Endo-periodontal lesion--endodontic approach.

Endo-perio lesions might be interdependent because of the vascular and anatomic connections between the pulp and the periodontium. The aim of this study is to emphasise that primary endodontic lesion heals after a proper instrumentation, disinfection and sealing of the endodontic space. The primary endodontic lesion with a secondary periodontal involvement first requires an endodontic therapy and, in the second stage, a periodontal therapy. The prognosis is good, with an adequate root canal treatment; it depends on the severity of the periodontal disease, appropriate healing time and the response to the treatment. A correct diagnosis is sometimes difficult; an accurate identification of the etiologic factors is important for an adequate treatment. Primary perio-endo lesion may heal after a proper disinfection and sealing of the endodontic system, the one-year follow-up radiograph showing bonny repair. Invasive periodontal procedures should be avoided at that moment. The microorganisms and by-products from the infected root canal may cross accessory and furcal canals and determine sinus tract and loss of attachment. In both clinical cases presented in this article, successful healing was obtained after a proper disinfection and sealing of the endodontic system.

External radicular resorption: selected cases and review of the literature.

External radicular resorption is a pathological process that generates the loss of cementum, dentin and bone, almost irreversibly, involving vital and pulpless teeth. The early stage is asymptomatic and might be diagnosed by a routine radiograph or a clinical examination. Radicular resorption appears because of cementoclastic, dentinoclastic or/and osteoclastic activity. The process of resorption is associated with a damage of the periodontal ligament as a result of injury and necrosis, macrophages are the first cells that are detected, followed by multinucleated cells, odontoclasts, which affect the cementum and dentin.

Sex differences in development of morphine tolerance and dependence in the rat.

RATIONALE: Several investigators have shown that male rodents are more sensitive than females to morphine's antinociceptive effects. OBJECTIVE: The present study was conducted to determine whether this sex difference is stable after chronic morphine treatment. RESULTS: Acutely administered morphine produced significantly greater hotplate and tail withdrawal antinociception in males than in females. In contrast, there were no sex differences in morphine's hotplate or tail withdrawal effects under repeated (1-week interval) dosing conditions. In a separate group of rats, after 2 weeks of twice-daily morphine treatment (10-20 mg/kg per injection), the ED50 for morphine's antinociceptive effects increased approximately 6.9-fold in males versus only 3.7-fold in females; chronic morphine treatment also disrupted the estrous cycle of females. In a separate group of rats treated with 10 mg/kg morphine twice daily for 5 days, treatment with naloxone (1.0 mg/kg) on day 6 produced greater withdrawal scores in males than in females. CONCLUSIONS: These experiments demonstrate sex differences in development of tolerance to and dependence on morphine in the rat.

Effect of gonadectomy on discriminative stimulus effects of morphine in female versus male rats.

In a previous study, we found sex differences in the potency of morphine as a discriminative stimulus; the present study was designed to determine whether sex differences in gonadal hormones contribute to sex differences in morphine's discriminative effects. Adult female and male rats were gonadectomized (GNDZ) or sham-gonadectomized (SHAM), and then trained to discriminate 3.0 mg/kg morphine from saline. The ED50 for morphine discrimination was significantly lower in females than in males (0.66 +/- 0.12 vs. 1.25 +/- 0.16 mg/kg, respectively); ED50 values in GNDZ rats were slightly higher than in SHAM rats. The time course of morphine discrimination was not significantly different in females and males, whether GNDZ or not. The micro agonist fentanyl completely substituted for morphine in all rats, with no group differences in ED50 value. The micro agonists buprenorphine and nalbuphine substituted for morphine in nearly all females and in all SHAM males, but in only four of seven GNDZ males. The kappa agonist U69,593 did not substitute for morphine in rats of any group. Most opioid agonists were significantly more potent in decreasing response rate in males than females, and in GNDZ than SHAM rats; morphine and nalbuphine also increased response rate above control in some females. A pA2 analysis of naltrexone in combination with morphine suggested that there were no significant differences among groups in receptors at which morphine produced its discriminative stimulus effects. Although hormone replacement in GNDZ female rats at the end of the study reinstated estrous cycling, it did not substantially alter the ED50 for morphine discrimination. Thus, sex differences in potency of morphine as a discriminative stimulus may not be due to sex differences in gonadal hormone milieu. The possibility that sex differences in reinforcement frequency on morphine versus saline levers caused the sex differences in morphine discrimination is discussed.

Sex differences in opioid antinociception.

Previous studies indicate that mu opioid agonists such as morphine may produce greater antinociception in male than in female rodents. The present study was designed to investigate the generality of this finding across dose, time and type of opioid agonist. In adult female and male Sprague-Dawley rats, time-effect curves were obtained for vehicle and three doses each of the mu agonists fentanyl and buprenorphine, the kappa agonists (5alpha,7alpha,8alpha)-(-)-N-methyl-[7-(1-pyrrolidinyl )-1-oxaspiro-(4,5)dec-8-yl]benzeneacetamide (U69,593) and bremazocine and the delta agonists [D-Pen2,D-Pen5]enkephalin (DPDPE) and deltorphin on the 52 degrees C hot-plate and tail-withdrawal (immersion) assays. There were sex differences in the antinociceptive effects of the two kappa agonists and the two delta agonists, but the differences were assay-, dose- and/or time-dependent. Peak effects of U69,593 on tail withdrawal and DPDPE on hot plate tended to occur earlier in females than in males, and bremazocine produced greater tail-withdrawal antinociception in females than in males, whereas the highest doses of the two delta opioids produced greater hot-plate antinociception in males than in females. These results contrast with several previous reports showing that male rodents are more sensitive than females to the antinociceptive effects of mu and kappa (but not delta) opioids. These discrepancies may be caused by the more comprehensive examination of sex differences across dose and time used in the present study; sex differences that are dose- or time-dependent may not be apparent if a single dose or time point is examined. In addition, repeated testing procedures used in the present study may produce different results than acute testing procedures would, if female and male rats develop opioid tolerance at different rates.