World Workshop on Oral Medicine VI: a systematic review of medication‐induced salivary gland dysfunction

The aim of this paper was to perform a systematic review of the pathogenesis of medication‐induced salivary gland dysfunction (MISGD). Review of the identified papers was based on the standards regarding the methodology for systematic reviews set forth by the World Workshop on Oral Medicine IV and the PRISMA statement. Eligible papers were assessed for both the degree and strength of relevance to the pathogenesis of MISGD as well as on the appropriateness of the study design and sample size. A total of 99 papers were retained for the final analysis. MISGD in human studies was generally reported as xerostomia (the sensation of oral dryness) without measurements of salivary secretion rate. Medications may act on the central nervous system (CNS) and/or at the neuroglandular junction on muscarinic, α‐and β‐adrenergic receptors and certain peptidergic receptors. The types of medications that were most commonly implicated for inducing salivary gland dysfunction were those acting on the nervous, cardiovascular, genitourinary, musculoskeletal, respiratory, and alimentary systems. Although many medications may affect the salivary flow rate and composition, most of the studies considered only xerostomia. Thus, further human studies are necessary to improve our understanding of the association between MISGD and the underlying pathophysiology.     

STRESS FRACTURES OF THE FEMORAL SHAFT IN MILITARY RECRUITS

Stress fractures amongst military recruits are limited to the lower extremities; yet involvement of the shaft of the femur is unusual. Seven such cases in a series of 352 stress fractures are presented. The importance of early recognition and management is emphasized with a view to prevent bony disruption in an otherwise easily treatable condition.KEY WORDS: Fractures stress, Femoral fractures     

Sternocostoclavicular hyperostosis: a review and report of 11 cases

Sternocostoclavicular hyperostosis is a benign ossifying diathesis of unknown etiology characterized by hyperostosis and soft-tissue ossification between the clavicles, anterior portion of the upper ribs, and manubrium, with variable hyperostosis or ankylosis in the spine and sacroiliac joints. Our cumulative experience with 11 cases is reported, with emphasis on radiographic features of the condition. Scintigraphic results in five patients and computed tomographic findings in one patient are presented. A review of the literature and our own material indicates that sternocostoclavicular hyperostosis may be more common than has been previously recognized.     

Kinetics of solvolysis and muscarinic actions of an N-methyl-N-(2-bromoethyl)amino analogue of oxotremorine

An N-methyl-N-(2-bromoethyl)amino analogue (2) of oxotremorine cyclized in phosphate buffer to an aziridinium ion (3). The first-order rate constants (k1) for the cyclization reaction at 22 and 37 degrees C (pH 7.3) were 0.14 and 0.85 min-1, respectively. Determination of k1 as a function of pH gave a pKa value of 5.6 for 2. The rate constants (k2) for the hydrolysis of 3 at 22 and 37 degrees C (pH 7.3) were 0.0083 and 0.040 min-1, respectively. Compound 3 was 3-fold more active than oxotremorine as a muscarinic agonist on the guinea pig ileum, whereas its nicotinic actions, as estimated on the frog rectus, were quite weak. Because of its greater rate of cyclization and the higher peak concentrations of the aziridinium ion which ensue, 2 may offer advantages over its (2-chloroethyl)amino analogue (1) as an alkylating ligand for muscarinic receptors.     

Influence of atropine and N-methyl atropine pretreatments on behavioral and physiological effects of the irreversible muscarinic agonist, BM123

The irreversible muscarinic agonist, BM123 (63 mu moles kg-1, IV), was shown to produce central and peripheral physiological signs characteristic of cholinergic agonists. It also induced hypothermia, elevated nociceptive thresholds, reduced locomotor activity and disrupted spontaneous alternation performance in rats. The centrally acting muscarinic antagonist, atropine (50 mu mole kg-1) prevented or reduced all the above effects of BM123 when given SC 40 min prior to the BM123 injection. In contrast, the peripherally acting muscarinic antagonist, N-methyl atropine, prevented only the peripheral effects and the elevated nociceptive thresholds. Habituation of activity during a 20 min session was observed in all groups despite different levels of general activity. These findings are consistent with a model in which atropine and N-methyl atropine compete with BM123 for reversible association with the muscarinic receptor. In the case of BM123 administered alone, the association results, first, in agonist effects and proceeds to form an irreversible complex. Our present results show that by competing with BM123 for mAChR sites during the initial, reversible state of the interaction, atropine blocks the cholinomimetic effects of the agonist during both this state and its otherwise subsequent irreversible state.     

妊娠糖尿病妇女使用门冬胰岛素或常规人胰岛素在疗效、安全性方面的比较

在一项随机、平行分组的开放试验中，27例妊娠糖尿病妇女（年龄30．7±6．3岁，HbA1c〈7％）随机分为门冬胰岛素治疗组（餐前5分钟注射）和常规人胰岛素治疗组（餐前30分钟注射）。试验时间为从诊断妊娠糖尿病（18～28周）至产后6周。研究期间两组的总体血糖水平均控制良好（试验开始和结束时HbA1c≤6％）。进餐试验时，试验6周时的平均血糖水平（门冬胰岛素组4．2±0．57mmol／L，常规人胰岛素组4．8±0．86mmol／L）略低于试验0周时（门冬胰岛素组4．9±0．59mmol／L，常规人胰岛素组5．1±0．36mmol／L）。