Risks and complications in rhinoplasty

Rhinoplasty is regarded to be associated with many risks as the expectations of patient and physician are not always corresponding. Besides of postoperative deformities many other risks and complications have to be considered

Operative treatment of functional facial skin disorders

The skin is the principal interface between the body and the surrounding world and thus serves as a protective barrier against trauma, temperature extremes and radiation. With receptors for pressure, movement, heat and cold, it also acts as sensory organ and through sweat secretion plays a role in thermoregulation and electrolyte metabolism. Not all of these functions are relevant to facial skin, however, cosmetic aspects are of vital importance

Telomere Shortening Impairs Regeneration of the Olfactory Epithelium in Response to Injury but Not Under Homeostatic Conditions

Atrophy of the olfactory epithelium (OE) associated with impaired olfaction and dry nose represents one of the most common phenotypes of human aging. Impairment in regeneration of a functional olfactory epithelium can also occur in response to injury due to infection or nasal surgery. These complications occur more frequently in aged patients. Although age is the most unifying risk factor for atrophic changes and functional decline of the olfactory epithelium, little is known about molecular mechanisms that could influence maintenance and repair of the olfactory epithelium. Here, we analyzed the influence of telomere shortening (a basic mechanism of cellular aging) on homeostasis and regenerative reserve in response to chemical induced injury of the OE in late generation telomere knockout mice (G3 mTerc−/−) with short telomeres compared to wild type mice (mTerc+/+) with long telomeres. The study revealed no significant influence of telomere shortening on homeostatic maintenance of the OE during mouse aging. In contrast, the regenerative response to chemical induced injury of the OE was significantly impaired in G3 mTerc−/− mice compared to mTerc+/+ mice. Seven days after chemical induced damage, G3 mTerc−/− mice exhibited significantly enlarged areas of persisting atrophy compared to mTerc+/+ mice (p = 0.031). Telomere dysfunction was associated with impairments in cell proliferation in the regenerating epithelium. Deletion of the cell cycle inhibitor, Cdkn1a (p21) rescued defects in OE regeneration in telomere dysfunctional mice. Together, these data indicate that telomere shortening impairs the regenerative capacity of the OE by impairing cell cycle progression in a p21-dependent manner. These findings could be relevant for the impairment in OE function in elderly people

Morphological Analysis of the olfactory epithelium at day 2 after Triton-X application.

<p>(A,B) Representative photographs of hematoxylin and eosin-stained sagittal sections of the OE, two days after intranasal injection of Triton-X in 6 month old (A) G3 <i>mTerc^−/−</i> and (B) <i>mTerc^+/+</i> mice. There are no significant differences between the two cohorts, both showing strong damage to 80–90% of the OE. The histograms show the percentage of the chemically damaged olfactory epithelium in <i>mTerc^+/+</i> and G3 <i>mTerc^−/−</i> mice at two days after Triton-X induced injury: (C) percentage of damaged epithelium of 0–4 cell layer thickness (P = 0.7887), (D) percentage of completely damaged epithelium of 0–2 cell layer thickness (P = 0.8208).</p

Telomere shortening does not affect homeostasis of the olfactory epithelium in aging mice.

<p>(A, B): Representative photographs of hematoxylin and eosin-stained longitudinal sections of the OE from 2–3 month old (A) <i>mTerc^+/+</i> and (B) G3 <i>mTerc^−/−</i> mice, and 10–12 month old (C) <i>mTerc^+/+</i> and (D) G3 <i>mTerc^−/−</i> mice. (E-J) Immunohistological analysis of longitudinal sections of the OE 10–12 month old (E, G, I) <i>mTerc^+/+</i> and (F, H, J) G3 <i>mTerc^−/−</i> mice: (E, F) Olfactory marker protein (OMP), (G, H) GAP43 and (I, J) proliferating cell nuclear antigen (PCNA). White arrows point to PCNA positive cells (G, H). (K) Histogram showing percentage of PCNA-positive cells in the OE of 10–12 month old <i>mTerc^+/+</i> and G3 <i>mTerc^−/−</i> mice (n = 10 mice per group, P = 0.4580).</p

Limited proliferation potential of the OE in telomere deficient mice.

<p>(A,B) Representative photographs of BrdU-stained longitudinal sections of the olfactory epithelium, 7 days after Triton-X treatment in (A) <i>mTerc^+/+</i> and (B) G3 <i>mTerc^−/−</i> mice. (C) Histogram showing BrdU positive cells in the OE of G3 <i>mTerc^+/+</i> and <i>mTerc^+/+</i> mice. Note that there is no significant difference of the ratio of BrdU positive cells v.s. negative cells between <i>mTerc^+/+</i> and G3 <i>mTerc^−/−</i> mice in injured olfactory epithelium of one cell layer thickness (P = 0.216) but there was a significant reduction of BrdU positive cells in G3 <i>mTerc^−/−</i> compared to <i>mTerc^+/+</i> mice in injured olfactory epithelium of three cell layer thickness (P = 0.008) and 5–6 cell layer thickness (P = 0.0293), n = 5 mice per group. (D) The histogram shows the percentage of the olfactory epithelium with incomplete regeneration (0–2 cell layer thickness) in 6–8 month mice of the indicated genotypes at 7 days after Triton-X induced injury. Note that <i>p21</i> deletion rescues regenerative defects in G3 <i>mTerc^−/−</i> mice. The cohorts in this experiment show an overall higher rate of tissue damage compared to the previous experiment depicted in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0027801#pone-0027801-g003" target="_blank">Figures 3</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0027801#pone-0027801-g004" target="_blank">4</a>.</p

Shortened telomeres in the olfactory epithelium of G3 <i>mTerc^−/−</i> mice.

<p>(A, B): Distribution of the mean telomere fluorescence intensity (TFI) of cells of the olfactory epithelium in 6–8 month old <i>mTerc^+/+</i> mice (A) and of G3 <i>mTerc^−/−</i> mice (B) (n = 4 mice per group). The dotted line shows the mean TFI of olfactory epithelial cells in mice of the two cohorts. Note that the olfactory epithelium of G3 <i>mTerc^−/−</i> have shorter telomeres than <i>mTerc^+/+</i> mice (P = 0.0207).</p