Evaluation of diffusion parameters and T2 values of the masseter muscle during jaw opening, clenching, and rest.

BACKGROUND: Diffusion-weighted imaging (DWI) and diffusion-tensor imaging (DTI) can be used to evaluate changes that accompany skeletal muscle contraction. PURPOSE: To investigate whether jaw opening or closure affect the diffusion parameters of the masseter muscles (MMs). MATERIAL AND METHODS: Eleven healthy volunteers were evaluated. Diffusion-tensor images were acquired to obtain the primary (λ(1)), secondary (λ(2)), and tertiary eigenvalues (λ(3)). We estimated these parameters at three different locations: at the level of the mandibular notch for the superior site, the level of the mandibular foramen for the middle site, and the root apex of the mandibular molars for the inferior site. RESULTS: Both λ(2) and λ(3) during jaw opening were significantly lower than that at rest at the superior (P = 0.006, P < 0.0001, respectively) and middle site (P = 0.004, P = 0.0001, respectively); however, the change in λ(1) was not significant. At the lower site, no parameter was significantly different at rest and during jaw opening. There was no significant difference in T2 between at rest (40.3 ± 4.4 ms) and during jaw opening (39.2 ± 2.7 ms; P = 0.12). The changes induced by jaw closure were marked at the inferior site. In the middle and inferior sites, the three eigenvalues were increased by jaw closure, and the changes in λ(1) (P = 0.0145, P = 0.0107, respectively) and λ(2) (P = 0.0003, P = 0.0001) were significant (especially λ(2)). CONCLUSION: The eigenvalues for diffusion of the MM were sensitive to jaw position. The recruitment of muscle fibers, specific to jaw position, reflects the differences in changes in muscle diffusion parameters.

Multiple congenitally missing teeth treated with autotransplantation and orthodontics.

Treatment of children with several congenitally missing teeth is challenging, because growth and development of the oral structures must be considered. The treatment options include retaining the deciduous teeth and postponing treatment until later or extracting the deciduous teeth and doing one of the following: allowing the space to close spontaneously, closing the space orthodontically, or in patients whose growth is finished, using a prosthetic or implant replacement. One other viable option, if donor teeth are available, is autotransplantation. The treatment plan for patients with missing teeth should be based on a comprehensive evaluation of the patient's age, occlusion, and space requirements as well as on the size and shape of the adjacent teeth. This case report presents the management of a patient in the early mixed dentition with multiple missing teeth. The treatment consisted of a combination of autotransplantation of the maxillary right first premolar to the mandibular right first premolar region and orthodontic treatment with a 5-year follow-up after autotransplantation.

Molecular imaging in masseter muscle observed by muscle function magnetic resonance imaging and 31 P-magnetic resonance spectroscopy in patients with a jaw deformity.

BACKGROUND: Skeletal mandibular protrusion would influence to the muscle fatigue of the masticatory muscles. Establishing a diagnostic procedures combining physiological and biochemical information is necessary for quantitative evaluation of masticatory muscle fatigue. OBJECTIVE: The transverse relaxation time (T2 time) of muscle functional magnetic resonance imaging (mfMRI), and 31 P-magnetic resonance spectroscopy (MRS) were used to investigate the reliability as parameters for measuring the masseter muscle in patients with skeletal mandibular prognathism. METHOD: The subjects were 19 patients diagnosed as skeletal mandibular protrusions and 19 healthy subjects as a control group. Transverse relaxation time (T2 value) determined by mfMRI along with creatine phosphate (PCr) and inorganic phosphorus (Pi) determined by 31 P-MRS before, during, and after clenching were used for molecular imaging of muscle fatigue. RESULTS: The average T2 value of the patient group was significantly higher than that of the healthy control group at rest. Furthermore, the average T2 value transiently increased in both groups during experimental clenching. The PCr and Pi showed a tendency toward a transient decrease and increases, respectively. The pH in the masseter muscle showed a transient decrease in both groups prior to and following experimental clenching. The pH in the masseter muscle of the patient group was significantly lower than that in the healthy control group at rest and recovery. CONCLUSION: We showed mfMRI and 31 P-MRS are useful for evaluating masseter fatigue during clenching, and the masseter muscle in the prognathic patients showed more severe fatigue than the healthy controls.

Assessment of the sequential change of the masseter muscle by clenching: a quantitative analysis of T1, T2, and the signal intensity of the balanced steady-state free precession.

BACKGROUND: The persistent muscle contractions during clenching are thought to cause some temporomandibular disorders. However, no report has so far evaluated the effect of clenching on the masticatory muscles by magnetic resonance imaging (MRI). PURPOSE: To investigate the effect of clenching with maximum voluntary contraction on the T(1), T(2), and signal intensity (SI) of the balanced fast field-echo (b FFE) of the masseter muscle. MATERIAL AND METHODS: A total of 11 volunteers participated. Multi-echo spin-echo echo-planar imaging was used for T(2) measurements, and multi-shot Look-Locker sequence for T(1) measurements. The Look-Locker sequence has been used for fast T(1) mapping and this method has been applied for the imaging of various tissues. In addition, the b FFE was used due to the high temporal resolution. These three sequences lasted for 10 min and the participants were instructed to clench from 60 s to 80 s after the start of the data acquisition. T(2), T(1), and SI were normalized compared to pre-clenching values. RESULTS: T(2) decreased by clenching, which reflected a decrease of tissue perfusion due to the mechanical pressure. It increased rapidly after the clenching (peak value, 1.11+/-0.03; peak time, 16.8+/-7.6 s after the clenching), which corresponded to the reactive hyperemia and later, it gradually returned to the initial values (half period, 2.22+/-0.84 min). The change in the SI of the b FFE was triphasic and similar to that of T(2) clenching. T(1) increased after the cessation of the clenching and later gradually decreased during the recovery periods. However, the change of T(1) was quite different from that of T(2), with a lower peak value (1.04+/-0.02), a later peak time (36.0+/-28.0 s), and a longer half period (4.76+/-3.40 min) (P<0.0001, 0.0066, 0.02, respectively). CONCLUSION: The change in T(2) was triphasic and we considered that it predominantly reflected the tissue perfusion.

Effect of clenching on T2 and diffusion parameters of the masseter muscle.

BACKGROUND: Persistent muscle contractions during clenching are considered to be one reason for temporomandibular disorders. However, no report has evaluated the effect of clenching on the masticatory muscles, as measured by magnetic resonance imaging (MRI). PURPOSE: To investigate whether clenching has an effect on either T(2) or the coefficients for diffusion of the masseter muscles (MM), and to evaluate the effect of the distribution of bite force on such indices. MATERIAL AND METHODS: Twenty-three subjects were examined. Bite force was measured by a pressure-sensitive sheet, and the force of the right and the left sides was calculated. MRI was used to evaluate T(2), the apparent diffusion coefficient (ADC), and the primary (lambda(1)), secondary (lambda(2)), and tertiary eigenvalues (lambda(3)). These indices on the stronger side of the bite force were compared to those on the weaker side. Thereafter, the indices were compared between at rest and during clenching. RESULTS: There was no significant difference in any of the indices (T(2), ADC, lambda(1), lambda(2), and lambda(3)) between the side of stronger bite force and the side with weaker. T(2) increased by clenching, and the difference was significant in the side with stronger bite force (P = 0.006). ADC, lambda(1), lambda(2), and lambda(3) increased significantly by clenching (P <0.01, P <0.01, P <0.01, and P <0.01, respectively) on both sides. The percentage of change of lambda(2) by clenching was 26.2+/-15.7% on the stronger side and 26.9+/-18.6% on the weaker side, which was significantly greater than either that of lambda(1) or lambda(3). CONCLUSION: The coefficients for diffusion of the MM were sensitive to change by clenching, and lambda(2) was the most sensitive. Moreover, the relative distribution of the bite forces had no effect on any of the indices.

Effect of exposure parameters and gutta-percha cone size on fracture-like artifacts in endodontically treated teeth on cone-beam computed tomography images.

OBJECTIVES: To ascertain the effects of exposure parameters (tube current and tube voltage) and the gutta-percha cone (GPC) size on root fracture-like artifacts obtained with cone-beam computed tomography (CBCT). METHODS: Fracture-like artifacts appearing on CBCT images of nine extracted human mandibular premolars filled with GPCs of size #50 or #80 were analyzed using six exposure factors: two tube voltages (80 kV and 110 kV); and three tube currents (4 mA, 7 mA, and 10 mA). On axial images, the gray value (GV) was recorded at three points: the mesiobuccal portion (MBP) as the sound dentin, the mesial portion (MP) as the artifact line, and the water area (WA). The rate of decrease in the GV (RDGV) of the artifact line was calculated using the formula: RDGV (%) = (GV of MBP - GV of MP) × 100/(GV of MBP - GV of WA). RESULTS: Comparison of the #80 group and the #50 group with equal tube voltages and tube currents shows that artifact lines in the #80 group were more obvious than those in the #50 group. The artifact lines with 80 kV were markedly more visible than those with 110 kV for each tube current and GPC size. Tube current changes did not affect the artifact line for any tube voltage or GPC size. CONCLUSIONS: For the reduction of artifacts, we recommend selection of higher tube voltages and lower tube currents when taking CBCT images of teeth with each GPC size.

Assessment of the relationship between impacted mandibular third molars and inferior alveolar nerve with dental 3-dimensional computed tomography.

PURPOSE: The purpose of this study was to assess the capacity of dental 3-dimensional computed tomography (3D-CT; limited cone-beam CT) to predict the exposure and injury of the inferior alveolar nerve (IAN) after mandibular third molar extractions. MATERIALS AND METHODS: This study was a retrospective case series of patients who presented for extraction of mandibular third molars. Subjects eligible for study enrollment were those who underwent preoperative dental 3D-CT because the mandibular third molars were determined to be extremely close to the IAN on panoramic radiogram. The predictive variable was the anatomic relation of the IAN and third molar apices and was a binary variable, contact or noncontact. The primary outcome variable was IAN exposure, and the secondary outcome variable was IAN injury. RESULTS: From January 2006 to August 2007, 1,853 mandibular third molars in 1,539 patients were extracted. Among them, dental 3D-CT was performed on 53 third molars in 47 patients. The mandibular third molars were judged to make contact with the mandibular canal on dental 3D-CT images in 35 cases (66%). Intraoperative IAN exposure was observed in 17 (49%) contact cases and 2 (11%) noncontact cases on dental 3D-CT images. Of 53 cases extracted after dental 3D-CT examinations, IAN injury occurred in 8 cases (15%). IAN exposure led to IAN injury in 36.8% of cases, whereas IAN injury occurred in only 2.9% of cases without IAN exposure. Although the incidence of IAN injury in the molar-canal contact cases was 23%, all 8 cases with IAN injury (100%) were included in these contact cases. CONCLUSION: When viewing the anatomic relation between the IAN and mandibular third molar root apices using dental 3D-CT, contact of the 2 anatomic structures results in an increased risk for IAN exposure or injury.

Amelogenin is a negative regulator of osteoclastogenesis via downregulation of RANKL, M-CSF and fibronectin expression in osteoblasts.

Amelogenin is a novel enamel matrix protein. Knockout mice showed enhanced osteoclast formation and resorption of tooth cementum. This study investigated the effects of amelogenin on osteoclastogenesis. In co-cultures with calvaria osteoblasts and purified bone marrow cells, amelogenin inhibited osteoclastogenesis dramatically. Furthermore, amelogenin inhibited the expression of receptor activator of nuclear factor kappaB ligand (RANKL), macrophage-colony stimulating factor (M-CSF) and fibronectin in osteoblasts, while RANKL expression was induced by fibronectin and inhibited by treatment with fibronectin small interfering RNA. These results suggest that the inhibitory effects of amelogenin on osteoclastogenesis lead to downregulation of RANKL, M-CSF and fibronectin production in osteoblasts.

Interaction between fibronectin and ß1 integrin is essential for tooth development.

The dental epithelium and extracellular matrix interact to ensure that cell growth and differentiation lead to the formation of teeth of appropriate size and quality. To determine the role of fibronectin in differentiation of the dental epithelium and tooth formation, we analyzed its expression in developing incisors. Fibronectin mRNA was expressed during the presecretory stage in developing dental epithelium, decreased in the secretory and early maturation stages, and then reappeared during the late maturation stage. The binding of dental epithelial cells derived from postnatal day-1 molars to a fibronectin-coated dish was inhibited by the RGD but not RAD peptide, and by a ß1 integrin-neutralizing antibody, suggesting that fibronectin-ß1 integrin interactions contribute to dental epithelial-cell binding. Because fibronectin and ß1 integrin are highly expressed in the dental mesenchyme, it is difficult to determine precisely how their interactions influence dental epithelial differentiation in vivo. Therefore, we analyzed ß1 integrin conditional knockout mice (Intß1lox-/lox-/K14-Cre) and found that they exhibited partial enamel hypoplasia, and delayed eruption of molars and differentiation of ameloblasts, but not of odontoblasts. Furthermore, a cyst-like structure was observed during late ameloblast maturation. Dental epithelial cells from knockout mice did not bind to fibronectin, and induction of ameloblastin expression in these cells by neurotrophic factor-4 was inhibited by treatment with RGD peptide or a fibronectin siRNA, suggesting that the epithelial interaction between fibronectin and ß1 integrin is important for ameloblast differentiation and enamel formation.

Value of computed tomography findings in differentiating between intraosseous malignant tumors and osteomyelitis of the mandible affecting the masticator space.

OBJECTIVES: We sought to evaluate the diagnostic efficacy of computed tomography (CT) images in the differentiation between intraosseous malignant tumors and osteomyelitis spreading into the masticator space. STUDY DESIGN: A retrospective evaluation was carried out by using CT images from 12 patients with intraosseous malignant tumors and 9 patients with osteomyelitis involving the masticator space and accompanying mandibular bone destruction. The following CT observations are discussed: (1) bone destruction pattern subdivided into spotty, gross, or permeative; (2) cortical bone expansion; (3) diffuse osteosclerotic changes; (4) periosteal reaction; (5) masticator muscle involvement; (6) enlargement of the facial muscle; and (7) attenuation in the subcutaneous adipose tissue. RESULTS: The pattern of permeative bone destruction, cortical bone expansion, and the enlargement of both the masseter and medial pterygoid muscles were all observed in patients with malignant tumors. In contrast, diffuse sclerotic change and a periosteal reaction were significant observations in patients with osteomyelitis. CONCLUSION: The efficacy of CT in establishing a differential diagnosis of malignant tumors or osteomyelitis is supported by this study.

Neurotrophic factor neurotrophin-4 regulates ameloblastin expression via full-length TrkB.

Neurotrophic factors play an important role in the development and maintenance of not only neural but also nonneural tissues. Several neurotrophic factors are expressed in dental tissues, but their role in tooth development is not clear. Here, we report that neurotrophic factor neurotrophin (NT)-4 promotes differentiation of dental epithelial cells and enhances the expression of enamel matrix genes. Dental epithelial cells from 3-day-old mice expressed NT-4 and three variants of TrkB receptors for neurotrophins (full-length TrkB-FL and truncated TrkB-T1 and -T2). Dental epithelial cell line HAT-7 expressed these genes, similar to those in dental epithelial cells. We found that NT-4 reduced HAT-7 cell proliferation and induced the expression of enamel matrix genes, such as ameloblastin (Ambn). Transfection of HAT-7 cells with the TrkB-FL expression construct enhanced the NT-4-mediated induction of Ambn expression. This enhancement was blocked by K252a, an inhibitor for Trk tyrosine kinases. Phosphorylation of ERK1/2, a downstream molecule of TrkB, was induced in HAT-7 cells upon NT-4 treatment. TrkB-FL but not TrkB-T1 transfection increased the phosphorylation level of ERK1/2 in NT-4-treated HAT-7 cells. These results suggest that NT-4 induced Ambn expression via the TrkB-MAPK pathway. The p75 inhibitor TAT-pep5 decreased NT-4-mediated induction of the expression of Ambn, TrkB-FL, and TrkB-T1, suggesting that both high affinity and low affinity neurotrophin receptors were required for NT-4 activity. We found that NT-4-null mice developed a thin enamel layer and had a decrease in Ambn expression. Our results suggest that NT-4 regulates proliferation and differentiation of the dental epithelium and promotes production of the enamel matrix.

Laminin alpha5 is required for dental epithelium growth and polarity and the development of tooth bud and shape.

In tooth development, the oral ectoderm and mesenchyme coordinately and reciprocally interact through the basement membrane for their growth and differentiation to form the proper shape and size of the tooth. Laminin alpha5 subunit-containing laminin-10/11 (LM-511/521) is the major laminin in the tooth germ basement membrane. Here, we have examined the role of laminin alpha5 (Lama5) in tooth development using laminin alpha5-null mouse primary dental epithelium and tooth germ organ cultures. Lama5-null mice develop a small tooth germ with defective cusp formation and have reduced proliferation of dental epithelium. Also, cell polarity and formation of the monolayer of the inner dental epithelium are disturbed. The enamel knot, a signaling center for tooth germ development, is defective, and there is a significant reduction of Shh and Fgf4 expression in the dental epithelium. In the absence of laminin alpha5, the basement membrane in the inner dental epithelium becomes discontinuous. In normal mice, integrin alpha6beta4, a receptor for laminin alpha5, is strongly localized at the basal layer of the epithelium, whereas in mutant mice, integrin alpha6beta4 is expressed around the cell surface. In primary dental epithelium culture, laminin-10/11 promotes cell growth, spreading, and filopodia-like microspike formation. This promotion is inhibited by anti-integrin alpha6 and beta4 antibodies and by phosphatidylinositol 3-kinase inhibitors and dominant negative Rho-GTPase family proteins Cdc42 and Rac. In organ culture, anti-integrin alpha6 antibody and wortmannin reduce tooth germ size and shape. Our studies demonstrate that laminin alpha5 is required for the proliferation and polarity of basal epithelial cells and suggest that the interaction between laminin-10/11-integrin alpha6beta4 and the phosphatidylinositol 3-kinase-Cdc42/Rac pathways play an important role in determining the size and shape of tooth germ.

Laminin alpha2 is essential for odontoblast differentiation regulating dentin sialoprotein expression.

Laminin alpha2 is subunit of laminin-2 (alpha2beta1gamma1), which is a major component of the muscle basement membrane. Although the laminin alpha2 chain is expressed in the early stage of dental mesenchyme development and localized in the tooth germ basement membrane, its expression pattern in the late stage of tooth germ development and molecular roles are not clearly understood. We analyzed the role of laminin alpha2 in tooth development by using targeted mice with a disrupted lama2 gene. Laminin alpha2 is expressed in dental mesenchymal cells, especially in odontoblasts and during the maturation stage of ameloblasts, but not in the pre-secretory or secretory stages of ameloblasts. Lama2 mutant mice have thin dentin and a widely opened dentinal tube, as compared with wild-type and heterozygote mice, which is similar to the phenotype of dentinogenesis imperfecta. During dentin formation, the expression of dentin sialoprotein, a marker of odontoblast differentiation, was found to be decreased in odontoblasts from mutant mice. Furthermore, in primary cultures of dental mesenchymal cells, dentin matrix protein, and dentin sialophosphoprotein, mRNA expression was increased in laminin-2 coated dishes but not in those coated with other matrices, fibronectin, or type I collagen. Our results suggest that laminin alpha2 is essential for odontoblast differentiation and regulates the expression of dentin matrix proteins.