Basaloid squamous cell carcinoma of the maxilla.

The study reports the first case of basaloid squamous cell carcinoma (BSCC) involving both the oral mucosa and the tuberosity area of the maxilla. The tumour showed many histological similarities to cases previously reported, though mitoses were not frequent. The immunoreactivity for cytokeratin, S-100, vimentin, Ki-67, p53, c-erbB-2 and bcl-2 was also investigated. Immunostaining for the bcl-2 protein showed a high extent of positive cells, although only a moderate staining intensity. Staining for c-erbB-2 was negative. The pathological findings and the immunoreactivity may indicate that BSCC is not as high a grade carcinoma as previously suggested. Additional studies are thus clearly needed to confirm or reject this impression.

Pulpal reactions in rat incisors to Caridex.

This study examined the in vivo effects of Caridex, a chemomechanical caries removal system, on rat pulpal tissue. Rat incisors were opened and the pulps exposed to Caridex or physiological saline and sealed with calcium hydroxide. After various time periods, teeth were extracted and examined by light microscopy. Histological evaluation revealed an almost identical response in both test and control teeth which consisted of a transient inflammatory reaction and a limited necrosis in adjacent pulp tissue. Within seven days, formation of hard tissue matrix was seen below the necrotic area and on pulpal walls. It was suggested that the high pH of Caridex may have contributed to the necrotizing effect of calcium hydroxide in adjacent pulp tissue and the formation of hard tissue matrix. Additionally, the solution is most probably bactericidal. The results suggest that the system can be used as a caries removal agent on humans without unfavourable side effects on the dental pulp.

Assessment of p53 and Ki-67 expression in snuff-induced lesions.

An immunohistochemical study of snuff-induced lesions with a monoclonal antibody (DO-7) specific to p53 mutant and wildtype antioncogene product demonstrated nuclear overexpression of the mutant protein in 45.9 nuclear profiles/mm2 epithelium (SEM 10.8; n = 15) compared with only 0.18 positively stained nuclear profiles/mm2 in the control group (SEM 0.18; n = 4). Furthermore, the biopsy material was also stained with the antibody Ki-67, which has been shown to be excellent for the estimation of the growth fraction in both normal and malignant human tissues. Ki-67 stained positive in 566.1 nuclear profiles/mm2 epithelium (SEM 85.0; n = 15) in the snuff-group compared with 20.2 nuclear profiles/mm2 (SEM 4.9; n = 4) in the control group. To the best of our knowledge, this is the first study showing overexpression of p53 protein and Ki-67 in snuff-induced lesions. The results may indicate that the p53 gene is involved in the initial events leading to subsequent malignant transformation of oral mucosa exposed to snuff. Furthermore, mutations of the p53 gene have been associated with increased cellular proliferation with greater risk of perpetuation of mutations and malignant transformation.

Evidence for a dentin-derived inhibitor of macrophage spreading.

The ability of macrophages to spread in vitro on mineralized and non-mineralized tissues extracted with guanidium hydrochloride (GuHCl) was studied in order to establish morphologic evidence for an extractable inhibitor of macrophage spreading present within dentin. Macrophages were seeded onto dentin, demineralized dentin, predentin and hyaline cartilage extracted with different concentrations of GuHCl. Macrophages were also seeded onto unextracted tissues. The results were evaluated with scanning electron microscopy after varying incubation periods. Macrophages readily attached and spread on extracted and unextracted dentin, extracted demineralized dentin, predentin, and hyaline cartilage. Cells seeded onto unextracted demineralized dentin, predentin, and hyaline cartilage attached, but showed no signs of spreading. It was concluded that an extractable inhibitor of macrophage spreading is present in the organic, non-collagenous component of dentin. This inhibitor may be responsible for the resistance of predentin and dentin to resorption.

Macrophage colonization of infected and non-infected dental tissues in vitro.

Attachment and spreading of phagocytes on a mineralized tissue surface is crucial for their proper resorptive function. In other studies, attachment and spreading have been shown to be highly dependent on the nature and composition of the surface. In the present study, peritoneal macrophages were cultured on infected and non-infected mineralized and non-mineralized dental tissues, which were examined with scanning electron microscopy at different observation periods. Although some cells had attached to non-infected predentin, only a few showed signs of spreading, even after long incubation times. This contrasted with the behavior of macrophages cultivated on enamel, mineralized dentin and infected predentin. Most of these cells showed spreading and the characteristics of active, phagocytosing cells. The reluctance of macrophages to spread on non-infected predentin was suggested to be due to the non-mineralized nature of this tissue, although an influence of endogenous resorption inhibitors cannot be excluded.

Evidence for a resorption inhibitor in dentin.

The ability of stimulated and unstimulated peritoneal macrophages to spread in vitro on different inorganic and organic components of dental tissues was studied in order to establish morphologic evidence in favor of a resorption inhibitor in dentin. Macrophages were seeded onto enamel, dentin, predentin, demineralized dentin and collagen-coated coverslips and examined with scanning electron microscopy after varying incubation periods. The cells readily attached and spread on enamel, dentin and collagen-coated coverslips. Cells attached but showed no signs of spreading when incubated on predentin or demineralized dentin. It was concluded that the resistance to resorption of predentin and dentin rests in the organic, non-collagenous component of the tissue, indicating the presence of a resorption inhibitor in dentin.

Evidence for an inhibitor of osteoclast attachment in dentinal matrix.

The ability of osteoclasts to colonize in vitro different preparations of dentin extracted with guanidinium hydrochloride (GuHCl) was studied in order to establish morphological evidence for an extractable inhibitor of osteoclast spreading within dentin. Osteoclasts were isolated from neonatal rats and seeded onto pieces of fully mineralized dentin, demineralized dentin and predentin extracted with GuHCl. Osteoclasts were also seeded onto unextracted tissues. The results were evaluated with scanning electron microscopy. Osteoclasts colonized and resorbed fully mineralized dentin, whereas clastic cells were not observed on unextracted demineralized dentin and predentin. In contrast to this, osteoclasts attached and spread on demineralized dentin and predentin extracted with GuHCl. It was concluded that the non-collagenous organic component of dentin contains an extractable inhibitor of osteoclastic attachment and spreading. It is tempting to speculate that the inhibitor may be responsible for the naturally occurring resistance of dentin to resorption.

Resorbing potential of different connective tissue types.

Pieces of dentin were implanted into five different connective tissues in rats and examined with scanning electron microscopy after observation periods of up to 2 weeks. Dentin-oclast-like cells, apparently involved in resorption of the implants, were only seen associated with periosteum and periodontal membrane. These findings indicate that the resorbing potential of connective tissues is related to their ability to induce bone formation.

Studies of the healing of bone grafts, and the incorporation of titanium implants in grafted bone: an experimental animal model.

An insufficient quality and amount of bone often necessitate the clinical use of implants together with bone transplants. The present study describes an experimental animal model for the study of implants in bone grafts. Circular defects were made bilaterally in the tibia of 36 rabbits. The defects received either autologous cortical bone (control), demineralized bone matrix (DBM), plasma-augmented DBM or were left empty (without bone graft). In all defects a titanium implant was centrally placed and anchored in the opposite cortex. Evaluation with light microscopic morphometry showed that the insertion of a threaded titanium implant centrally in a cortical defect was followed by a spontaneous healing of the defect after 6 mon. After 6 wk, all implants in cortical grafts were well integrated with a significantly higher bone-to-implant contact than in the DBM and plasma-augmented groups. After 6 mon, all experimental groups had a mean bone area within the threads ranging between 69% and 80% and a mean bone-to-implant contact between 31% and 42%. The results from the present study indicate that the model allows comparative studies on the early formation, resorption and remodelling of bone around implants after modification of implant, graft and host properties.