Implant soft tissue dehiscences compromise not only the aesthetics of the supported restorations but implant survival in the long run. The aim of this narrative review was to briefly present the causative factors of buccal peri-implant soft tissue dehiscences (PSTDs), how these are classified, and the current therapeutic approaches. Implant malposition and the thin peri-implant phenotype are the two major determinants for the occurrence of PSTDs, but other risk factors have also been identified. The most common surgical procedure for treating PSTDs is the split-thickness coronally advanced flap combined with either a connective tissue graft or acellular dermal matrix materials. However, depending on the class and subtype of the dehiscence, the combination of surgical techniques with modifications in the restoration may further ameliorate the final result. In general, within a five-year follow-up period, most techniques lead to a satisfactory aesthetic result, although full coverage of the implant/abutment surface is not always achievable, especially in more extended lesions.

Periodontal disease (PD) is a chronic inflammatory oral condition with potentially important systemic sequelae. We sought to determine whether the presence of PD in patients with severe carotid disease was associated with morphological features consistent with carotid plaque instability. A total of 52 dentate patients hospitalized for carotid endarterectomy (CEA) had standardized assessments of their periodontal status, including measurements of probing pocket depth (PPD), clinical attachment level (CAL) and bleeding on probing (BoP). Carotid plaque morphology was assessed by ultrasound using the gray scale median (GSM) score and by immunohistochemistry using anti-CD68 and anti-alpha-actin antibodies, markers for macrophages and smooth muscle cells (SMCs) respectively. In total 30/52 patients (58%) had PD. Significant associations were noted between low GSM on ultrasound and each mm in PPD (p = 0.001), each mm in CAL (p = 0.002) and with a 10% increase in BoP (p = 0.009). Using the standardized PERIO definition the association remained robust (aOR = 10.4 [95% CI:2.3–46.3], p = .002). Significant associations were also observed with high macrophage accumulation and each individual PD measure (p < 0.01 for PPD, CAL and BoP) and with the PERIO definition (aOR = 15 [95% CI:1.8–127.8], p = .01). Similarly, low SMC density was also significantly associated with individual measures of PD (p < 0.05 for PPD, CAL and BoP), but not with the PERIO definition (aOR 3.4 [95% CI:0.9–12.8], p = .07). The presence of PD was significantly associated with both ultrasound and immunohistochemistry features of carotid plaque instability in patients undergoing CEA.

During the last few decades there has been a growing interest in understanding the involvement of epigenetics in the pathogenesis and treatment of periodontal disease. Noncoding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), may serve as epigenetic modifiers affecting the expression of genes involved in the pathogenesis of inflammatory and autoimmune diseases. There is increasing evidence supporting the idea that the function of all three types of ncRNAs seems to be interdependent. LncRNAs can act as miRNA decoys, while circRNAs can act as miRNA sponges, leading to the re-expression of miRNA target genes. The purpose of this review is to evaluate the expression patterns of ncRNAs in periodontal disease. Studies demonstrate a positive correlation between miRNA expression and periodontitis; however, this cannot be claimed for lncRNAs and circRNAs, which appear to be differentially expressed in periodontitis patients. Several studies have also suggested utilizing ncRNAs as diagnostic and prognostic biomarkers in periodontitis, or even as potential therapeutic targets; Nevetheless, the evidence to support this is premature. Future well-designed research remains necessary to establish the functional role of ncRNAs in the evolution and progression of periodontal disease.

Oxidative stress plays a significant role in the pathophysiology of periodontal disease (PD). Therefore, it is reasonable to suggest that a diet rich in antioxidants, such as several vitamins and essential minerals, may positively affect periodontal health. However, the evidence from the relevant literature is yet inconclusive. Studies evaluating the levels of intake of nutritional antioxidants in relation to periodontal status demonstrate contradictory results. This inconsistency could be attributed to heterogeneity in study design and methodological limitations, such as the small sample size, the assessment of periodontal status based on partial mouth measurements that usually underestimate the actual severity of PD, the lack of adjustment for confounders, which may obscure any potential but weak effect of nutrition, and the use of a 24 h recall to assess nutrient intake. Regarding the intervention studies that evaluated the effect of nutritional antioxidant supplementation as an adjunct to periodontal therapy, again, the results are not consistent. Few studies are randomized, and often different nutritional supplements are combined, making it difficult to distinguish the actual effect of each nutrient. Moreover, the dosage and duration of use of these supplements vary, rendering comparisons impossible. Therefore, better designed studies are necessary for the future. The assessment methods used for both PD and vitamin/mineral intake need to be more accurate and standardized to improve comparability. Also, prospective longitudinal and randomized controlled studies are important to establish the optimal dosing and the long-term effects of vitamin/mineral supplementation on periodontal health in different patient populations.

Periodontal diseases, including both gingivitis and periodontitis, occur commonly among pregnant individuals. Both gingivitis and periodontitis are associated with adverse pregnancy outcomes (APOs) such as early pregnancy loss, preterm birth, preeclampsia, low birth weight, and stillbirth. This review highlights that the strongest mechanistic evidence linking periodontal diseases with APOs involves the domains of systemic inflammation, including increased pro‐inflammatory cytokines and activation of matrix metalloproteases associated with preterm labor, and microbial translocation involving hematogenous dissemination of periodontopathic bacteria to the fetoplacental unit. Yet, other mechanistic domains remain underexplored, including maladaptive myelopoiesis with alterations of neutrophil activity, immune player trafficking with autoantibody development, masticatory dysfunction‐diet interactions that may further increase risk of critical vitamin and nutritional deficiencies related to both periodontitis and APOs, and functional dysregulation of the oral microbiome including generation of nitric oxide that could impact pregnancy outcomes. Additionally, specific underlying vulnerabilities unique to pregnancy such as increased hormone production such as progesterone and cortisol likely impact the risk of periodontal diseases in pregnancy. By delving into these critical mechanistic domains, this review reveals both current understanding and critical areas for future research to overcome deficits in knowledge pertaining to how periodontal diseases in pregnancy lead to APOs. Elucidating these novel insights can promote scientific advancement, facilitate the development of novel interventions that prevent and/or treat periodontal diseases in pregnancy, and concurrently improve the lives and well‐being of pregnant individuals and their children worldwide.