Maria Angela Naval Machado

Influence of anti-inflammatory administration in collagen maturation process during orthodontic tooth movement

Bone formation is essential to orthodontic tooth movement and bone is formed by collagen. To analyze the collagen maturation process on bone matrix neoformed under nonsteroidal and steroidal treatment during orthodontic tooth movement by polarized microscopy, male Wistar rats (n = 90) were randomly divided into three groups (n = 30): C (control), NSAID (potassium diclofenac) and SAID (disodic phosphate dexamethasone). The animals of the C group received 0.9% saline solution; NSAID group received 5 mg/kg potassium diclofenac (CATAFLAM®); and SAID group received 2 mg/kg phosphate dissodic dexamethasone (DEXANIL®). Animals were sacrificed 3, 7 or 14 days after the placement of orthodontic appliances and the upper first molars were processed histologically and stained with picrosirius. Bone formation was evaluated under polarized light microscopy and 4.5 Image Pro‐Plus® software calculated the percentage of immature/mature collagen present in the groups. On the third days after force application, SAID and NSAID groups showed greater proportion of immature collagen than C group. On the seventh and fourteenth days, there was a lower proportion of mature collagen only in the SAID group (P < 0.001). These data demonstrate that dexamethasone delays the collagen maturation process in established bone matrix. Microsc. Res. Tech., 2011.

Low virulent oral Candida albicans strains isolated from smokers.

It is widely accepted that tabagism is a predisposing factor to oral candidosis and cumulate data suggest that cigarette compounds may increase candidal virulence. To verify if enhanced virulence occurs in Candida albicans from chronic smokers, a cohort of 42 non-smokers and other of 58 smokers (all with excellent oral conditions and without signs of candidosis) were swabbed on tong dorsum and jugal mucosa. Results showed that oral candidal loads do not differ between smoker and non-smokers. Activities of secreted aspartyl-protease (Sap), phospholipase, chondroitinase, esterase-lipase, and haemolysin secretions were screened for thirty-two C. albicans isolates. There were detected significant increments in phospholipasic and chondroitinasic activities in isolates from non-smokers. For other virulence factors, no differences between both cohorts were achieved.

Effects of Fluoxetine and Venlafaxine and Pilocarpine on Rat Parotid Glands

This study assessed the effect of the antidepressants, Fluoxetine and Venlafaxine, on the size (GS), mass (M), cellular volume (CV), of rat parotid salivary glands and salivary flow rate (SFR), as well as the secretagogue action of pilocarpine on this flow. Ninety animals were divided into 9 treatment groups with the antidepressants, antidepressants associated with the application of pilocarpine, antidepressants and physiologic serum, physiologic serum (control) and pilocarpine (positive control). Thirty hours after the end of treatment, saliva collection began, to determine the SFR. Next, the salivary glands were removed, GS and M measured, and the specimens processes for histomorphometric analysis and CV determination. The variable GS presented statistically significant increase among the groups that were treated for 30 days with Fluoxetine (p=0.0002) and Venlafaxine (p=0.0112) when compared with the group treated with physiologic serum (control). The group treated with Fluoxetine for 30 days revealed increase in M (p=0.0190) and diminished SFR (p=0.0031), statistically significant, when compared with the control group. CV revealed increase in acinic cells between the Fluoxetine (30 days) (p=0.0005) and Venlafaxine (30 days) (p=0.0004) groups as well, when compared with the control group. The group treated with Venlafaxine for 60 days in association with pilocarpine presented SFR similar to the control group treated for 60 days. Both Fluoxetine and Venlafaxine reduced the SFR and caused increase in CV, resulting in hypertrophy of the glands, with Fluoxetine having a more pronounced anticholinergic action. The pilocarpine increased the SFR in the group that received Venlafaxine.

Cytopathological Changes Induced by the Crack Use in Oral Mucosa

Aims: To evaluate cytological alterations, inflammation, and microbial charge of the oral mucosa epithelium in crack users in in terms of the amount and duration of use. Methods: Two hundred thirty four crack users (case group) and 120 non-users (control group) participated in this study. Clinically healthy epithelial cells were collected from the posterior mouth floor, using the conventional exfoliative cytology. Some of the aspects evaluated were as follows: Papanicolaou classification, nuclear area (NA), cytoplasmic area (CA), nuclear/cytoplasmic area ratio (NA/CA), inflammation, microbial charge, keratinization, enucleated superficial cells, and binucleation. Results: The average time of crack consumption was 9.8 years (±7.1) and the average quantity of use was 13.97 g/week (±18.5). The average NA values and NA/CA ratio were increased and CA values were decreased in the case group compared to those in the controls (p < 0.05). Papanicolaou class II, intense inflammation, and intense microbial charge were more prevalent in the case group than in the controls (p < 0.05). There was a significant association between high quantity of smoked crack rocks per week and increased CA values, absence of keratinization, and presence of enucleated superficial cells (p < 0.05). Conclusion: Crack use seemed to induce inflammatory alterations and early indicators of malignant transformation on the oral mucosa epithelium.

HIV Infection Induces Morphometrical Changes on the Oral (Buccal Mucosa and Tongue) Epithelial Cells

The aim of this study was to assess morphological and morphometrical alterations of oral squamous epithelial cells in type 1 HIV infected individuals. Oral smears were collected from tongue and buccal mucosa of 30 HIV infected (experimental) and 30 non-infected (control) individuals by liquid-based exfoliative cytology. The cells were morphologically analyzed and the nuclear area (NA), the cytoplasmic area (CA) and the nucleus-to-cytoplasm area ratio (NA/CA) were calculated. No morphological differences were found between the groups. The mean values of CA were decreased in tongue (P=.00006) and buccal mucosa (P=.00242) in HIV infected individual, while mean values of NA were increased (P=.00308 and .00095, respectively) in the same group. NA/CA ratio for experimental group was increased in both collected places, with P=.00001 (tongue) and P=.00000 (buccal mucosa). This study revealed that HIV infection was able to induce morphometrical changes on the oral epithelial cells.

Effect of Physical Activity on the Lesion Repair Process in the Gastrocnemius Muscle of Rats

The present study aimed to evaluate the effect of a progressive load of physical activity on a musculoskeletal injury in rats. Sixty-four rates were divided into two groups: experimental group (EG), which underwent physical activity (swimming) with a progressive load, and the control group (CG), which was not submitted to this program. The training was carried out according to an adapted version of the Goncalves (1999) swimming system. Injuries were caused to the gastrocnemic muscle by inducing 40% NaOH. On days 2, 7, 14, and 21 after inducing muscle injury, the animals from both EC and CG were sacrificed. The injured area was removed and processed. The neutrophils, macrophages, lymphocytes, and plasmocytes were quantified by hematoxylin and eosin (HE GC=2.48±1.00; p=0.006) and lymphocytes (GE=2.12±0.82; GC=0.06±0.82; p=0.037) after 2 days, and of macrophages (GE=15.74±3.00; GC=6.02±1.95; p=0.007) and lymphocytes (GE=2.01±0.78; GC=0.14±0.09; p=0.044) after 7 days, could be observed in the EG when compared to the CG; however, the opposite was true for neutrophils (GE=48.12±17.04; GC=105.54±12.25; p=0.005). After 14 days, a smaller quantity of neutrophils (GE= 32.70±10.26; GC= 90.96±17.62; p= 0.044) and a larger quantity of plasmocytes (GE=9.06±3.84; GC=0.68±0.53; p=0.028) could be observed in the EG as compared to the CG. A greater area of type III collagen could be observed in the EG when compared to the CG over a 14-day period (GE=44.90±16.15; GC=0.74±0.40; p=0.000) and a 21-day period (GE=13.19±9.09; GC=1.02±0.94; p=0.029), whereas the opposite could be observed for type I collagen. The physical activity promoted an increase in the deposition of type III collagen in the muscle injury. This activity accelerated the repair process after 14 days, possibly moderated by the larger number of inflammatory cells, while after 21 days, the lesion presented a lesser resistance.

Preclinical alterations of oral epithelial cells in contact with orthodontic appliances.

AIM This study evaluated the behavior of oral epithelial cells in contact with orthodontic appliances. METHODS Oral epithelial cells of clinically normal buccal mucosa were obtained by liquid-based exfoliative cytology from 22 orthodontic patients. The following regions were evaluated: a) oral mucosa exposed to friction from orthodontic brackets; b) oral mucosa exposed to friction from the tube on the orthodontic band, and c) oral mucosa not exposed to friction (control area). Nuclear (NA) and cytoplasmic (CA) areas and NA/CA ratio were assessed by an image analysis system. Cell morphology and cellularity were also analyzed by Papanicolaou technique. RESULTS The NA of the cells in contact with orthodontic brackets and bands were smaller than the control area. Cells in contact with the brackets showed the greatest reduction in CA in comparison with the cells subjected to friction from the tube, and the control group. Smears classified as type I predominated in all regions analyzed, although type II were predominant, together with superficial epithelial cells, mainly in the oral mucosa in contact with the band tube. CONCLUSION Preclinical alterations in the epithelial cells of oral mucosa, caused by orthodontic appliances, are reduction in NA, increase in cell keratinization and inflammatory features, especially in the band tube area.

Surgical treatment of maxillary transverse deficiency: retrospective study of 14 patients

IntroductionThe diversity of the proposed techniques in the treatment of maxillary transverse deficiency in adults reflects the conflicting opinions about the primary area of resistance to maxillary expansion in the craniofacial skeleton. In order to evaluate the efficiency of the surgical expansion in which no osteotomies of the pterygomaxillary junction were made, we have carried out a retrospective study with 14 patients with maxillary transverse deficiency, who were treated from 2003 to 2006.Material and methodsIn the study, models were made prior to and after surgery, and the intercanine and intermolar distances and the improvement of the interocclusal relationships were analyzed. Breathing function and the complications that occurred during and after the surgeries were also analyzed.ResultsAll expansions were carried out according to pre-surgical planning so that expansion completely corrected the crossbite, resulting in the desired final occlusion for all patients. Intraoperative complications were limited to one Hyrax appliance deformation. Two patients had minor postoperative complications that included wound dehiscence and pain. Improvements in nasal breathing were observed in all patients that complained of breathing problems prior to the surgery.ConclusionThe satisfactory results obtained turns the surgical protocol described in this study recommended for the treatment of maxillary transverse deficiency in adults. Importantly, we found that pterygomaxillary osteotomy is not essential for maxillary expansion. The morbidity of the procedure was low with fairly minor complications, and surgically assisted rapid maxillary expansion was shown to improve nasal breathing.