Evaluation of peri-implant marginal tissues around tissue-level and bone-level implants in patients with a history of chronic periodontitis.

OBJECTIVE: To evaluate clinical and radiographic characteristics in peri-implant marginal tissues in patients with a history of chronic periodontitis, rehabilitated using tissue-level or bone-level implants. MATERIAL AND METHODS: Using a split-mouth design, 20 patients with a history of chronic periodontitis were selected and received two different implants, tissue-level group (n = 20) and the bone-level group (n = 20). Peri-implant probing depth, relative peri-implant mucosal margin position, relative peri-implant clinical attachment level, peri-implant plaque index and peri-implant bleeding on probing were evaluated at prosthesis installation, 1, 3, 6, 12 and 24 months after implant loading. Radiographic marginal bone level was evaluated at implant insertion, prosthesis installation, 6 and 24 months after implant loading. RESULTS: The mean difference of peri-implant marginal bone resorption from implant installation to 24 months in function was 0.75 ± 1.12 mm for the tissue-level group and 0.70 ± 0.72 mm for the bone-level group. No statistically significant difference was found between groups at all assessment periods for clinical and radiographic peri-implant evaluation. CONCLUSION: Under a rigid supportive therapy, both approaches performed likewise regarding clinical and radiographic parameters for rehabilitation of patients with a history of chronic periodontitis.

Periodontal clinical and microbiological characteristics in healthy versus generalized aggressive periodontitis families.

AIM: Generalized aggressive periodontitis (GAP) is a severe and multifactorial disease in which a familial aggregation and a specific microbiological profile have been suggested. Thus, this case-control study evaluated the clinical and subgingival microbial profile of GAP subjects and their families compared to healthy families. METHODS: Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family should have at least one child between 6 and 12 years old. Plaque index (PI), gingival index (GI), and periodontal probing depth (PPD), as well as Porphyromonas gingivalis, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans (Aa) amounts (by qPCR), were assessed from all subjects. RESULTS: Children of GAP families showed a higher PI, GI, and PPD when compared to children of healthy families (p ≤ 0.05). A higher frequency of detection and amounts of Aa was observed in GAP children compared to children of healthy families (p ≤ 0.05). Moreover, a significant association between Aa amounts and gingival bleeding was observed in children (p ≤ 0.05, r = 0.37). CONCLUSION: Children from GAP families have worst clinical conditions, i.e. higher levels of PI, GI, and PPD, a more pathogenic microbiological profile, and the amount of Aa are associated with a higher marginal inflammation.

Effects of basic fibroblast growth factor on density and morphology of fibroblasts grown on root surfaces with or without conditioning with tetracycline or EDTA.

A study was conducted to evaluate in vitro the effect of root surface conditioning with basic fibroblast growth factor (b-FGF) on morphology and proliferation of fibroblasts. Three experimental groups were used: non-treated, and treated with 50 microg or 125 microg b-FGF/ml. The dentin samples in each group were divided into subgroups according to the chemical treatment received before application of b-FGF: none, or conditioned with tetracycline-HCl or EDTA. After contact with b-FGF for 5 min, the samples were incubated for 24 h with 1 ml of culture medium containing 1 x 10(5) cells/ml plus 1 ml of culture medium alone. The samples were then subjected to routine preparation for SEM, and random fields were photographed. Three calibrated and blind examiners performed the assessment of morphology and density according to two index systems. Classification and regression trees indicated that the root surfaces treated with 125 microg b-FGF and previously conditioned with tetracycline-HCl or EDTA presented a morphology more suggestive of cellular adhesion and viability (P = 0.004). The density of fibroblasts on samples previously conditioned with EDTA, regardless of treatment with b-FGF, was significantly higher than in the other groups (P < 0.001). The present findings suggest that topical application of b-FGF has a positive influence on both the density and morphology of fibroblasts.

Root instrumentation with an erbium:yttrium-aluminum-garnet laser: effect on the morphology of fibroblasts.

OBJECTIVE: The purpose of this study was to evaluate the effect of erbium:yttrium-aluminum-garnet laser instrumentation of root surfaces on the morphology of fibroblasts from continuous lineage. METHOD AND MATERIALS: Dentinal slices with 4 mm2 of surface area were obtained from teeth extracted for severe periodontal involvement. Specimens were assigned to one of three treatment groups: group 1, application of the laser with an energy level of 250 mJ at 103 pulses per second; group 2, application of the laser with an energy level of 80 mJ at 166 pulses per second; and group 3, similar to group 2, but with concomitant water irrigation of the device. The specimens were incubated in multiwell plates containing cell culture media. After 24 hours, the specimens were submitted to routine preparation for scanning electron microscopy. Three independent and blind examiners used photomicrographs to evaluate the morphology of the fibroblasts: 0 = without cells; 1 = flat cells; 2 = round cells; and 3 = combination of round and flat cells. RESULTS: Statistical analysis indicated that there were significant differences among treatment groups and that group 3 was significantly different from groups 1 and 2. CONCLUSION: There was no difference between groups 1 and 2 in the morphology of fibroblasts. Laser instrumentation with concomitant irrigation impaired the adhesion of fibroblasts to dentinal surfaces.

Correction of hypophosphatasia-associated mineralization deficiencies in vitro by phosphate/pyrophosphate modulation in periodontal ligament cells.

BACKGROUND: Mutations in the liver/bone/kidney alkaline phosphatase (ALPL) gene in hypophosphatasia (HPP) reduce the function of tissue non-specific alkaline phosphatase (ALP), resulting in increased pyrophosphate (PP(i)) and a severe deficiency in acellular cementum. We hypothesize that exogenous phosphate (P(i)) would rescue the in vitro mineralization capacity of periodontal ligament (PDL) cells harvested from HPP-diagnosed patients, by correcting the P(i)/PP(i) ratio and modulating expression of genes involved with P(i)/PP(i) metabolism. METHODS: Ex vivo and in vitro analyses were used to identify mechanisms involved in HPP-associated PDL/tooth root deficiencies. Constitutive expression of PP(i)-associated genes was contrasted in PDL versus pulp tissues obtained from healthy individuals. Primary PDL cell cultures from patients with HPP (monozygotic twin males) were established to assay ALP activity, in vitro mineralization, and gene expression. Exogenous P(i) was provided to correct the P(i)/PP(i) ratio. RESULTS: PDL tissues obtained from healthy individuals featured higher basal expression of key PP(i) regulators, genes ALPL, progressive ankylosis protein (ANKH), and ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), versus paired pulp tissues. A novel ALPL mutation was identified in the twin patients with HPP enrolled in this study. Compared to controls, HPP-PDL cells exhibited significantly reduced ALP and mineralizing capacity, which were rescued by addition of 1 mM P(i). Dysregulated expression of PP(i) regulatory genes ALPL, ANKH, and ENPP1 was also corrected by adding P(i), although other matrix markers evaluated in our study remained downregulated. CONCLUSION: These findings underscore the importance of controlling the P(i)/PP(i) ratio toward development of a functional periodontal apparatus and support P(i)/PP(i) imbalance as the etiology of HPP-associated cementum defects.

Hypophosphatasia-associated deficiencies in mineralization and gene expression in cultured dental pulp cells obtained from human teeth.

INTRODUCTION: Mutations in the gene ALPL in hypophosphatasia (HPP) reduce the function of tissue nonspecific alkaline phosphatase, and the resulting increase in pyrophosphate (PP(i)) contributes to bone and tooth mineralization defects by inhibiting physiologic calcium-phosphate (P(i)) precipitation. Although periodontal phenotypes are well documented, pulp/dentin abnormalities have been suggested in the clinical literature although reports are variable and underlying mechanisms remains unclear. In vitro analyses were used to identify mechanisms involved in HPP-associated pulp/dentin phenotypes. METHODS: Primary pulp cells cultured from HPP subjects were established to assay alkaline phosphatase (ALP) activity, mineralization, and gene expression compared with cells from healthy controls. Exogenous P(i) was provided to the correct P(i)/PP(i) ratio in cell culture. RESULTS: HPP cells exhibited significantly reduced ALP activity (by 50%) and mineral nodule formation (by 60%) compared with the controls. The expression of PP(i) regulatory genes was altered in HPP pulp cells, including reduction in the progressive ankylosis gene (ANKH) and increased ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1). Odontoblast marker gene expression was disrupted in HPP cells, including reduced osteopontin (OPN), dentin matrix protein 1 (DMP1), dentin sialophosphoprotein (DSPP), and matrix extracellular phosphoprotein (MEPE). The addition of P(i) provided a corrective measure for mineralization and partially rescued the expression of some genes although cells retained altered messenger RNA levels for PP(i)-associated genes. CONCLUSIONS: These studies suggest that under HPP conditions pulp cells have the compromised ability to mineralize and feature a disrupted odontoblast profile, providing a first step toward understanding the molecular mechanisms for dentin phenotypes observed in HPP.