|
Ellies et al. (1999)
|
BTX-A (Botox®).
2.5 U |
19 rats Wistar (200-360 g). Females. Right submandibular gland. |
Analysis after 7, 14 and 28 days of application. Histological processing (HE), morphometric studies and Immunohistochemistry for acetylcholinesterase (AChE). |
Immunoreactivity weaker on days 7, 14 and 28 in the treated group. Nuclear counting slightly higher than the controls. No change in acinar volume. |
|
Ellies et al. (2000)
|
BTX-A (Botox®).
2.5 U. |
16 rats Wistar (200-360 g). Females. Right parotid gland. |
Analysis after 7, 14 and 28 days of application. Histological processing (HE), morphometric studies and Immunohistochemistry for acetylcholinesterase. |
Weak immunoreactivity observed in the group treated on days 7 and 14, but stronger on day 28. Nuclear counting slightly lower than in controls. Slight increase in acinar volume. |
|
Ellies et al. (2003)
|
BTX-A (Botox®).
2.5 U. |
10 rats Wistar (200-360 g). Females. Parotid gland and right submandibular. |
Analysis after 7, 14 and 28 days of application. Immunohistochemistry for Neuronal nitric oxide synthase (nNOS). |
Weak immunoreactivity observed proportional to the increasing of toxin exposure time in the treatment group. |
|
Ellies (2003)
|
BTX-A. Dose and brand not informed. |
Rats. Sex and weight not informed. Submandibular and parotid glands. |
Immunohistochemistry for acetylcholinesterase and neuronal nitric oxide synthase. Morphometric studies. |
Decreased immunoreactivity of acetylcholinesterase and neuronal nitric oxide synthase in the treated groups. Normal glandular parenchyma. Small increase in cell volume. |
|
Yuan et al. (2004)
|
BTX-A (Prosigne®).
2.5 U. |
18 rats Wistar (210-280 g). Females. Right submandibular gland. |
Analysis after 6, 10 and 30 days of application. Histological processing (HE) and Immunohistochemistry for substance P |
Temporary atrophy of the acinar and ductal cells. No inflammatory process. Weak immunoreactivity in the treated group. |
|
Ellies et al. (2006a)
|
BTX-A (Botox®).
2.5 U. |
20 rats Wistar (200-360 g). Females. Right submandibular gland. |
Analysis after 5, 7, 14 and 28 days of after application. Immunohistochemistry for Neuronal nitric oxide synthase. |
Weak immunoreactivity observed proportional to the increasing of toxin exposure time in the treatment group. |
|
Ellies et al. (2006b)
|
BTX-A (Botox®).
2.5 U. |
20 rats Wistar (200-360 g). Females. Right parotid gland. |
Analysis after 5, 7, 14 and 28 days of after application. Immunohistochemistry for Neuronal nitric oxide synthase. |
Weak immunoreactivity observed proportional to the increasing of toxin exposure time in the treatment group. |
|
Coskun et al. (2007)
|
BTX-A (Botox®).
2.5 U. |
15 rats Wistar (275-325 g). Females. Right submandibular gland. |
Analysis after 14 and 28 days of application. Histological processing (HE) and ultrasonography. |
Reduction in size of the glands, but with no permanent histological changes in the cells. Lymphocytic infiltration. |
|
Teymoortash et al. (2007)
|
BTX-A, B ou A/B
(Botox®).
BTX-A: 5 U; BTX-B: 250 U (1:50, conversion factor). |
18 rats Wistar (250-300 g). Males. Right submandibular gland. |
Analysis after 14 days of application. Macroscopic, histological processing (HE), immunohistochemistry, immunohistochemistry for amylase and transmission electron microscopy (TEM). |
Reduced weight of the gland. Acini more compressed and with a smaller area. Lower immunoreactivity in the treated groups. Ultrastructural changes in the treated group. |
|
Gerlinger et al. (2007)
|
BTX-A. 8 U. Brand not informed. |
3 rabbits (2.5 kg). Males. Right submandibular gland. |
Analysis after 8 weeks of application. |
Significant histological changes not observed and temporary reduction in saliva production. |
|
Wen et al. (2009)
|
BTX-A (Prosigne®).
2.5 U. |
18 rats Wistar (210-280 g). Females. Right parotid gland. |
Analysis after 7, 12 and 35 days of application. Histological processing (HE) and immunohistochemistry for vasoactive intestinal polypeptide. |
Temporary cell atrophy and decrease in immunoreactivity in the treated group. |
|
Shan et al. (2013)
|
BTX-A (Prosigne®).
10 U and 5U. |
30 rabbits (2.4+/-0.3 kg). Males. Left submandibular gland. |
10 U – Analysis after 1 week;
5 U – Analysis after 1, 2, 4 and 12 weeks. Histological processing (HE), TEM, Tunel (apoptosis), immunofluorescence for AQP5, salivary flow and PCR for M3. |
Size reduction of acinar cells, fibrosis, ultrastructural changes in the treated group, decreased salivary flow, apoptosis in acinar and ductal cells in the treated, inhibition of the M3 receptor, and location of AQP5 in the cell cytoplasm. |
|
Younis et al. (2013)
|
BTX-A (Botox®).
2 U. |
15 rats Wistar (150-200 g). Males. Right parotid gland. |
Analysis after 20 days of application. Histological processing (HE) and TEM. |
Reduction in the size of the acini, with less secretory granules and with extensive and coarse vacuoles. Larger interlobular spaces. Ultrastructural changes in the treated group. |
|
Xu et al. (2015)
|
BTX-A (Prosigne®).
1, 2, 3 and 10 U. |
30 rats Sprague-Dawley (230-250 g). Males. Left submandibular gland. |
Analysis 1, 2, 4, 12 and 24 weeks after application. Measurement of Saliva Secretion; Western Blotting; Immunohistochemistry for SNAP-25 and immunofluorescence for aquaporin 5 (AQP5); Cell Culture and Transfection; Cell Surface Biotinylation and Western Blotting; Cell Surface Biotinylation and Immunocytofluorescence; Preparation of Cytoplasm and Membrane Fractions. |
Reduced salivary flow in a dose-dependent; SNAP-25 immunostaining was decreased; proteolysis of SNAP-25 in the treated groups; decreased AQP5 immunofluorescence; and redistribution of AQP5 (diffuse cytoplasmic distribution) in the treated groups. |
Histological and immunohistochemical findings of the action of botulinum toxin in salivary gland: systematic review