The maxillary blood supply is essential for preserving the vitality of the affected maxillary region, integration of the grafting material, and wound healing such as following sinus floor elevation. Although it is well established that edentulous maxillae demonstrate a decreasing vascularity as bone resorption progresses, the vascular conditions relevant to sinus floor elevation procedures have not been investigated yet. This study deals with maxillary arteries relevant to sinus floor elevation surgery and examines the vascularization of the lateral maxilla after tooth loss. The vessels of the lateral maxilla of 18 maxillary specimens (10 male, 8 female, mean age 67 years) were prepared anatomically and the local main arteries, the number of macroscopically discernible branches and anastomoses, their calibers, and the distance between the caudal main branches and the alveolar ridge recorded. The lateral maxilla is supplied by branches of the posterior superior alveolar artery (PSAA) and the infraorbital artery (IOA) that form an anastomosis in the bony lateral antral wall, which also supplies the Schneiderian membrane. This intraosseous anastomosis was found in all of the specimens. Eight of 18 also showed an extraosseous anastomosis between PSAA and IOA, vestibular to the antral wall, giving off an average of 3 branches cranially and 5 branches caudally. The two anastomoses form a double arterial arcade to supply the lateral antral wall and, partly, the alveolar process. The PSAA had a mean caliber of 1.6 mm and exhibited an average of 2 endosseous and 1 extraosseous branches. The IOA had a mean diameter of 1.6 mm and showed an average of 1 endosseous and 3 extraosseous branches. The mean distance between the intraosseous anastomosis and the alveolar ridge was 19 mm in 2 defined measuring sites. Its mean length was 44.6 mm. The epiperiosteal vestibular anastomosis was situated further cranially at a mean distance of 23 to 26 mm from the alveolar ridge and had a mean length of 46 mm. The rather large caliber of the vessels supplying the lateral antral wall seems to be crucial to the fact that the periosteal blood supply is maintained even in severe maxillary atrophy and after complete disappearance of the centro-medullary vessels.

1. Denervated fast extensor digitorum longus (EDL) muscles of adult rats were stimulated electrically for up to 4 months with a 'slow' pattern resembling the activity in soleus (Sol) motor units and examined with antibodies against myosin heavy chains (MHCs). 2. The normal EDL contained, on average, 45% type IIB, 29% type IIX, 23% type IIA and 3% type I fibres. All type IIB and almost all type IIX fibres disappeared during the first 3 weeks of stimulation. They were replaced by type IIA and type I fibres, whose percentages increased to about 75 and 15, respectively. Type IIA fibres remained at 75% for nearly 2 months and were then gradually replaced by type I fibres during the next 2 months. The transformation occurred sequentially in the order II BÏII X II A I, the first step (II BÏII X II A) occurring after a short delay (2 weeks) and the last step (II A I in originally IIB or IIX fibres) after a long delay (> 2 months). During the transformation coexpression of MHCs occurred. 3. It appears that the transformation to type I fibres occurred in pre-existing type II fibres since no signs of fibre damage or regeneration were observed. 4. Normal EDL was also stimulated through an intact nerve with the same pattern for up to 37 days. The effects on fibre type distributions were identical to those observed in the denervated EDL. The result indicated that the Sol-like pattern of evoked muscle activity, rather than nerve-derived trophic influences or denervation per se, was primarily responsible for the fast to slow transformation.

No abstract

For prevention of DAIH the distal venous graft diameter is not important, while the local compliance of an autologous vein is a predictive factor for DAIH formation and thus long-term patency.

Bronchial wall thickness on thin-section CT scans should be evaluated with window centers between -250 and -700 HU and with window widths greater than 1,000 HU. Other than window settings, notably window widths less than 1,000 HU, can lead to substantial artificial thickening of bronchial walls.