Assessing the proposed association between DED and gluten‐free diet introduction in celiac children

A strong association between celiac disease (CD) and dental enamel defects (DEDs) have been extensively reported, however, the nature of this relationship is still unclear. The aim of this study was to evaluate DEDs phenotype in CD individuals according to the time they were introduced to a gluten‐free diet (GFD). Forty‐five CD individuals were examined by a pediatric dentist. DEDs were classified according to the type of affected teeth. CD individuals were classified into two groups (with or without DEDs) and the differences between these groups were tested using chi‐square or Fisher´s exact tests and t‐test to compare differences between means. The Pearson coefficient test was used to evaluate the degree of the correlation between the age of GFD introduction and number of affected teeth. Individuals with MIH were introduced earlier to the GFD (p = 0.038). An association was also observed for molar DED (p = 0.013). In conclusion, our study suggested an association between a specific type of DED and the time that CD individuals were introduced to a GFD.     

Amelogenin specific IgA and IgG in children with untreated coeliac disease

Children with untreated coeliac disease (CD) may develop enamel defects. Moreover, children with untreated CD have increased serum levels of gliadin reactive IgG, which may cross‐react to amelogenin. The aim of this study was to investigate reactivity of anti‐gliadin IgA and IgG to amelogenin in children with untreated CD. Blood samples from patients with CD (n = 75) and from disease controls (n = 24) were analysed for IgA and IgG reactivities to amelogenin (Emdogain) and to gliadin by ELISA. Whereas children with CD had statistically significantly higher serum levels of anti‐amelogenin IgA, only those with the most severe CD (Marsh 3c) had significantly higher anti‐amelogenin IgG immune reactivity than the disease controls. Western blotting confirmed that the IgA and IgG immune reactivity was to the amelogenin‐specific bands in Emdogain and to a 22‐kDa human recombinant amelogenin. Cross‐inhibition studies revealed that the anti‐amelogenin immune reactivity was not only caused by anti‐gliadin cross‐reactivity but also included amelogenin selective immune reactivity. Some controls had high levels of anti‐amelogenin IgA and IgG, similar to children with CD. Thus, anti‐amelogenin IgA and IgG may not only be involved in the aetiology of CD‐associated enamel defects but may also interfere with enamel maturation in non‐coeliac children.     

Enamel defects in children with coeliac disease.

AIM: This was to investigate the prevalence of enamel developmental defects in a group of children with a history of coeliac disease. METHODS: A study group of children attending the Dept. Paediatrics (Leeds General Infirmary), born between 1985 and 1986 and subsequently diagnosed and treated for coeliac disease (CD) were recruited. A group of age/sex-matched children attending the Paediatric Dentistry department were used as a control group (Cont). Examinations were carried out for enamel defects and opacities (DDE index), dmf, dmfs, DMF and DMFS (BASCD method), and a full medical and dental history were obtained. RESULTS: Significantly more children in the CD group had a greater number of enamel defects than controls for both primary (p=<0.02) and permanent (p=<0.001) dentitions. Opacities in both primary and permanent teeth were statistically significantly greater in the CD group than controls (p=<0.04 and p=<0.001 respectively). Dental caries in both primary and permanent dentitions was less in the CD group compared with the control group of children. CONCLUSION: Coeliac disease was associated with an increased prevalence of developmental enamel defects.     

Prevalence and distribution of developmental enamel defects in primary dentition of Chinese children 3–5 years old

Abstract A total of 1344 children, 3–5 yr old, from two rural counties, Haidian and Miyun, close to Beijing, China, were examined in 1992. A modified DDE Index was employed in this study, and a pre-designed formula was used to calculate an enamel detect score (EDS) for each individual in the study. Oral examination was performed by one dentist under natural light using a standard mouth mirror and dental probe. Developmental enamel lesions were diagnosed without drying or cleaning the teeth prior to examination. Results from this study showed that primary teeth with defective enamel were seen in 23.9% of the children examined, opacity in 1.6%, and hypoplasia in 22.2%. Among the teeth, maxillary central and lateral incisors were affected by enamel hypoplasia most often (40.8% and 39.2%), followed by maxillary canines (25.7%), maxillary 1st molars (22.1%), and mandibular 1st molars (18.5%). The enamel defects occurred more frequently on the buccal surfaces of teeth than on any other surface. The study did not find a significant association of the children's age, family socioeconomic status, and anthropometric measurements with the distribution of enamel defects. However, there was a significantly higher prevalence of teeth with defects in males compared to females (P < 0.001), as well as mean tooth surfaces with defects (P < 0.05), and mean EDS (P < 0.05). Children born prematurely were shown to have four times more enamel lesions than children who were full term (P < 0.01). Children with low birth weight also showed a statistically significant higher prevalence of enamel defects (P < 0.05) and a greater severity of hypoplastic lesions measured by EDS (P < 0.05) than those with normal birth weight. The results indicate that nutrition during fetal development is important in determining normal development of enamel in primary teeth. Nutritional status (diagnosed by anthropometric measurements) after the critical period was not associated with enamel defects induced earlier in life. The study suggested, therefore, that nutrition is important for maintaining proper development of the teeth only during the critical period when teeth are susceptible to the formation of defects.     

Dental enamel defects in children with coeliac disease

OBJECTIVE: The aim of this study was to investigate whether Dutch children with proven coeliac disease show specific dental enamel defects, and to asses whether children with the same gastrointestinal complaints, but proved no-coeliac disease, lack these specific dental enamel defects. MATERIALS AND METHODS: Eighty-one children (53 coeliac patients and 28 control subjects) were examined during the period 2003-2004 in the Oral Surgery Outpatient Clinic of the Academic Medical Centre in Amsterdam. RESULT: Twenty-nine (55%) coeliac patients had enamel defects against 5 (18%) control subjects. In the coeliac disease group, the enamel defects were diagnosed as specific in 20 (38%) children, compared with 1 (4%) in the control group. Statistical analysis showed significantly more specific enamel defects in children with coeliac disease than in children in the control group (chi(2) = 12.62, d.f. = 2, P = 0.002). CONCLUSION: This study showed significantly more specific enamel defects in Dutch children with coeliac disease as compared with children in the control group. Dentists could play an important role in recognizing patients with coeliac disease.     

Prevalence and distribution of developmental enamel defects in children with cerebral palsy in Beijing,China

International Journal of Paediatric Dentistry 2011; 21: 23–28 Aim. To investigate the prevalence and distribution of developmental enamel defects in children with cerebral palsy (CP) in Beijing, China. Design. A total of 135 children aged 1.5–6 years with moderate or severe congenital CP diagnosed in Beijing Boai Hospital from year 2005 to 2009 were recruited. The children underwent dental examination at the hospital dental clinic. Results. Enamel defects (opacity and/or hypoplasia) were found in 44 (32.6%) out of 135 CP children. Enamel hypoplasia was found in 35 (25.9%) of the CP children, opacity alone was found in 5 (3.7%) of the CP children, and mixed defects (opacity and hypoplasia) was found in 4 (3.0%) of the CP children. Most of the enamel defects were located symmetrically in the primary incisors and first molars. 42.4% of children with enamel defects were born prematurely (<37 weeks) where as only 23.2% of them were born at normal gestational age. No statistically significant difference in the prevalence of enamel defects was found in relation to birth weight (P > 0.05). Conclusions. A high prevalence of developmental enamel defects was found among the children with CP. The prevalence of defects varied with the tooth type and was associated with gestational age of the children.     

Enamel defects associated with coeliac disease: putative role of antibodies against gliadin in pathogenesis

Enamel defects in the permanent teeth of patients with coeliac disease (CD) are often reported as an atypical manifestation, sometimes being suggestive of an undiagnosed atypical disease. We proposed to explore the pathogenesis of these oral defects, which are poorly studied. Sequence analyses of proteins from gluten (gliadins) and of proline-rich enamel proteins (amelogenin and ameloblastin) suggested the presence of common antigenic motifs. Therefore, we analyzed, by ELISA and western blotting, the reactivity of sera from patients with CD against gliadin and enamel-derived peptides. Correlation analyses between the levels of specific antibodies against gliadin and enamel derived peptides and inhibition experiments confirmed the presence of cross-reactive antibodies. Immunoblot analysis revealed that the most prominent component in enamel matrix derivative (of approximately 18.6 kDa), identified by an amelogenin-specific antibody, is recognized by sera from patients with CD; in addition, several fractions of pure gliadin were recognized by amelogenin-specific antibody. In agreement, sera from mice immunized with enamel matrix-derived proteins generated antibodies that recognized a peptide (of approximately 21.2 kDa) derived from gliadin. In conclusion, antibodies against gliadin generated in patients with CD can react in vitro with a major enamel protein. The involvement of anti-gliadin serum in the pathogenesis of enamel defects in children with untreated CD can be hypothesized on the basis of these novel results.     

Oral health in preschool children with cerebral palsy: a case–control community‐based study

International Journal of Paediatric Dentistry 2010; 20: 330–335 Objectives. To assess and compare the oral health status of preschool children with and without cerebral palsy (CP). Methods. Preschool children with CP (72) were recruited from 23 Special Child Care Centers in Hong Kong. An age (±3 months) and gender matched sample of preschool children from mainstream preschools were recruited as the control group. Dental caries status, gingival health status, tooth wear, developmental defect of enamel, malocclusion, dental trauma and oral mucosal health were assessed and compared between the two groups. Results. Significant differences in gingival health status were found between children with and without CP (mean plaque index scores, P = 0.001 and mean gingival index scores, P < 0.05). Tooth wear involving dentine was more prevalent among CP children (P < 0.001), as were evidence of anterior open‐bite (P < 0.001) and oral mucosal lesions (P < 0.05). Children with and without CP had similar caries experiences (P > 0.05), prevalence of enamel defects (P > 0.05) and dental trauma (P > 0.05). Conclusions. Differences of oral health status exist among preschool children with and without CP. Preschool children fare worse in terms of gingival health, tooth wear, oral mucosal health and malocclusion.     

Macroscopic enamel defects of primary anterior teeth--types, prevalence, and distribution

A total of 40.7% of 509 exfoliated primary anterior teeth from children who were healthy products of uneventful pregnancies exhibited at least one macroscopic enamel defect. Twenty percent of the teeth exhibited hypoplastic defects (HD), 12.4% exhibited white-cream opacities (WCO), and 9.8% exhibited yellow-brown opacities (YBO). Slightly more than a third (33.6%) of the teeth had defects we considered to be developmental enamel defects (DED). The occurrence of DED did not vary with gender, side of mouth, individual tooth types, or racial background. DED occurred with increased frequency on maxillary teeth, facial surfaces, and the middle third of affected surfaces. These locations have thicker enamel than other sites and may be more susceptible to insult if vulnerability is a function of metabolic demand of the rapidly secreting ameloblasts. Twenty-five per cent of the maxillary incisors and 10.1% of the mandibular incisors exhibited HD whose locations coincided with enamel forming at birth. A third (33.3%) of the canines exhibited HD, which occurred most commonly in the middle third of the facial surfaces. These defects are believed to occur approximately six months postnatally and may be primarily due to mechanical trauma. YBO most commonly occurred on the middle third of the facial surfaces, while WCO on the gingival third. Neither YBO nor WCO followed a chronologic pattern.     

Comparison of the Proportion of Non‐Classic (CD14+CD16+) Monocytes/Macrophages in Peripheral Blood and Gingiva of Healthy Individuals and Patients With Chronic Periodontitis

Background: Monocyte subsets with low CD14 expression that coexpress CD16 (CD14+CD16+) are called non‐classic or hyperinflammatory monocytes. Previous studies have reported an increase in the percentage of CD14+CD16+ monocytes in the peripheral blood of patients with chronic periodontitis (CP). To our knowledge, there are no reports demonstrating the presence of CD14+CD16+ monocyte–derived macrophages (MDMs) in the gingival tissue. The objective of this study is to identify the proportion of non‐classic (CD14+CD16+) monocytes/macrophages in peripheral blood and gingiva of healthy individuals and patients with CP. Methods: A total of 60 individuals (n = 30 per group) were recruited for the study. Group 1 included 30 individuals with healthy gingiva, and group 2 included 30 patients with CP. Direct immunofluorescent staining was done in 200 μL whole‐blood and single‐cell suspensions obtained from gingival tissue, with fluorochrome‐conjugated monoclonal antibodies against CD14, CD16, and human leukocyte antigen‐DR (HLA‐DR), and subjected to flow cytometric analysis. Results: The mean percentage of CD14+CD16+ monocytes in the peripheral blood of healthy individuals was 9.10% ± 1.39%, and for patients with CP it was 14.18% ± 2.69% (P <0.05). The mean percentage of CD14+CD16+ MDMs in the gingival tissue of healthy individuals was found to be 0.93% ± 0.33%, whereas in patients with CP, it was 1.92% ± 0.78% (P <0.01). Non‐classic monocytes/macrophages showed a high median fluorescent intensity for HLA‐DR (DR++). Conclusion: This study demonstrates an increased proportion of CD14+CD16+HLA‐DR++ monocytes/macrophages in the peripheral blood and gingiva of patients with CP.     

Dental caries experience and Molar-Incisor Hypomineralization

Abstract

Objective. This cross-sectional study assessed the prevalence and severity of the enamel defects, known as Molar-Incisor Hypomineralization (MIH) and its relationship to dental caries. Materials and methods. A sample of 1157 schoolchildren (population based), aged 6–12 years, of the Araraquara city-Brazil, was evaluated according to the European Academy of Paediatric Dentistry (EAPD) criteria by two trained examiners. The dental impact caused by MIH was evaluated with the Decayed, Missing and Filled Teeth (DMFT) index (WHO). Data were analyzed using ANOVA and Chi-square tests (p < 0.05). The socioeconomic status was collected using a questionnaire answered by parents. Results. The prevalence of MIH was 12.3%. Mild impairment was the most frequent diagnosis. DMFT of children with MIH was 0.89 (±1.18), which are higher than those of the unaffected group (0.43 ± 1.01). An association was found between dental caries only in the permanent dentition of children with MIH (p = 0.0001). Family income was considered low in 85% of the families of children with MIH in the public system, while in private school it was 18% (p < 0.05). Conclusion. The prevalence of MIH in Araraquara was associated with greater caries experience in the permanent dentition.     

Developmental defects of enamel in a group of New Zealand children: their prevalence and some associated etiological factors

Abstract The prevalence of developmental defects of enamel was assessed in 243 children aged 12–14 yr using the FDI Index. The teeth were not cleaned or dried prior to examination for which fibre optic lighting was used. At least one tooth with defective enamel was seen in 63% of children with a demarcated white opacity present in 44% of children. The enamel was abnormal in 11.7% of teeth, diffuse patchy opacities and demarcated while opacities occurring in 4.4 and 4.2%, respectively. Although defects were found most frequently in the maxillary central incisors, the ranking order of prevalence and the distribution for demarcated and diffuse opacities was quite different. Sex, residence, and the common childhood illnesses did not alter the prevalence of defects which was, however, increased significantly in 22 children with a history of a serious illness or accident (0.01 > P > 0.001). The prevalence of the diffuse opacities was significantly increased with increased exposure to fluoride either in tablets nr in the drinking water (0.01 > P > 0.001).     

Clinical Outcomes After Treatment of Non‐Contained Intrabony Defects With Enamel Matrix Derivative or Guided Tissue Regeneration: A 12‐Month Randomized Controlled Clinical Trial

Background: The purpose of this study is to compare the healing of deep, non‐contained intrabony defects (i.e., with a ≥80% 1‐wall component and a residual 2‐ to 3‐wall component in the most apical part) treated with either an enamel matrix derivative (EMD) or guided tissue regeneration (GTR) after 12 months. Methods: In this randomized, controlled clinical trial, 40 subjects with 40 defects affecting single‐rooted teeth were treated. The defects were treated with EMD alone or with a non‐resorbable titanium‐reinforced membrane. No grafting materials were used. At baseline and after 12 months, clinical parameters including probing depths (PDs) and clinical attachment levels (CAL) were recorded. The difference in CAL gain was the primary outcome. Results: At baseline, the intrabony component of the defects amounted to 8.5 ± 2.2 mm at EMD‐treated sites and 8.6 ± 1.7 mm at GTR‐treated sites (P = 0.47). The mean CAL gain at sites treated with GTR was significantly greater (P <0.001) than that at sites treated with EMD (4.1 ± 1.4 mm versus 2.4 ± 2.2 mm, respectively). GTR therapy, compared to EMD application alone, significantly (P = 0.01) increased the probability of CAL gain ≥4 mm (79.2% versus 11.3%, respectively) and significantly (P = 0.01) decreased the probability of residual PDs ≥6 mm (3% versus 79.3%, respectively). Conclusion: Although the outcomes of open‐flap debridement alone were not investigated, the application of EMD alone appeared to yield less PD reduction and CAL gain compared to GTR therapy in the treatment of deep, non‐contained intrabony defects.     

MBL2, MASP2, AMELX, and ENAM gene polymorphisms and dental caries in Polish children

Oral Diseases (2012) 18 , 389–395 Objective: The aim of the study was to examine whether the MBL2 C(‐290)G and G161A, MASP2 A359G, AMELX C287T and C522T, and ENAM C2452T polymorphisms are associated with dental caries. Subjects and methods: Genomic DNA of 95 Polish children with ‘higher caries experience’ (HC) and 84 subjects with ‘lower caries experience’ (LC) belonging to two age‐groups (5 and 13 years old) was extracted from the buccal mucosa. SNPs were genotyped with PCR‐RFLP methods. Results: Among 5‐year‐old children, we found significantly higher percentage of subjects carrying MBL2 (‐290)G allele in HC group compared with LC group (43.2%vs 17.6%, P = 0.023). MBL2 C(‐290)G–G161A C–G haplotype was overrepresented in LC group in 5‐year‐olds (P = 0.01), while the opposite association was observed in 13‐year‐olds, where C–G was overrepresented in HC group (P = 0.028). In 5‐year‐old children, the frequency of MBL2 G–G haplotype was higher in HC group compared with LC subjects (P = 0.045), while the opposite association (with borderline significance) was observed in 13‐year‐old children (P = 0.057). SNPs in MASP2, AMELX, and ENAM were not associated with dental caries. Conclusion: MBL2 gene polymorphism is associated with caries experience in Polish children, but the direction of this association seems to be opposite in primary and permanent dentition.     

Prenatal and neonatal risk factors for the development of enamel defects in low birth weight children

Oral Diseases (2010) 16 , 257–262 Objective: To analyse the influence of several prenatal and neonatal risk factors in the development of enamel defects in low birth weight children. Subjects and methods: Children between 4 and 5 years of age (n = 102) were classified into: Group 1) 52 low birth weight (<2500 g); Group 2) 50 normal birth weight (≥2500 g). Medical history, prenatal and neonatal variables were collected. Enamel defects were evaluated with the modified Developmental Defects of Enamel Index. Results: The prevalence of hypoplasia and average number of affected teeth were significantly higher in group 1 than in group 2 (59.6%vs 16% and 1.6 vs 0.3 respectively). Low gestational age was linked to a higher prevalence of hypoplastic (P = 0.027) and combined defects (P = 0.001). Children with neonatal risk factors (low Apgar scores, parenteral nutrition, orotracheal intubation, mechanical ventilation and acidosis) developed defects more frequently (P < 0.05). Defects were symmetrically distributed in children who were not intubated; in those who required intubation they concentrated on the left maxillary teeth (P < 0.05). Smoking during pregnancy, young maternal age and multiple birth were significantly associated to developmental defects. Conclusions: The prevalence of enamel defects in primary dentition is significantly influenced by birth weight, gestational age and several systemic factors. Orotracheal intubation probably plays an important role as a result of laryngoscope trauma on the maxilla.     

The erosion and abrasion-inhibiting effect of TiF(4) and NaF varnishes and solutions on enamel in vitro

International Journal of Paediatric Dentistry 2011; 22: 11–16 Objective. Previous in vitro study has shown that TiF₄ varnish might reduce enamel erosion. No data regarding the effect of this experimental varnish on enamel erosion plus abrasion, however, are available so far. Thus, this in vitro study aimed to analyse the effect of TiF₄ compared with NaF varnishes and solutions, to protect against enamel erosion with or without abrasion. Methods. Enamel specimens were pre‐treated with experimental‐TiF₄ (2.45% F), experimental‐NaF (2.45% F), NaF‐Duraphat (2.26% F), and placebo varnishes; NaF (2.26% F) and TiF₄ (2.45% F) solutions. Controls remained untreated. The erosive challenge was performed using a soft drink (pH 2.6) 4 × 90 s/day (ERO) and the toothbrushing abrasion (ERO+ABR) 2 × 10 s/day, for 5 days. Between the challenges, the specimens were exposed to artificial saliva. Enamel loss was measured profilometrically (μm). Results. Kruskal–Wallis/Dunn tests showed that all fluoridated varnishes (TiF₄–ERO:0.53 ± 0.20, ERO+ABR:0.65 ± 0.19/NaF‐ERO:0.94 ± 0.18, ERO+ABR:1.74 ± 0.37/Duraphat‐ERO:1.00 ± 0.37, ERO+ABR:1.72 ± 0.58) were able to significantly reduce enamel loss when compared with placebo varnish (ERO:3.45 ± 0.41/ERO+ABR:3.20 ± 0.66) (P < 0.0001). Placebo varnish, control (ERO:2.68 ± 0.53/ERO+ABR:3.01 ± 0.34), and fluoridated (NaF‐ERO:2.84 ± 0.09/ERO+ABR:2.40 ± 0.21/TiF₄‐ERO:3.55 ± 0.59/ERO+ABR:4.10 ± 0.38) solutions did not significantly differ from each other. Conclusion. Based on the results, it can be concluded that the TiF₄ varnish seems to be a promising treatment to reduce enamel loss under mild erosive and abrasive conditions in vitro.     

Enamel Matrix Derivative,Alone or Associated With a Synthetic Bone Substitute,in the Treatment of 1‐ to 2‐Wall Periodontal Defects

Background: In this study, we compare the effects of enamel matrix derivative (EMD) associated with a hydroxyapatite and β‐tricalcium phosphate (HA/β‐TCP) implant to EMD alone and to open‐flap debridement (OFD) when surgically treating 1‐ to 2‐wall intrabony defects. Methods: Thirty‐four patients, exhibiting ≥3 intraosseous defects in different quadrants, were each treated by OFD, EMD, or EMD + HA/β‐TCP in each defect. At baseline and 12 and 24 months, a complete clinical and radiographic examination was done. Pre‐therapy and post‐therapy clinical (probing depth [PD], clinical attachment level [CAL], and gingival recession [GR]) and radiographic (defect bone level [DBL] and radiographic bone gain [RBG]) parameters for the different treatments were compared. Results: After 12 and 24 months, almost all the clinical and radiographic parameters showed significant changes from baseline within each group (P <0.001). Differences in PD, CAL, and DBL scores were also seen among the three groups at the 12‐ and 24‐month visits (P <0.001). At 12 and 24 months after treatment, the EMD + HA/β‐TCP group showed significantly greater PD reduction (4.00 ± 0.42 mm; 4.25 ± 0.63 mm), CAL gain (3.47 ± 0.65 mm; 3.63 ± 0.91 mm), and RBG (3.17 ± 0.69 mm; 3.35 ± 0.80 mm) and less GR increase (0.56 ± 0.37 mm; 0.63 ± 0.42 mm) compared with the OFD and EMD groups (P <0.05). Conclusion: Our data support the hypothesis that the adjunct of an HA/β‐TCP composite implant with EMD may improve the clinical and radiographic outcomes of the surgical treatment of unfavorable intrabony defects.     

Histomorphometric and mineral degradation study of Ossceram: a novel biphasic B-tricalcium phosphate, in critical size defects in rabbits

Objective: To carry out a histomorphometric analysis of a new highly porous (95%) biphasic calcium phosphate (hydroxyapatite 60%/B‐tricalcium phosphate 40%), used to fill critical size defects in rabbit tibiae, supplementing histomorphometric findings with radiographic thermal imaging, EDX analysis and Ca/P ratio mapping at different time stages. Materials and methods: Two critical size defects of 6 mm diameter were created in both tibiae of 21 New Zealand rabbits, test group (Ossceram^®) and control group. Histomorphometric, radiographic thermal imaging, EDX and element mapping analysis were performed at 15, 30 and 60 days after graft insertion. Results: Histomorphometric analysis at 30 days showed more new bone formation in defects filled with Ossceram^® 4.41 ± 0.23 mm than the test group 1.94 ± 0. 28 mm (P<0.05). Element analysis revealed higher percentages of Ca (42.33 ± 2.8%) and P (1.3 ± 0.8%) in the test group than in the control group (P<0.05). Element mapping showed that Ca and P were concentrated in medullar and cortical zones in the test group but were concentrated only in cortical zones in the control group. Test group histomorphometry at 60 days showed complete closure of the cortical defect 5.37 ± 0.32 mm more than the control group 2.3 ± 0.54 mm. There was no cortical defect closure or medullar bone formation in the control group (P<0.05). Element analysis revealed higher percentages of Ca (32.26 ± 21.7%) and P (1.5 ± 0.3%) in the test group than in the control group (P<0.05). Conclusion: Defects of a critical size in a rabbit tibia model can be sealed using a highly porous biphasic calcium phosphate; this supports new bone formation, creates a bridge between borders and facilitates bone ingrowth. Furthermore, this study observed partial dissolution of the mineral phase of the graft material and its incorporation into the surrounding bone. Radiographic thermal imaging may be used to supplement histological and chemical analyses.     

Clinical Outcomes Following Regenerative Therapy of Non‐Contained Intrabony Defects Using a Deproteinized Bovine Bone Mineral Combined With Either Enamel Matrix Derivative or Collagen Membrane

Background: The purpose of this study is to compare clinical outcomes in the treatment of deep non‐contained intrabony defects (i.e., with ≥70% 1‐wall component and a residual 2‐ to 3‐wall component in the most apical part) using deproteinized bovine bone mineral (DBBM) combined with either enamel matrix protein derivative (EMD) or collagen membrane (CM). Methods: Forty patients with multiple intrabony defects were enrolled. Only one non‐contained defect per patient with an intrabony depth ≥3 mm located in the interproximal area of single‐ and multirooted teeth was randomly assigned to the treatment with either EMD + DBBM (test: n = 20) or CM + DBBM (control: n = 20). At baseline and after 12 months, clinical parameters including probing depth (PD) and clinical attachment level (CAL) were recorded. The primary outcome variable was the change in CAL between baseline and 12 months. Results: At baseline, the intrabony component of the defects amounted to 6.1 ± 1.9 mm for EMD + DBBM and 6.0 ± 1.9 mm for CM + DBBM sites (P = 0.81). The mean CAL gain at sites treated with EMD + DBBM was not statistically significantly different (P = 0.82) compared with CM + DBBM (3.8 ± 1.5 versus 3.7 ± 1.2 mm). No statistically significant difference (P = 0.62) was observed comparing the frequency of CAL gain ≥4 mm between EMD + DBBM (60%) and CM + DBBM (50%) or comparing the frequency of residual PD ≥6 mm between EMD + DBBM (5%) and CM + DBBM (15%) (P = 0.21). Conclusion: Within the limitations of the present study, regenerative therapy using either EMD + DBBM or CM + DBBM yielded comparable clinical outcomes in deep non‐contained intrabony defects after 12 months.