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Structured Abstract Authors – Ueki K, Nakagawa K, Takatsuka S, Yamamoto E, Laskin DM Objective – To assess the relationship between skeletal morphology and stress direction on the temporomandibular joint (TMJ) by a two-dimensional rigid body spring model (RBSM). Design – Lateral cephalograms were analyzed and the information was processed with afortran analysis program. Setting and Sample Population – The subjects were 149 patients (54 men and 95 women, mean age 21.8 ± 5.9 years) from Kanazawa University Hospital and the School of Dentistry, Virginia Commonwealth University. Of the 149 cases, 48 were skeletal class I, 54 were class II, and 47 were class III. The patients had no TMJ symptoms or abnormalities. Outcome Measure – The force vector on the condyle, its direction (Ph angle), the degree of the vector (Ph) and the displacement vector (u, v), and the rotational angle ( θ) of the mandibular body were calculated by RBSM. Results – The direction of the force vector (Ph angle) on the condyle was 24.83°± 4.67° in the class II group, 21.04°± 5.59° in the class I group, and 19.58 ± 7.57° in the class III group. The Ph angle of the class II group was significantly larger than those of the class I and III groups ( p < 0.05). Conclusions – This study suggests that differences in skeletal patterns induce differences in stress distribution on the TMJ; the morphology of the TMJ was also associated with stress direction and distribution on the condyle. [ABSTRACT FROM AUTHOR]

Background Netherton syndrome (NS) is a severe autosomal recessive disorder characterized by ichthyosiform erythroderma, bamboo hair and atopy. The disease is caused by mutations in the SPINK5 gene, which encodes a putative serine protease inhibitor, LEKTI (lymphoepithelial Kazal-type-related inhibitor). Previous studies have clearly shown a crucial role for LEKTI in skin barrier formation. Objectives To identify pathogenic mutations in two Japanese siblings with NS, and further to investigate the consequences of the mutations at the protein level. Methods To screen for mutations in the SPINK5 gene, all of its exons and splice junctions were amplified by polymerase chain reaction and directly sequenced. In addition, immunohistochemical staining of LEKTI, desmoglein (Dsg) 1 and elafin was performed with their specific antibodies. Results Mutation analysis resulted in the identification of compound heterozygous mutations, Q713X and R790X, in the SPINK5 gene of both patients. The former one is a novel mutation. Immunohistochemical studies in one patient demonstrated a complete absence of LEKTI and a strong expression of elafin in the patient's skin. Dsg1 was normally expressed in our patient. Conclusions In this report, we describe compound heterozygous mutations in the SPINK5 gene in two Japanese siblings with NS. The result of immunohistochemistry shows LEKTI deficiency and upregulation of elafin in the skin of one patient. Furthermore, our data indicate that degradation of Dsg1 does not always occur in NS. [ABSTRACT FROM AUTHOR]

To determine whether or not aggrecanase in synovial fluid can be used as a biochemical marker in the diagnosis of temporomandibular joint disorder (TMJD). Forty-four samples of synovial fluid were obtained from 35 patients with internal derangement or osteoarthritis and 15 control samples from 10 asymptomatic volunteers. Aggrecanase in the synovial fluid was examined by immunoblotting. The incidence of aggrecanase expression in TMJD group were significantly higher than that in the normal control group ( P < 0.05). Those with severe OA and anterior disc displacement without reduction showed significantly high expression of aggrecanase compared with other disease subgroups ( P < 0.05). These findings suggested that aggrecanase could be a potential biochemical marker for cartilage degeneration in the TMJD. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine whether or not matrix metalloproteinases (MMPs) in synovial fluid are helpful in the biochemical diagnosis of temporomandibular joint (TMJ) disorder (TMD). We examined the synovial fluid from 38 TMD patients with disc displacement and 20 volunteers by gelatin zymography and immunoblotting analysis to clarify the involvement of the joint pathology from the viewpoint of expression of MMPs. Two gelatinolytic enzymes, MMP-2 and -9, were detected in the samples. The incidences of expression, except for pro-MMP-2, in anterior disc displacement (ADD) without reduction (ADD w/o R) were significantly higher than in ADD with reduction (ADD w R) (P<0.05). Quantitative analysis showed that the degree of MMP-2 and -9 expression in ADD w/ o R were higher than in ADD w R. These data suggest that the presence or absence of disc reduction is a major turning point in the process of joint destruction, and these MMPs are useful as biochemical markers for TMD diagnosis. [ABSTRACT FROM AUTHOR]

Matrix metalloproteinase (MMP)-2 is expressed in osteoarthritic cartilage and synovial fluid and is thought to be involved in the degradation of cartilage extracellular matrix. However, MMP-2 expression and osteoarthritic changes in internal derangement of the temporomandibular joint are unknown. In the present study, we have examined the histological relationship between osteoarthritic changes on articular cartilage with or without articular disc perforation, and MMP-2 expression, in 85 mandibular condyles from cadavers. The expression and tissue immunolocalization of MMP-2 in fibrocartilages from these condyles was examined histochemically. The Mankin grade of histological criteria for specimens with disc perforation was significantly higher than that of specimens without perforation. MMP-2 immunostaining was positive in the cytoplasm of chondrocytes and in their surrounding matrix. There was a linear correlation between MMP-2-positive cell rates and Mankin grade. Our data suggest that MMP-2 plays an important role in fibrocartilage degradation in internal derangement of the temporomandibular joint. [ABSTRACT FROM AUTHOR]