Role of toll-like receptor 2 in inflammation and alveolar bone loss in experimental peri-implantitis versus periodontitis.

BACKGROUND AND OBJECTIVE: Peri-implantitis and periodontitis are different entities in immune characteristics even though they share similar features in clinical and radiologic signs. Toll-like receptor 2 (TLR-2), one of the key pathogen-recognition receptors in the innate immune system, plays an important role in the progression of periodontitis. However, the role of TLR-2 in peri-implantitis remains unclear. The objective of this study was to investigate the role of TLR-2 in inflammation and alveolar bone loss in a murine model of ligature-induced peri-implantitis and to compare it with ligature-induced periodontitis. MATERIAL AND METHODS: Smooth-surface titanium implants were placed in the alveolar bone of the left maxillary molars of wild-type (WT) and Tlr2 knockout (Tlr2-KO) mice 6 weeks after tooth extraction. Silk ligatures were applied to the left implant fixtures and the right maxillary second molars to induce peri-implantitis and periodontitis 4 weeks after implant placement. Two weeks after ligation, bone loss around the implants and maxillary second molars was analysed by micro-computed tomography (micro-CT), and inflammation around the implants and maxillary second molars was assessed at the same time point using histology and TRAP staining, respectively. Expression of mRNA for proinflammatory cytokines (interleukin-1ß [Il1ß], tumor necrosis factor-α [Tnfα]), an anti-inflammatory cytokine (interleukin-10 [Il10]) and osteoclastogenesis-related cytokines (Rankl, osteoprotegerin [Opg]) were evaluated, in gingival tissue, using real-time quantitative PCR (RT-qPCR). RESULTS: The success rate of implant osseointegration was significantly higher in Tlr2-KO mice (85.71%) compared with WT mice (53.66%) (P = .0125). Micro-CT revealed significantly decreased bone loss in Tlr2-KO mice compared with WT mice (P = .0094) in peri-implantitis. The levels of mRNA for Il1ß (P = .0055), Tnfα (P = .01) and Il10 (P = .0019) in gingiva were significantly elevated in the peri-implantitis tissues of WT mice, but not in Tlr2-KO mice, compared with controls. However, the gingival mRNA ratios of Rankl/Opg in peri-implant tissues were significantly upregulated in both WT (P = .0488) and Tlr2-KO (P = .0314) mice. Ligature-induced periodontitis exhibited similar patterns of bone loss and inflammatory cytokine profile in both groups of mice, except that the level of Il10 was elevated (P = .0114) whereas the Rankl/Opg ratio was not elevated (P = .9755) in Tlr2-KO mice compared with control mice. Histological findings showed increased numbers of TRAP-positive cells and infiltrated inflammatory cells in ligature-induced peri-implantitis in both WT (P < .01) and Tlr2-KO mice (P < .05), and the numbers of both types of cell were significantly higher in WT mice than in Tlr2-KO mice (P < .01). CONCLUSION: This study suggests that TLR-2 mediates bone loss in both peri-implantitis and periodontitis. However, different molecular features may exist in the pathogenesis of the two diseases.

Antibiotic administration alleviates the aggravating effect of orthodontic force on ligature-induced experimental periodontitis bone loss in mice.

BACKGROUND AND OBJECTIVES: It is recognized that orthodontic force (OF) has an aggravating effect on the progression of destructive periodontitis if periodontitis have not been well controlled. However, the underlying mechanism is not completely clear. This study was to investigate the effect of antibiotic administration on OF-aggravated, ligature-induced experimental periodontitis in mice. MATERIAL AND METHODS: C57BL/6 mice (male, 8 wk old) were divided into three groups (n = 8). Silk ligatures (SL) were tied around the maxillary right (group 1) or both (groups 2 and 3) first molars on day 0, removed on day 8 and systemic antibiotics was administered through drinking water (group 3) since day 8. OF was applied on the maxillary right first molars since day 13 (groups 2 and 3). All mice were killed on day 20. RESULTS: Total oral bacteria load was significantly higher in group 2 when compared to group 1 on day 20, whereas such count was greatly reduced in group 3 when antibiotics were administered. Periodontal bone loss was significantly increased on SL side vs. control side in group 1. Periodontal bone loss was significantly increased on OF + SL side vs. SL side in group 2 (p < 0.05) but not in group 3 when systemic antibiotics were administered. Gingival mRNA and protein expressions of receptor activator of nuclear factor kappa-B ligand/osteoprotegerin were significantly increased on OF + SL side vs. SL side in group 2 (p < 0.01) but not in group 3. However, comparable levels of tartrate-resistant acid phosphatase-positive cell formation within periodontal space and tooth movement were observed on OF + SL side in groups 2 and 3. CONCLUSION: Our results suggest that reduction of oral bacterial load by antibiotic administration alleviate orthodontic force-aggravated periodontitis bone loss.

Correlation of mandibular impacted tooth and bone morphology determined by cone beam computed topography on a premise of third molar operation.

PURPOSE: To determine the width and morphology of the mandible in the impacted third molar region, and to identify the location of the mandibular canal prior to planning impacted third molar operations. METHODS: Cone beam computed tomography (CBCT) data of 87 mandibular third molars from 62 Japanese patients were analyzed in this study. The width of the lingual cortical bone and apex-canal distance were measured from cross-sectional images in which the cortical bone was thinnest at the lingual side in the third molar region. Images were used for measuring the space (distance between the inner border of the lingual cortical bone and outer surface of the third molar root), apex-canal distance (distance from the root of the third molar tooth to the superior border of the inferior alveolar canal) and the cortical bone (width between the inner and outer borders of the lingual cortical bone). RESULTS: The means of the space, apex-canal distance and lingual cortical width were 0.31, 1.99, and 0.68 mm, respectively. Impacted third molar teeth (types A-C) were observed at the following frequencies: type A (angular) 37 %; type B (horizontal), 42 %; type C (vertical), 21 %. The morphology of the mandible at the third molar region (types D-F) was observed as: type D (round), 49 %; type E (lingual extended), 18 %; and type F (lingual concave), 32 %. CONCLUSIONS: The width and morphology of the mandible with impacted teeth and the location of the mandibular canal at the third molar region could be clearly determined using cross-sectional CBCT images.

Detection of periodontal pathogens in newborns and children with mixed dentition.

We report the age-related prevalence of red complex periodontal pathogens, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, along with four strains of orange complex pathogens. The bacteria present in samples isolated from tongue, cheek, and subgingival sulcus in edentulous newborns and children with mixed dentition were monitored by polymerase chain reaction (PCR). P. gingivalis was not detected in any site of any subject in the two groups tested. However, T. denticola was not only found in the 6-13 years age group, but also in edentulous newborns at a relatively high prevalence, indicating non-dentition-related colonization by T. denticola. Campylobacter rectus, Prevotella intermedia, T. forsythia, Eikenella corrodens, and Parvimonas micra were found in the oral cavity of most subjects belonging to the 6-13 years age group compared to newborns. This suggested a pronounced association between these colonizing bacteria and the presence of teeth. There was also a strong relation between T. denticola and T. forsythia for their prevalence in the subgingival sulcus of the 6-13 years age group (p < 0.0001), but not in the other sites tested, suggesting that the colonization of dentition-related T. forsythia may be associated with the increased prevalence of non-dentition-related T. denticola in the subgingival sulcus. Overall, these results suggest that dentition is a key determinant of bacterial colonization, especially orange complex bacteria and the red complex bacterium T. forsythia.

DC-STAMP Is an Osteoclast Fusogen Engaged in Periodontal Bone Resorption.

Dendritic cell-specific transmembrane protein (DC-STAMP) plays a key role in the induction of osteoclast (OC) cell fusion, as well as DC-mediated immune regulation. While DC-STAMP gene expression is upregulated in the gingival tissue with periodontitis, its pathophysiological roles in periodontitis remain unclear. To evaluate the effects of DC-STAMP in periodontitis, anti-DC-STAMP-monoclonal antibody (mAb) was tested in a mouse model of ligature-induced periodontitis ( n = 6-7/group) where Pasteurella pneumotropica ( Pp)-reactive immune response activated T cells to produce receptor activator of nuclear factor kappa-B ligand (RANKL), which, in turn, promotes the periodontal bone loss via upregulation of osteoclastogenesis. DC-STAMP was expressed on the cell surface of mature multinuclear OCs, as well as immature mononuclear OCs, in primary cultures of RANKL-stimulated bone marrow cells. Anti-DC-STAMP-mAb suppressed the emergence of large, but not small, multinuclear OCs, suggesting that DC-STAMP is engaged in the late stage of cell fusion. Anti-DC-STAMP-mAb also inhibited pit formation caused by RANKL-stimulated bone marrow cells. Attachment of ligature to a second maxillary molar induced DC-STAMP messenger RNA and protein, along with elevated tartrate-resistant acid phosphatase-positive (TRAP+) OCs and alveolar bone loss. As we expected, systemic administration of anti-DC-STAMP-mAb downregulated the ligature-induced alveolar bone loss. Importantly, local injection of anti-DC-STAMP-mAb also suppressed alveolar bone loss and reduced the total number of multinucleated TRAP+ cells in mice that received ligature attachment. Attachment of ligature induced significantly elevated tumor necrosis factor-α, interleukin-1ß, and RANKL in the gingival tissue compared with the control site without ligature ( P < 0.05), which was unaffected by local injection with either anti-DC-STAMP-mAb or control-mAb. Neither in vivo anti- Pp IgG antibody nor in vitro anti- Pp T-cell response and resultant production of RANKL was affected by anti-DC-STAMP-mAb. This study illustrated the roles of DC-STAMP in promoting local OC cell fusion without affecting adaptive immune responses to oral bacteria. Therefore, it is plausible that a novel therapeutic regimen targeting DC-STAMP could suppress periodontal bone loss.

Origin, splicing, and expression of rodent amelogenin exon 8.

Amelogenin RNA transcripts undergo extensive alternative splicing, and MMP-20 processes the isoforms following their secretion. Since amelogenins have been ascribed cell-signaling activities, we asked if a lack of proteolytic processing by MMP-20 affects amelogenin signaling and consequently alters amelogenin splice site selection. RT-PCR analyses of amelogenin mRNA between control and Mmp20(-/-)mice revealed no differences in the splicing pattern. We characterized 3 previously unidentified amelogenin alternatively spliced transcripts and demonstrated that exon-8-encoded amelogenin isoforms are processed by MMP-20. Transcripts with exon 8 were expressed approximately five-fold less than those with exon 7. Analyses of the mouse and rat amelogenin gene structures confirmed that exon 8 arose in a duplication of exons 4 through 5, with translocation of the copy downstream of exon 7. No downstream genomic sequences homologous to exons 4-5 were present in the bovine or human amelogenin genes, suggesting that this translocation occurred only in rodents.

Bone repair of rabbit mandibular transsection using rhBMP-2 and atelocollagen gel.

This experimental was carried out using 12 rabbits. A rabbit experimental mandibular transsection was reconstructed with 10mug of rhBMP-2 and 1% atelocollagen gel. The transsection gap was fixed with a titanium plate and screws, and covered with poly (lactic-co-glycolic acid) co-polymer (PLGA) membrane. Histopathological examination of 1-week specimens revealed that many spindle cells had proliferated and invaded blood clots, and a small amount of immature trabecular bone was formed in the transsection gap. In 2 and 3-week specimens, bone formation was gradually increased in the fibro-vascular tissues of the site. These histological findings were also observed in the control group specimens, but the bone formation was slightly less than in the experimental group. The results suggest the effectiveness of atelocollagen gel as a carrier of rhBMP-2 and PLGA as a covering membrane in this rabbit mandibular transsection reconstruction model.

The biological properties of a novel ethyl methacrylate resin.

A novel ethyl methacrylate (EMA) resin was developed to overcome the tissue, organ and systemic damage associated with the residual monomer of conventional methyl methacrylate (MMA) resin bone cement. EMA resin is a chemical/ photopolymerizable material and is easy to handle during clinical procedures. The biocompatibility of EMA was evaluated in accordance with ISO10993-6. No inflammatory response was observed 1 and 9 weeks after implantation in the dorsal subcutaneous tissue of ddY mice. EMA resin also demonstrated better biocompatibility when compared with conventional bone cements. Poly-L-lactic acid (PLLA) was used as a carrier for bone morphogenetic protein (BMP) and added to the EMA slurry. The EMA-PLLA composite membrane was sticky and BMP readily adhered to its surface. The EMA-PLLA-BMP composite membrane induced new bone formation, the new bone growing in the shape of the EMA in the thigh muscle pouch of ddY mice. This novel EMA resin has many potential clinical applications.

New antibody immobilization method via functional liposome layer for specific protein assays.

A specific protein assay system based on functional liposome-modified gold electrodes has been demonstrated. To fabricate such assay system, a liposome layer was initially grown on top of a gold layer. The liposome layer contained two kinds of functional molecules: biotin molecules for the binding sites of streptavidin and N-(10,12-pentacosadiynoic)-acetylferrocene molecules for the facile redox probe in electrochemical detections. Then, streptavidin was attached on the functional liposme-modified layer using the interaction of streptavidin-sbiotin complex. On the streptavidin-attached surface, antibody molecules, anti-human serum albumin antibodies could be immobilized without any secondary antibodies. AFM imaging of the streptavidin-attached liposome surface revealed a uniform distribution of closely packed streptavidin molecules. In situ quartz-crystal microbalance and electrochemical measurements demonstrated that the wanted antibody-antigen reactions should occur with high specificity and selectivity. Our specific antibody assay system, based on a functional liposome modified electrode, can be developed further to yield sophisticated structures for numerous protein chips and immunoassay sensors.

Potassium channel-blockers as therapeutic agents to interfere with bone resorption of periodontal disease.

UNLABELLED: Inflammatory lesions of periodontal disease contain all the cellular components, including abundant activated/memory T- and B-cells, necessary to control immunological interactive networks and to accelerate bone resorption by RANKL-dependent and -independent mechanisms. Blockade of RANKL function has been shown to ameliorate periodontal bone resorption and other osteopenic disorders without affecting inflammation. Development of therapies aimed at decreasing the expression of RANKL and pro-inflammatory cytokines by T-cells constitutes a promising strategy to ameliorate not only bone resorption, but also inflammation. Several reports have demonstrated that the potassium channels Kv1.3 and IKCa1, through the use of selective blockers, play important roles in T-cell-mediated events, including T-cell proliferation and the production of pro-inflammatory cytokines. More recently, a potassium channel-blocker for Kv1.3 has been shown to down-regulate bone resorption by decreasing the ratio of RANKL-to-OPG expression by memory-activated T-cells. In this article, we first summarize the mechanisms by which chronically activated/memory T-cells, in concert with B-cells and macrophages, trigger inflammatory bone resorption. Then, we describe the main structural and functional characteristics of potassium channels Kv1.3 and IKCa1 in some of the cells implicated in periodontal disease progression. Finally, this review elucidates some recent advances in the use of potassium channel-blockers of Kv1.3 and IKCa1 to ameliorate the clinical signs or side-effects of several immunological disorders and to decrease inflammatory bone resorption in periodontal disease. ABBREVIATIONS: AICD, activation-induced cell death; APC, antigen-presenting cells; B(K), large conductance; CRAC, calcium release-activated calcium channels; DC, dendritic cell; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IFN-gamma, interferon-gamma; IP(3), inositol (1,4,5)-triphosphate; (K)ir, inward rectifier; JNK, c-Jun N-terminal kinase; I(K), intermediate conductance; LPS, lipopolysaccharide; L, ligand; MCSF, macrophage colony-stimulating factor; MHC, major histocompatibility complex; NFAT, nuclear factor of activated T-cells; RANK, receptor activator of nuclear factor-kappaB; T(CM), central memory T-cells; T(EM), effector memory T-cells; TNF, tumor necrosis factor; TRAIL, TNF-related apoptosis-inducing ligand; OPG, osteoprotegerin; Omp29, 29-kDa outer membrane protein; PKC, protein kinase C; PLC, phospholipase C; RT-PCR, reverse-transcriptase polymerase chain-reaction; S(K), small conductance; TCR, T-cell receptor; and (K)v, voltage-gated.

Bovine tooth-derived bone morphogenetic protein.

Eight groups of dental tissues were mechanically dissected from the mandibles of one-year-old steers; they were then defatted and decalcified in HCl. The noncollagenous proteins were extracted with various solvents from collections of tissue and bio-assayed for osteo-inductive activity. Collectively, the hard tissue (dentin, enamel, and cementum) noncollagenous proteins were fractionated by molecular sieve chromatography, hydroxyapatite affinity chromatography, and ion exchange chromatography. Osteo-inductive activity of each protein fraction was determined by implantation in the quadriceps muscle pouch of mice. The quantity of bone was measured by computerized image analysis. From 71% to 83% of 41 implants of dental hard tissues induced bone formation. The quantity of bone was greater from unerupted than from erupted teeth. Dental soft tissues that had no osteo-inductive activity were rich in a 14-kDa protein, presumably matrix gamma-carboxyglutamic acid-rich proteins. Proteins with Mr of from 15 to 28 kDa were associated with osteo-inductive activity. Components with Mr greater than 28 kDa had no activity. These observations suggest that bovine teeth have a selection of osteo-inductive proteins that is comparable in range of MW to bovine bone morphogenetic protein.

Changes in collagen types during the healing of rabbit tooth extraction wounds.

Three alpha chains of type V collagen--alpha 1 (V), alpha 2 (V), and alpha 3 (V)--were initially demonstrated together with the expected collagen types I and III in the pepsin-soluble fraction of both normal mandibular bone and tooth extraction wound tissues of rabbits, as analyzed by sodium dodecyl sulfate-gel electrophoresis. The total collagen content of each extraction wound, as determined by the hydroxyproline assay, was observed to increase continuously from day 5 through day 17 and then leveled off or decreased. The ratio of type V to type I collagen was significantly higher in the initial stage of wound healing and decreased sharply down to the level of mandibular bone by day 5. The ratio of type III to type I collagen in the pepsin-soluble fraction increased and reached a maximum on day 5, whereas it was maximal on day 7 in the cyanogen bromide-soluble fraction, and thereafter decreased gradually in both fractions. The ratio for the pepsin-soluble fraction was, however, significantly higher than that for the cyanogen bromide-soluble fraction in the early stage of wound healing.

Cytokine profiles of T-lymphocytes from gingival tissues with pathological pocketing.

Periodontal disease is an infection in which destruction occurs at sites remote from the infection, resulting in pathological pocketing. Intervening between the infection and the destruction is a dense mononuclear inflammatory infiltrate. It has been suggested that this infiltrate might have characteristics and the destructive potential of Th1-type T lymphocytes. To ascertain the nature of the infiltrates we investigated the expression of mRNA for IL-2, IL-5, and IFN-gamma by gingival mononuclear cells (GMC) from healthy (n = 8) or adult periodontitis (AP) patients (n = 25) by using cytokine-specific reverse-transcription/polymerase-chain-reaction (RT-PCR). GMC, as obtained from patients' tissues, expressed IL-2, IFN-gamma, or IL-5 mRNA. Significantly higher proportions of GMC from AP patients expressed IL-2 and IFN-gamma mRNA than did those from healthy subjects. IFN-gamma was the most consistent cytokine message detected. In other experiments, gingival T-lymphocytes (n = 12) and CD4+ and CD8+ gingival T-lymphocytes (n = 16) were isolated from gingival tissues removed surgically from AP patients. AP gingival T-lymphocytes expressed mRNA for IL-2, IFN-gamma, or IL-6 prior to stimulation. After stimulation with Con A, the cells significantly up-regulated IL-5 and IL-6 message expression. Both CD4+ and CD8+ gingival T-lymphocytes expressed IFN-gamma, IL-5, and some IL-2. This cumulative cytokine profile observed in these experiments is consistent with the predominance of Th1-type cells in pathological tissues and with Th2-type cells, which can also be present, being up-regulated under appropriate stimulation. Importantly, CD4+ and CD8+ lymphocytes were shown to express T1- and T2-type cytokine message, emphasizing the potential for CD8+ T-lymphocytes to participate in periodontal disease pathology.

A new sensitive method for determining endotoxin in whole blood.

We developed a microplate method for determining endotoxin in whole blood with Endospecy, an endotoxin-specific chromogenic limulus test reagent. The factors in blood that would interfere with the test were successfully removed by exposing samples to 0.66 mol/l HNO3 containing 0.25% Triton X-100. Recoveries of various endotoxins spiked into whole blood of humans and experimental animals were almost complete, and were not enhanced by sample dilution. Normal endotoxin concentration in human whole blood was less than 10 pg/ml in reference to Escherichia coli 0111:B4 endotoxin. Measurements on paired whole blood and platelet-rich plasma (PRP) samples from 50 normal and 132 diseased subjects showed a good correlation (r = 0.901, P less than 0.01). This microplate whole blood method has advantages over the conventional PRP method in that it requires less time, less amount of sample and limulus reagent, and less risk of contamination during the procedure.

High conversion in asymmetric hydrolysis during permeation through enzyme-multilayered porous hollow-fiber membranes.

We describe a novel porous hollow-fiber support for immobilizing aminoacylase in multilayers. Epoxy-group-containing polymer chains were grafted onto a porous hollow-fiber membrane by radiation-induced graft polymerization of glycidyl methacrylate, and subsequently a diethylamino group as an anion-exchange group was introduced into the graft chain. Aminoacylase was adsorbed in multilayers by allowing the amioacylase buffer solution to permeate through the pores across the hollow fiber; the graft chains provided three-dimensional space for the enzymes because of their electrostatic repulsion. The adsorbed enzyme at a degree of multilayer binding of 15 was cross-linked with glutaraldehyde to prevent leakage. An acetyl-DL-methionine solution was allowed to permeate through the pores surrounded by the aminoacylase-immobilized graft chain. Production of L-methionine was observed at a 4.1 mol/h per L of the fiber for a space velocity of 200 h(-1), defined as the flow rate of the effluent penetrating the outside surface of the hollow fiber divided by the membrane volume including the lumen.

Immunohistochemical localization of collagenase inhibitor in bovine dental pulp, pulp cells in monolayer culture, and in some oral connective tissues.

The development of an antiserum, monospecific to the collagenase inhibitor, from bovine dental pulps permitted localization of immunoreactive inhibitor protein, by means of both immunofluorescence and immunoperoxidase-staining techniques in sections of bovine dental pulps. The immunoreactive inhibitor protein in bovine dental pulps is present both in cells and extracellular matrices. When cultured in Eagle minimal essential medium, coronal pulps from bovine-unerupted teeth were shown, by assay of the medium, to produce only about 1/10 of the amount of inhibitor produced by the root pulps. When compared by immunohistochemical observation, however, essentially no differences in fluorescent activity was found between coronal and root pulps. Specific cytoplasmic staining was seen both in explanted root-pulp tissues and in immature fibroblast-like pulp cells from monolayer cell cultures of bovine root pulps, which indicate that the pulp cells are responsible for inhibitor production. Sections of dental follicle and gingiva from the same animal, showed a distribution of immunoreactive inhibitor protein similar to that in dental pulps.

Epidemiological study of oral leukoplakia based on mass screening for oral mucosal diseases in a selected Japanese population.

The purpose of this study was 1) to show the epidemiological status of oral leukoplakia in a selected population of 3131 Japanese (504 women, 2627 men, aged 18-63 yr, mean age 35.9 yr), and 2) to estimate of the validity of the diagnosis of oral leukoplakia by general practitioners. Seventy-seven individuals were detected as having leukoplakia, a prevalence of 2.5%; 2.7% and 1.0% for men and women, respectively, a difference that is statistically significant (P less than 0.001). The percentage of smokers was 75.3% for patients with leukoplakia and 47.8% for individuals detected as not having leukoplakia, a difference which is statistically significant (P less than 0.001). Of 77 leukoplakia patients, 37 cases (48.1%) received a clinically confirmed diagnosis and 27 patients were diagnosed in further examination as having leukoplakia. These results can also be expressed by a positive predictive value of 0.73 and a false positive ratio of 0.27 for the diagnosis of leukoplakia in the primary mass screening by general practitioners. The results of this study suggest that in order to carry out an efficient oral health program in Japan, the objects for mass screening for leukoplakia might be better limited to men over 30 and women over 40 yr of age.

Prevalence study of oral mucosal lesions in a selected Cambodian population.

The aim of this study was to investigate the epidemiology of oral mucosal lesions in a selected Cambodian population to obtain pilot data useful in planning an oral health data base for the country. Due to unstable conditions in Cambodia, the validity of population data related to present census information is highly questionable. Therefore, prior to this investigation a census registration was carried out using local health workers as registrars in nine villages of a commune. In the period July 4-31, 1991, a total of 1319 individuals (953 women, 366 men, 15-99 yr) were examined by one oral surgeon in the nine villages of Kok Trop Commune, Kandal Stung District, southwest of the capital Phnom Penh. Clinical diagnoses were based on WHO criteria. Information on smoking habits, betel nut chewing habits, and alcohol use was collected by 4 Khmer dental personnel. In total, 71 lesions were recorded in 64 (4.9%) individuals. Leukoplakia was found in 1.1%, lichen lesions in 1.8%, candidosis in 1.4%, submucous fibrosis in 0.2%, cancer in 0.1% and other diagnoses in 0.8%. The prevalence of leukoplakia was 2.2% and 0.6% among men and women respectively, a statistically significant difference (P < 0.05). There were significantly more smokers (P < 0.01) among subjects with leukoplakia (64.3%) than among those without this lesion (28.6%). All subjects with lichen lesions were women. The age-adjusted relative risk for developing lichen among betel nut chewers as compared to non-chewers was 3.3.(ABSTRACT TRUNCATED AT 250 WORDS)

A clinicopathological study of ameloblastomas.

72 cases of ameloblastoma were obtained from the files of the Department of Pathology, School of Dentistry, Aichi-Gakuin University for the years January 1970 through December 1983. The cases were analyzed with respect to sex, age, duration, site histopathology, and treatment. Of 72 patients, 63 had no previous therapy, while 9 received their initial treatment elsewhere. There were 38 males and 34 females, a ratio of 1.2: 1. At the time of diagnosis, the ages of all patients ranged from 11 to 71 years, with an average of 36.6 years. About 65% of patients were in the 2nd, 3rd, and 4th decades of life. The duration of symptoms varied from 2 days to 5 years, with an average of 12.6 months. 69 cases occurred in the mandible, with the molar-ramus region being the most frequent site of involvement. Only 3 were found in the maxilla. The left side of the mandible was affected 1.6 times more frequently than the right. Histopathologically, 44 cases were of the plexiform type, 15 the follicular, 10 the acanthomatous, and 2 the basal cell type. Only 1 case was of the granular cell type. Most of the findings in the present study agreed with previous available data from the literature on ameloblastomas.

Healing after removal of benign cysts and tumors of the jaws. A radiologic appraisal.

A retrospective review of the radiographic findings after removal of benign jaw cysts (n = 31) and ameloblastomas (n = 24) was carried out. The radiographic features of the site margins and interior contents were classified into four categories. In most patients radiographic changes were detected between 1 and 4 months after removal of the lesion, and complete bone healing was found 4 months or more after surgery. Radiographic changes included "spiculed" or "trabecular" contents within the interior of the surgical site. The fourth month was found to be the optimum time for follow-up radiographic examination for the early detection of residual lesions. In nine (53%) of the patients who had ameloblastoma, recurrent lesions were noted within or at the periphery of the original surgical sites 6 to 10 years after the initial tumor removal.