One-third of smokers primarily use menthol cigarettes and usage of these cigarettes leads to elevated serum nicotine levels and more difficulty quitting in standard treatment programmes. Previous brain imaging studies demonstrate that smoking (without regard to cigarette type) leads to up-regulation of β2*-containing nicotinic acetylcholine receptors (nAChRs). We sought to determine if menthol cigarette usage results in greater nAChR up-regulation than non-menthol cigarette usage. Altogether, 114 participants (22 menthol cigarette smokers, 41 non-menthol cigarette smokers and 51 non-smokers) underwent positron emission tomography scanning using the α4β2* nAChR radioligand 2-[18F]fluoro-A-85380 (2-FA). In comparing menthol to non-menthol cigarette smokers, an overall test of 2-FA total volume of distribution values revealed a significant between-group difference, resulting from menthol smokers having 9–28% higher α4β2* nAChR densities than non-menthol smokers across regions. In comparing the entire group of smokers to non-smokers, an overall test revealed a significant between-group difference, resulting from smokers having higher α4β2* nAChR levels in all regions studied (36–42%) other than thalamus (3%). Study results demonstrate that menthol smokers have greater up-regulation of nAChRs than non-menthol smokers. This difference is presumably related to higher nicotine exposure in menthol smokers, although other mechanisms for menthol influencing receptor density are possible. These results provide additional information about the severity of menthol cigarette use and may help explain why these smokers have more trouble quitting in standard treatment programmes.

Context Despite progress in tobacco control, secondhand smoke (SHS) exposure remains prevalent worldwide and is implicated in the initiation and maintenance of cigarette smoking. Objective To determine whether moderate SHS exposure results in brain α4β2* nicotinic acetylcholine receptor (nAChR) occupancy. Design, Setting, and Participants Positron emission tomography scanning and the radiotracer 2-[18F]fluoro-3-(2(S)azetidinylmethoxy) pyridine (also known as 2-[18F]fluoro-A-85380, or 2-FA) were used to determine α4β2* nAChR occupancy from SHS exposure in 24 young adult participants (11 moderately dependent cigarette smokers and 13 nonsmokers). Participants underwent two bolus-plus-continuous-infusion 2-FA positron emission tomography scanning sessions during which they sat in the passenger’s seat of a car for 1 hour and either were exposed to moderate SHS or had no SHS exposure. The study took place at an academic positron emission tomography center. Main Outcome Measure Changes induced by SHS in 2-FA specific binding volume of distribution as a measure of α4β2* nAChR occupancy. Results An overall multivariate analysis of variance using specific binding volume of distribution values revealed a significant main effect of condition (SHS vs control) (F1,22=42.5, P <.001) but no between-group (smoker vs nonsmoker) effect. Exposure to SHS led to a mean 19% occupancy of brain α4β2* nAChRs (1-sample t test, 2-tailed, P <.001). Smokers had both a mean 23% increase in craving with SHS exposure and a correlation between thalamic α4β2* nAChR occupancy and craving alleviation with subsequent cigarette smoking (Spearman ρ= −0.74, P =.01). Conclusions Nicotine from SHS exposure results in substantial brain α4β2* nAChR occupancy in smokers and nonsmokers. Study findings suggest that such exposure delivers a priming dose of nicotine to the brain that contributes to continued cigarette use in smokers. This study has implications for both biological research into the link between SHS exposure and cigarette use and public policy regarding the need to limit SHS exposure in cars and other enclosed spaces.

Objective To create a treatment algorithm for focal grade 3 or 4 cartilage defects of the knee using both classic and novel cartilage restoration techniques. Design A comprehensive review of the literature was performed highlighting classic as well as novel cartilage restoration techniques supported by clinical and/or basic science research and currently being employed by orthopedic surgeons. Results There is a high level of evidence to support the treatment of small to medium size lesions (<2-4 cm2) without subchondral bone involvement with traditional techniques such as marrow stimulation, osteochondral autograft transplant (OAT), or osteochondral allograft transplant (OCA). Newer techniques such as autologous matrix-induced chondrogenesis and bone marrow aspirate concentrate implantation have also been shown to be effective in select studies. If subchondral bone loss is present OAT or OCA should be performed. For large lesions (>4 cm2), OCA or matrix autologous chondrocyte implantation (MACI) may be performed. OCA is preferred over MACI in the setting of subchondral bone involvement while cell-based modalities such as MACI or particulated juvenile allograft cartilage are preferred in the patellofemoral joint. Conclusions Numerous techniques exist for the orthopedic surgeon treating focal cartilage defects of the knee. Treatment strategies should be based on lesion size, lesion location, subchondral bone involvement, and the level of evidence supporting each technique in the literature.

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Purpose of Review The purpose of the review is to discuss the relevant pathoanatomy, management, complications, and technical considerations for recurrent patellofemoral instability (PFI) in the pediatric population. Special consideration is given to recent literature and management of the patient with repeat instability following surgery. Recent Findings Patellar stabilization surgery is in principle dependent upon restoration of normal patellofemoral anatomy and dynamic alignment. Historically, treatment options have been numerous and include extensor mechanism realignment, trochleoplasty, and more recently repair and/or reconstruction of the medial patellofemoral ligament (MPFL) as a dynamic check rein during initial knee flexion. In skeletally immature patients, preference is given to physeal-sparing soft tissue procedures. While medial patellofemoral ligament reconstruction has become a popular option, postoperative failure is a persistent issue with rates ranging from 5 to 30% for PFI surgery in general without any single procedure (e.g., distal realignment, MPFL reconstruction) demonstrating clear superiority. Failure of surgical patellar stabilization is broadly believed to occur for three main reasons: (1) technical failure of the primary stabilization method, (2) unaddressed static and dynamic pathoanatomy during the primary stabilization, and (3) intrinsic risk factors (e.g., collagen disorders, ligamentous laxity). Summary PFI is a common orthopedic condition affecting the pediatric and adolescent population. Treatment of repeat instability following surgery in the PFI patient requires understanding and addressing underlying pathoanatomic risk factors as well as risks and reasons for failure.