Apoptosis-associated markers in oral lichen planus.

Hypothesizing that loss of basal cells in oral lichen planus is due to apoptosis, we evaluated LP specimens for apoptosis-regulating proteins [positive regulators Bcl-xS, Bax, Fas/Fas-ligand, p53, and negative regulators (anti-apoptotic) Bcl-2, Bcl-xL and compared results with reactions in normal mucosa and chronically inflamed gingiva. Also, sections were evaluated with an in situ TUNEL assay that identifies apoptotic DNA fragments. Basal keratinocytes in normal buccal mucosa, nonspecific gingivitis, and LP were negative for Bcl-2 protein, but melanocytes and lymphoid cells were positive. Keratinocyte staining for Bcl-x was negative to weak in normal buccal mucosa and gingivitis, and moderate in LP. Keratinocytes (especially upper prickle cells) in all tissues stained similarly for Bax at weak to moderate levels. Also, no differences in Fas and Fas-ligand staining were evident. Prominent p53-positive staining was seen in all LP biopsies (10-100% of basal keratinocytes) but not in normal buccal mucosa and gingivitis. Few basal keratinocytes in 5/10 LP cases exhibited a positive in situ signal for DNA fragment-associated apoptosis. That the Bcl-2 family of proteins and Fas/Fas-ligand were detected in normal and diseased tissues, and were occasionally expressed differently in oral LP, supports the notion that apoptosis is a potential mechanism of keratinocyte loss, especially in LP. The pattern of p53 staining in oral LP suggests over-expression of wild-type protein; a phenomenon that would arrest the cell cycle to allow repair of damaged DNA, or trigger apoptosis. While immunohistochemical evidence for apoptosis-associated basal keratinocyte death in LP was slight, it appeared that it may be p53 protein, and possibly Bcl-x associated.

Augmentation of the atrophic mandible with a vascularized rib graft.

A patient with a 29-year history of denture wearing had her mandible augmented with a vascularized rib graft. The rib was contoured to fit the arch of the mandible and vascularized by means of the facial arteries to the intercostal vessels. The nutrient artery was not included in the vascularized bone graft. Cortical cancellous bone chips were packed around the rib to augment the buccal surface of the rib graft. Periosteal perfusion and vascularity of the transferred rib were well documented at 1 week, 1 month, and 6 months postoperatively by radionuclide scintigraphy. It is now 24 months after surgery and the patient began wearing a denture 2 months after the rib transfer. She underwent a split-thickness skin graft vestibuloplasty and floor-of-the-mouth lowering 12 months following the rib transfer with improvement in her denture-wearing capabilities, which has remained constant for 10 months. Vertical resorption of the graft at 3 months was 10 percent, at 6 months 15 percent, and it has stabilized at 25 percent.

Detection of degenerative disease of the temporomandibular joint by bone scintigraphy: concise communication.

Nine patients with facial pain were evaluated with limited bone scans. The scintigrams correlated with microscopy in all patients (eight positive, one negative), although radiographs correlated with microscopy in only five patients (four positive, one negative). The degenerative disease process in the temporomandibular joint was more extensive in the patients with radiographic and scintigraphic abnormalities than in those with scintigraphic abnormalities alone. The limited bone scan appears useful in detecting early degenerative changes in the temporomandibular joint.