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1.
Article in English | MEDLINE | ID: mdl-37655970

ABSTRACT

Mucogingival deformities around implants are frequent findings in clinical practice and often present as inadequate keratinized tissue and insufficient mucosal thickness. Phenotype modification therapy can increase peri-implant mucosal thickness and the amount of keratinized mucosa, improving the long-term clinical outcomes of implants. Free gingival graft (FGG) is considered the gold standard to increase keratinized mucosa; however, FGGs on lingual aspects of implants are less predictable due to technique sensitivity and often present with insufficient gain in tissue thickness ue to limited blood supply. The Semilunar Lingualized Apically Positioned Flap (SLAP) with subperiosteal tunnel connective tissue graft (CTG) can increase both peri-implant mucosal thickness and keratinized mucosal width circumferentially. SLAP consists of one full-thickness, semilunar incision within keratinized mucosa on the buccal, and two vertical releasing incisions mesial and distal of the implant, extending lingually into the alveolar mucosa. The tissue is apically positioned lingual to the implant, and sutured in place creating buccal space for CTG via buccal subperiosteal tunneling. SLAP is a minimally invasive and predictable approach in improving peri-implant mucosal phenotype. This case reports demonstrates gain in peri-implant mucosal thickness and the amount of keratinized mucosa over a 10-month period utilizing SLAP with subepithelial CTG.

2.
Front Immunol ; 12: 705206, 2021.
Article in English | MEDLINE | ID: mdl-34290715

ABSTRACT

Different body systems (epidermis, respiratory tract, cornea, oral cavity, and gastrointestinal tract) are in continuous direct contact with innocuous and/or potentially harmful external agents, exhibiting dynamic and highly selective interaction throughout the epithelia, which function as both a physical and chemical protective barrier. Resident immune cells in the epithelia are constantly challenged and must distinguish among antigens that must be either tolerated or those to which a response must be mounted for. When such a decision begins to take place in lymphoid foci and/or mucosa-associated lymphoid tissues, the epithelia network of immune surveillance actively dominates both oral and gastrointestinal compartments, which are thought to operate in the same immune continuum. However, anatomical variations clearly differentiate immune processes in both the mouth and gastrointestinal tract that demonstrate a wide array of independent immune responses. From single vs. multiple epithelia cell layers, widespread cell-to-cell junction types, microbial-associated recognition receptors, dendritic cell function as well as related signaling, the objective of this review is to specifically contrast the current knowledge of oral versus gut immune niches in the context of epithelia/lymphoid foci/MALT local immunity and systemic output. Related differences in 1) anatomy 2) cell-to-cell communication 3) antigen capture/processing/presentation 4) signaling in regulatory vs. proinflammatory responses and 5) systemic output consequences and its relations to disease pathogenesis are discussed.


Subject(s)
Allostasis , Homeostasis , Immunity, Mucosal/immunology , Immunologic Surveillance/immunology , Intestinal Mucosa/immunology , Mouth Mucosa/immunology , Adaptive Immunity , Animals , Antigen Presentation , Bacterial Translocation/immunology , Cell Adhesion Molecules/physiology , Cell Communication , Dendritic Cells/immunology , Dysbiosis/immunology , Epithelial Cells/immunology , Humans , Inflammation , Intercellular Junctions/physiology , Intestinal Mucosa/cytology , Microbiota , Mouth Mucosa/cytology , Mucus/physiology , Organ Specificity , Saliva/immunology , Signal Transduction
3.
Med Int (Lond) ; 1(2): 4, 2021.
Article in English | MEDLINE | ID: mdl-36699146

ABSTRACT

The effect of weight loss on the periodontal condition remains unclear. The present prospective study thus aimed to evaluate the effect of weight loss on the periodontal status of 57 obese patients (BMI ≥30 kg/m2) with ages ranging from 18 to 60 years, at 12 months following bariatric surgery. Demographic, biological and behavioral variables were analyzed. All participants underwent a periodontal examination, including plaque index (PI), bleeding on probing (BOP), pocket depth (PD) and clinical attachment level (CAL). Anthropometric measurements, such as weight, height and body mass index (BMI) were calculated. Fisher's exact test, ANOVA, Bonferroni, Spearman's rank correlation and Wilcoxon signed-rank tests were used for the statistical analysis (P<0.05). Prior to surgery, 49% of patients were classified as having obesity class I, 33% as obesity class II and 18% as obesity class III. Variables, such as BMI and PD exhibited statistically significant differences among the obesity class I, II and III groups (P<0.05). As regards periodontal diagnosis, 37% of patients were classified as having gingivitis, 46% as having periodontitis stages I-II, and 17% as having periodontitis stages III-IV. BMI, PI, BOP and PD exhibited statistically significant differences following bariatric surgery (P<0.0001). No statistically significant differences were observed in the CAL (P>0.05). Thus, the findings of the present study suggest that weight loss was associated with decreased periodontal inflammation and an improved plaque control following bariatric surgery. CAL remained unaltered during the study period.

4.
Front Immunol ; 11: 591255, 2020.
Article in English | MEDLINE | ID: mdl-33363538

ABSTRACT

The current paradigm of onset and progression of periodontitis includes oral dysbiosis directed by inflammophilic bacteria, leading to altered resolution of inflammation and lack of regulation of the inflammatory responses. In the construction of explanatory models of the etiopathogenesis of periodontal disease, autoimmune mechanisms were among the first to be explored and historically, for more than five decades, they have been described in an isolated manner as part of the tissue damage process observed in periodontitis, however direct participation of these mechanisms in the tissue damage is still controversial. Autoimmunity is affected by genetic and environmental factors, leading to an imbalance between the effector and regulatory responses, mostly associated with failed resolution mechanisms. However, dysbiosis/infection and chronic inflammation could trigger autoimmunity by several mechanisms including bystander activation, dysregulation of toll-like receptors, amplification of autoimmunity by cytokines, epitope spreading, autoantigens complementarity, autoantigens overproduction, microbial translocation, molecular mimicry, superantigens, and activation or inhibition of receptors related to autoimmunity by microorganisms. Even though autoreactivity in periodontitis is biologically plausible, the associated mechanisms could be related to non-pathologic responses which could even explain non-recognized physiological functions. In this review we shall discuss from a descriptive point of view, the autoimmune mechanisms related to periodontitis physio-pathogenesis and the participation of oral dysbiosis on local periodontal autoimmune responses as well as on different systemic inflammatory diseases.


Subject(s)
Autoimmunity , Dysbiosis/immunology , Host-Pathogen Interactions/immunology , Microbiota/immunology , Animals , Autoantibodies/immunology , Autoantigens/immunology , Autoimmune Diseases/etiology , Autoimmune Diseases/metabolism , Biomarkers , Cytokines/metabolism , Disease Susceptibility , Epigenesis, Genetic , Epitopes/immunology , Humans , Periodontitis/etiology , Periodontitis/metabolism , Porphyromonas gingivalis/immunology , Receptors, Immunologic/metabolism
5.
J Med Life ; 13(4): 629-634, 2020.
Article in English | MEDLINE | ID: mdl-33456615

ABSTRACT

This case report describes the diagnosis, multidisciplinary treatment, and long-term follow-up of a severely compromised tooth in a patient who was referred for assessing a gingival recession. Clinical evaluation of the left maxillary canine showed 12 mm of mid-buccal gingival recession, probing depth of 14 mm on the mesial-buccal aspect, and grade III mobility. A periapical radiograph revealed extensive periapical and lateral radiolucency. The first step of the treatment was to carry out oral hygiene instructions and full-mouth debridement. After that, endodontic treatment was performed immediately. Periodontal reevaluation four months after endodontic therapy revealed that probing depths of all sites were within 3 mm and periapical radiograph showed a slight decrease in periapical and lateral radiolucency. It was subsequently decided to perform root coverage with a laterally positioned flap and subepithelial connective tissue graft. Six months after surgery, the root surface showed 1 mm recession, representing root coverage of 91.7% and a gain of attachment of 13 mm. The patient was enrolled in a 6-month supportive periodontal therapy. Treatment outcomes were evaluated over 18 years, with successful radiographic and clinical results throughout the follow-up period. The successful management of endo-periodontal lesions requires an accurate diagnosis, which is imperative to provide proper therapy in the correct treatment sequence.


Subject(s)
Endodontics , Patient Care Team , Periodontal Diseases/pathology , Female , Follow-Up Studies , Gingival Recession/diagnostic imaging , Gingival Recession/pathology , Gingival Recession/surgery , Humans , Male , Middle Aged , Periodontal Diseases/diagnostic imaging , Surgical Flaps , Sutures , Tooth/diagnostic imaging , Tooth/pathology , Tooth/surgery , Treatment Outcome
6.
Br Dent J ; 227(3): 235-239, 2019 Aug.
Article in English | MEDLINE | ID: mdl-31399683

ABSTRACT

Obesity and periodontitis are among the most common non-communicable diseases, and epidemiological studies report the influence of obesity in the onset and progression of periodontitis. Data indicate that increased body mass index, waist circumference, percentage of subcutaneous body fat, and serum lipid levels are associated with increased risk to develop periodontitis. The underlying biological mechanisms of this association involve adipose tissue-derived cytokines, such as tumour necrosis factor-α and interleukin-6, which affect whole-body metabolism and contribute to the development of a low-grade systemic inflammation. Multiple studies report a positive association between these two diseases across diverse populations. Obesity does not appear to impair the success of periodontal therapy. However, currently available evidence is variable and therefore inconclusive. Despite the limited evidence about recommendations on treatment planning, oral healthcare professionals need to be aware of the complexity of obesity to counsel their patients about the importance of maintaining healthy body weight and performing good oral hygiene procedures.


Subject(s)
Obesity , Periodontitis , Body Mass Index , Body Weight , Humans , Waist Circumference
7.
J Periodontol ; 87(11): 1320-1332, 2016 Nov.
Article in English | MEDLINE | ID: mdl-27498712

ABSTRACT

BACKGROUND: The aim of this systematic review is to evaluate whether use of local or systemic antimicrobials would improve clinical results of non-surgical periodontal therapy for smokers with chronic periodontitis (CP). METHODS: Medical Literature Analysis and Retrieval System Online, Excerpta Medica Database, and The Cochrane Central Register of Controlled Trials were searched up to and including March 2016. Randomized clinical trials of duration of at least 6 months were included if they reported on treatment of smokers (≥10 cigarettes per day for minimum 12 months) with CP with non-surgical periodontal therapy either alone or associated with local or systemic antimicrobials. Random-effects meta-analyses were undertaken to evaluate mean differences in probing depth (PD) and clinical attachment level (CAL). RESULTS: Of 108 potentially eligible articles, seven were included. Most individual studies (75%) testing locally delivered antibiotics reported that smokers benefited from this treatment approach. Pooled estimates found additional PD reduction of 0.81 mm (P = 0.01) and CAL gain of 0.91 mm (P = 0.01) at sites with baseline PD ≥5 mm. Conversely, meta-analysis on systemic use of antimicrobials failed to detect significant differences in mean changes from baseline, and only one trial supported their use. CONCLUSIONS: In smokers with CP, adjunctive use of local antimicrobials improved efficacy of non-surgical periodontal therapy in reducing PD and improving CAL at sites presenting PD ≥5 mm before treatment. Current evidence does not demonstrate similar gains when scaling and root planing plus systemic antimicrobial/antibiotics were associated with therapy.


Subject(s)
Anti-Infective Agents/therapeutic use , Chronic Periodontitis/drug therapy , Dental Scaling , Smokers , Anti-Bacterial Agents , Follow-Up Studies , Humans , Periodontal Attachment Loss , Randomized Controlled Trials as Topic , Root Planing
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