Background: The treatment of leprosy reactions (LRs) involves thalidomide, corticosteroids, and other immunomodulatory medications. This study evaluated the effect of these treatments on the association between periodontitis and LRs, as well as factors associated with LRs.
Methods: This case–control study was conducted on 283 individuals followed at a leprosy outpatient clinic in Brazil. The case group was comprised of 158 individuals presenting type 1 or type 2 LRs, and the control group of 125 leprosy individuals without reactions. A complete oral examination was performed to diagnose periodontitis, the independent variable. Antireaction medication used was collected from medical records, and participants were classified according to the use of prednisone and/or thalidomide, time of use, or non-use of medication. Socioeconomic–demographic, clinical, and lifestyle covariables were collected by interview. Unconditional logistic regression analysis by subgroups evaluated the effect of antireaction medication on the association between periodontitis and LRs, estimating the odds ratio with a 95% confidence interval (OR; 95% CI).
Results: A relationship between periodontitis and LRs was observed only in the subgroup using the association prednisone and thalidomide: ORadjusted = 0.32; 95% CI = 0.11–0.95. Conversely, more severe periodontal clinical parameters were observed in cases versus controls. Several socioeconomic, health conditions, and lifestyle factors were associated with the presence of LRs.
Conclusions: Although periodontal disease indicators were worse among the cases, the findings showed a negative relationship between periodontitis and LRs in individuals receiving associated prednisone and thalidomide. These medications appear to influence the inflammatory cascade between diseases, modifying and masking the manifestations of periodontitis.
This study was designed to test the hypothesis that the leptin receptor (LepR) regulates changes in periodontal tissues and that the overexpression of the receptor for resolvin E1 (ERV1) prevents age- and diabetes-associated alveolar bone loss.
LepR-deficient transgenic (TG) mice were cross-bred with those overexpressing ERV1 (TG) to generate double-TG mice. In total, 95 mice were divided into four experimental groups: wild type (WT), TG, LepR deficient (db/db), and double transgenic (db/db TG). The groups were followed from 4 weeks up to 16 weeks of age. The natural progression of periodontal disease without any additional method of periodontitis induction was assessed by macroscopic and histomorphometric analyses. Osteoclastic activity was measured by tartrate-resistant acid phosphatase (TRAP) staining.
At 4 weeks, ERV1 overexpression prevented weight gain. From Week 8 onward, there was a significant increase in the weight of db/db mice with or without ERV1 overexpression compared to the WT mice, accompanied by an increase in glucose levels. By 8 weeks of age, the percentage of bone loss in the LepR deficiency groups was significantly greater compared to WT mice. ERV1 overexpression in the db/db TG mice prevented early alveolar bone loss; however, it did not impact the development of diabetic bone loss in aging mice after the onset of weight gain and diabetes.
The findings suggest that the overexpression of ERV1 prevents LepR-associated alveolar bone loss during the early phases of periodontal disease by delaying weight gain, diabetes onset, and associated inflammation; however, LepR deficiency increases susceptibility to naturally occurring inflammatory alveolar bone loss as the animal ages, associated with excess weight gain, onset of diabetes, and excess inflammation.
To explore the correlation between short-chain fatty acids (SCFAs) in the peri-implant sulcular fluid (PISF) and peri-implant diseases.
PISF samples were obtained from implants that have been placed for at least 5 years, and peri-implant clinical parameters were examined. Gas chromatography-mass spectrometry and high-performance liquid chromatography were used to detect SCFAs in PISF. The correlation between SCFAs and clinical parameters was analyzed by Spearman's correlation. SCFAs related to peri-implant disease were identified by logistic regression and ranked by random forest analysis.
Eighty-six implants were divided into a peri-implant health group (PIH-group, 35 implants), peri-implant mucositis group (PIM-group, 25 implants), and peri-implantitis group (PI-group, 26 implants) according to clinical and radiographic examination results. The PIM-group had significantly lower formic acid detection rate than the other two groups (p < 0.001). The PIM-group had significantly higher levels of acetic, propionic, and isovaleric acids than the PIH-group (p < 0.05). The PI-group had significantly higher levels of propionic, butyric, isobutyric, valeric, and isovaleric acids than the PIH-group (p < 0.05). The PI-group had significantly higher levels of butyric, isobutyric, and isovaleric acids than the PIM-group (p < 0.05). SCFAs (apart from hexanoic and succinic acids) were significantly and positively correlated with clinical parameters (p < 0.05). SCFAs related to peri-implant disease were ranked as follows: butyric, isovaleric, isobutyric, propionic, acetic, formic, and lactic acids.
Elevated specific SCFAs are correlated with peri-implant disease. Recognition of this correlation may help in early identification of peri-implant disease and guide further clinical interventions.
Bacterial-induced inflammation instigates the destruction of hard and soft tissues surrounding teeth in periodontitis. In severe cases, the increased number and activity of osteoclasts induces the resorption of alveolar bones, ultimately leading to tooth loss. Because of their diverse chemical structures and bioactivities, natural compounds are often suggested to treat a wide variety of diseases, including inflammatory disorders.
In the present study, we demonstrated an inhibitory effect of gossypetin, a hexahydroxy flavone, on osteoclast differentiation and bone resorption using in vitro culture of osteoclasts from mouse bone marrow macrophage (BMM) precursors and in vivo model of ligature-induced periodontitis in mice.
Gossypetin significantly reduced the differentiation of osteoclasts from mouse BMM precursors in the presence of the receptor activator of nuclear factor κB ligand (RANKL). In vitro, gossypetin inhibited critical signaling events downstream of RANKL including the auto-amplification of nuclear factor of activated T-cells, cytoplasmic 1, Ca2+ oscillations, and the generation of reactive oxygen species. In a mouse ligature-induced periodontitis model, the administration of gossypetin significantly reduced osteoclastogenesis and alveolar bone resorption. Furthermore, gossypetin prevented the ligature-induced increase in macrophages and T cells and reduced the production of tumor necrosis factor-α and interleukin-6.
Taken together, these results show anti-osteoclastogenic and anti-inflammatory effects of gossypetin, suggesting the potential use of this natural compound in periodontitis.
The primary purpose of this two-arm, parallel design, randomized controlled study is to compare healing of the palatal tissue donor site when platelet-rich fibrin (PRF) is used as a wound dressing compared to the use of a hemostatic agent. Secondary outcomes of patient pain perception and analgesic intake were also evaluated.
Seventy-four patients receiving free gingival grafts were randomized to receive either PRF (test) or hemostatic agent (control) as a palatal wound dressing by patients selecting a sealed envelope containing their group assignment (initially 37 envelopes for PRF group and 37 for hemostatic agent group). Patient pain assessment and analgesic consumption were documented using a 21-point numerical scale (NMRS-21) at 24, 48, and 72 hours post-surgery. At 1-, 2-, 3-, and 4-week follow-up appointments palatal early healing index (PEHI) scores including wound color, epithelialization, presence or absence of swelling, granulation tissue, and bleeding on gentle palpation were generated by direct intraoral examination by a blinded examiner unaware of the patients’ treatment group.
NMRS-21 pain scores showed a significant reduction in pain over time in both groups, with no significant difference between groups at any time point. No significant between-group difference was found in the amount of analgesics taken by patients at 24, 48, and 72 hours. There was significant improvement in PEHI scores over the 4-week time period in both groups, but there was no significant difference in PEHI score at each time point (1, 2, 3, 4 weeks) between groups.
Study findings suggest that there is no difference in early palatal wound healing, patient pain perception, or analgesic consumption between use of PRF or a hemostatic agent as donor-site wound dressings.
Increasing evidence indicates that periodontitis contributes to systemic low-grade inflammation. Porphyromonas gingivalis is strongly associated with periodontitis, and antibodies against the bacterium may be used as a serological proxy to account for periodontal status, when studying diseases associated with periodontitis. The aim of the present study is to identify an easily accessible and reliable serological biomarker for determination of periodontal status and oral carriage of the bacterium.
Saliva and serum samples were collected from periodontally healthy controls (n = 27), and patients with periodontitis stage II (n = 12) or stages III or IV (n = 44). Serum levels of immunoglobulin G (IgG) antibodies against intact and fragmented P. gingivalis, recombinant gingipains (RgpA and RgpB), and the bacteria Escherichia coli and Capnocytophaga ochracea as controls were quantified with a multiplex bead-based assay. P. gingivalis was identified in saliva using quantitative polymerase chain reaction (qPCR).
Serum IgG antibodies against P. gingivalis whole bacteria were good indicators of periodontitis (area under the curve [AUC]: 0.75, 95% confidence interval [CI]: 0.64–0.85). The same was observed for levels of antibodies against P. gingivalis fragments (AUC: 0.78, 95% CI: 0.68–0.88). Likewise, levels of antibodies against P. gingivalis whole bacteria or P. gingivalis fragments were good indicators of oral carriage of P. gingivalis (AUC: 0.92, 95% CI: 0.86–0.98 and AUC: 0.96, 95% CI: 0.92–1, respectively). Conversely, antibodies against recombinant RgpA and RgpB were not good indicators of periodontitis or oral carriage of the bacterium. None of the antibody levels differed significantly between stage II and stage III or IV periodontitis.
Serum IgG antibody levels against heat-inactivated whole P. gingivalis proved to be the preferable biomarker for periodontitis and oral carriage of the bacterium.
To date, the clinical evidence regarding the effectiveness of alveolar ridge preservation (ARP) in restricting alveolar bone height and width change after extraction at periodontally compromised molar extraction sockets still remains controversial. This retrospective cohort study aims to evaluate the effect of ARP in molars extracted for periodontal reasons.
Retrospective data were collected from patient electronic records from January 2019 to December 2023. Patients with Stage III/IV periodontitis who underwent extraction of molars for periodontal reasons were screened for eligibility. The outcomes included the horizontal and vertical dimensions of alveolar bone. The need for additional augmentation procedure during implantation was also evaluated. A linear regression model was used to adjust for known confounders.
A total of 80 sockets were included in this study, of which 27 sockets received ARP therapy after extraction while 53 sockets experienced natural healing (NH). ARP resulted in significantly less bone height change in the periodontally compromised molar sites compared to the NH group (p < 0.001). In sockets displaying a height disparity of >2 mm between the buccal and palatal/lingual walls, the ARP group exhibited advantageous outcomes in terms of ridge width change, surpassing the NH group (p = 0.004). Moreover, the percentage for additional augmentation was significantly reduced in the ARP compared to the NH group (p = 0.006). Age, sex, smoking, jaw, location, and buccal wall thickness did not show any significant effect on bone height change.
ARP had benefits on limiting ridge resorption subsequent to molar extraction for periodontal reasons.
Implant surface decontamination is a critical step in peri-implantitis treatment. The aim of this study was to assess the effect chemotherapeutic agents have on reosseointegration after treatment on ligature-inducted peri-implantitis.
Six male canines had 36 implants placed and ligatures were placed around them for 28 weeks to establish peri-implantitis. The peri-implant defects were randomly treated by 1 of 3 methods: 0.12% chlorhexidine (CHX test group), 1.5% sodium hypochlorite (NaOCl test group), or saline (Control group). Sites treated with NaOCl and CHX were grafted with autogenous bone, and all sites then either received a collagen membrane or not. Histology sections were obtained at 6 months postsurgery to assess percentage of reosseointegration.
Thirty-five implants were analyzed (CHX: 13; NaOCl: 14; Control:8). NaOCl-treated sites demonstrated reosseointegration with direct bone-to-implant-contact on the previously contaminated surfaces (42% mean reosseointegration), which was significantly higher than Controls (p < 0.05). Correspondingly, clinical improvement was noted with a significant reduction in probing depth from 5.50 ± 1.24 mm at baseline to 4.46 ± 1.70 mm at 6-months postsurgery (p = 0.006). CHX-treated sites demonstrated a nonsignificant reosseointegration of 26% (p > 0.05); however, in the majority of cases, the new bone growth was at a distance from the implant surface without contact. Probing depths did not improve in the CHX group. The use of membrane did not influence reosseointegration or probing depths (all p > 0.05).
Titanium implants with peri-implantitis have the capacity to reosseointegrate following regenerative surgery. However, treatment response is contingent upon the chemotherapeutic agent selection. Additional chemical treatment with 1.5% NaOCl lead to the most favorable results in terms of changes in defect depth and percentage of reosseointegration as compared to CHX, which may hinder reosseointegration.
The purpose of this study was to conduct survival analysis of teeth following clinical crown lengthening procedures (CLPs) and crown insertions via a retrospective cohort study.
Patient- and tooth-related data were collected from 268 participants who received CLPs from 2009 to 2015. The Kaplan–Meier curve and the log-rank tests were used to estimate the probability of survival and compare the survival probabilities among different variables. A Cox multivariate proportional hazard regression model was used to investigate the collective effects of root canal treatment (RCT) and the types of opposing dentition.
The rate of tooth loss was 21.6% during the observation period from 1 to 14 years, with 58 teeth extracted. The most attributable reason for tooth extraction was coronal tooth fracture, followed by endodontic failure such as root fracture. The survival probability was 0.87 at 5 years and 0.7 at 10 years. No significant differences in the survival probabilities were found among different providers and locations, the presence of a post, and the types of crowns. The hazard ratio for tooth loss was 6.3, 95% confidence interval (CI) [2.6 to 20.9] in the teeth with RCT (p < 0.001) and 2.4, 95% CI [1.1 to 4.8] in the teeth occluding implant-retained prostheses (p = 0.016).
Tooth loss following CLPs and crown insertions appeared least among the teeth without RCT when occluding natural teeth, while tooth loss was most among the teeth with RCT when occluding implants.
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