Survival of resin-bonded bridgework provided for post-orthodontic hypodontia patients with missing maxillary lateral incisors.

OBJECTIVE: To analyse the clinical performance and factors influencing the survival of resin-bonded bridgework provided for hypodontia patients with missing maxillary lateral incisors, following orthodontic treatment to open, maintain or redistribute the missing tooth space. DESIGN: A retrospective analysis of patients treated at a single centre using case notes with all patients invited for review to corroborate findings. SETTING: Departments of Orthodontics, Child Dental Health and Restorative Dentistry, Newcastle upon Tyne Dental Hospital and School. SUBJECTS AND METHODS: Between 1989-2000, 59 suitable hypodontia patients were identified of whom 45 had complete records. For these patients 73 resin-bonded bridges (RBBs) were provided. Following invitation, 24 patients attended for a review appointment. The survival of the RBBs, grade of operator providing treatment, duration of post-orthodontic retention, the influence of design, presence of pontic contact in static and dynamic excursions, and the effect of habits were assessed. Life table, Kaplan-Meier and Cox regression analysis were carried out for the 73 RBBs with complete records. A separate analysis of the RBBs provided for patients who attended for the invited review did not show a higher failure rate than those patients who did not attend. Therefore both sets of data were combined. RESULTS: Of the 73 RBBs provided, 30 had debonded on at least one occasion (41.1%), six of these debonds were due to trauma (20%). The mean survival time of all the restorations was 59.3 months, with a median survival time of 59 months. Senior members of staff (Consultant, Senior Lecturer or Specialist Trainee) provided most restorations (n = 39) and achieved the highest mean survival of 72.6 months and median survival time of 100+ months. RBBs provided by junior staff and students had significantly lower survival times (p <0.05) compared with senior staff. Risk of failure was 3.9 times greater with junior staff and 2.5 times greater with students (p = 0.01 and p = 0.02, respectively). Analysis of all the other factors investigated showed no statistical difference in survival times or in hazard ratios. Analysis of fixed/fixed versus cantilevered bridges was limited by the number of fixed/fixed bridges (n = 11), and only two cantilevered bridges with multiple abutments were provided; both failed within one month. CONCLUSION: RBBs provided for post-orthodontic hypodontia patients with missing maxillary lateral incisors can for many patients be an acceptable and definitive restoration. Experienced staff achieved the best results, but why this should be was not explained by the individual factors analysed in this study.

ETV6-NTRK3 gene fusions and trisomy 11 establish a histogenetic link between mesoblastic nephroma and congenital fibrosarcoma.

Congenital mesoblastic nephroma (CMN) is an infantile spindle cell tumor of the kidney that is subdivided into "classical" and "cellular" forms based on the degree of cellularity and mitotic activity. The histogenesis of CMN remains obscure, but relationships to other pediatric renal neoplasms have been proposed. However, cellular CMN is virtually identical histologically to congenital fibrosarcoma (CFS), a malignant tumor of fibroblasts in children of the same age group. Moreover, cytogenetic studies have reported common trisomies in CFS and cellular CMN, particularly of chromosome 11. We show here that t(12;15)(p13;q25)-associated ETV6-NTRK3 gene fusions described in CFS are also present in cellular CMN. ETV6-NTRK3 chimeric transcripts were detected in 8 of 9 cellular CMNs and 2 of 2 mixed CMNs. In contrast, all of the four classical CMNs tested were negative, as were cases of Wilms' tumor and clear cell sarcoma of the kidney. Moreover, we found trisomy 11 only in cellular or mixed CMNs with the ETV6-NTRK3 gene fusion. Our studies indicate that classical and cellular CMN have different genetic features and support the concept that cellular CMN is histogenetically related to CFS. They also provide insight into potential mechanisms involved in the transformation of the classical into the cellular form of CMN.

A mitotic function for the high-mobility group protein HMG20b regulated by its interaction with the BRC repeats of the BRCA2 tumor suppressor.

The inactivation of BRCA2, a suppressor of breast, ovarian and other epithelial cancers, triggers instability in chromosome structure and number, which are thought to arise from defects in DNA recombination and mitotic cell division, respectively. Human BRCA2 controls DNA recombination via eight BRC repeats, evolutionarily conserved motifs of ∼35 residues, that interact directly with the recombinase RAD51. How BRCA2 controls mitotic cell division is debated. Several studies by different groups report that BRCA2 deficiency affects cytokinesis. Moreover, its interaction with HMG20b, a protein of uncertain function containing a promiscuous DNA-binding domain and kinesin-like coiled coils, has been implicated in the G2-M transition. We show here that HMG20b depletion by RNA interference disturbs the completion of cell division, suggesting a novel function for HMG20b. In vitro, HMG20b binds directly to the BRC repeats of BRCA2, and exhibits the highest affinity for BRC5, a motif that binds poorly to RAD51. Conversely, the BRC4 repeat binds strongly to RAD51, but not to HMG20b. In vivo, BRC5 overexpression inhibits the BRCA2-HMG20b interaction, recapitulating defects in the completion of cell division provoked by HMG20b depletion. In contrast, BRC4 inhibits the BRCA2-RAD51 interaction and the assembly of RAD51 at sites of DNA damage, but not the completion of cell division. Our findings suggest that a novel function for HMG20b in cytokinesis is regulated by its interaction with the BRC repeats of BRCA2, and separate this unexpected function for the BRC repeats from their known activity in DNA recombination. We propose that divergent tumor-suppressive pathways regulating chromosome segregation as well as chromosome structure may be governed by the conserved BRC motifs in BRCA2.

Management of patients with reduced oral aperture and mandibular hypomobility (trismus) and implications for operative dentistry.

Reduced oral aperture and mandibular mobility/trismus are relatively common conditions that can be encountered in patients attending general dental practice, community dental practice and district general or dental teaching hospitals. All dental specialties may see patients with these conditions, and regardless of which environment or specialty, both patient and clinician may experience significant problems. The purpose of this opinion-based paper is to identify and review the causes of such conditions, to review the development of problems encountered for patients and clinicians, and to identify options to treat or manage the conditions.