 636 bp for PCEA-IE180 cassettes and 523 bp for DNA polymerase (UL30), which was used as a reference (Fig. 4, panel B). Specific fragments could be amplified from the PRV-TER (Fig. 4, panel B, lane C), PRV-CEA (Fig. 4, Panel B, lane D) and vBecker2 (Fig. 4, Panel B, lane A) by using specific primers for each promoter but not from the PBAC90 (Fig. 4, Panel B, lane B).