Gingival recession development in orthodontic patients: studies on gingival phenotype diagnostics, local and systemic biomarkers, and the impact of orthodontic treatment on gingival recession development

Gingival recession refers to the apical displacement of the gingival margin from the cemento-enamel junction, resulting in exposure of the root of the tooth. Recessions can be localized, involving a single surface and tooth or may involve more tooth surfaces and/or teeth. Exposure of the root surface often causes a esthetic concerns, dentin hypersensitivity and increased susceptibility to root caries. Gingival recessions have been found to be more frequent in mandibular than maxillary teeth, and on buccal than lingual surfaces, especially within creasing age and have been found in persons with both good and poor oral hygiene. Several factors are associated with the etiology of gingival recessions; these are often categorized in predisposing and causative factors. A possible etiological factor for gingival recession is orthodontic tooth movement. The precise mechanism, nevertheless, by which orthodontic treatment influences the occurrence of recessions remains unclear, since bone dehiscence development during orthodontic treatment, per se, does not always lead to recession. It has been, therefore, assumed that the presence of a bone dehiscence before the beginning of orthodontic therapy is a prerequisite for the development of gingival recession. The retrospective and uncontrolled design of the available studies up to date, have not yet allowed the elucidation of the treatment- or patient- related risk factors for the development of gingival recession. The overall aims of this thesis were: • to determine whether or not orthodontic treatment is associated with the development of gingival recession and to quantify its magnitude and significance. • to document possible periodontal and systemic factors that are linked with gingival recession before, during or after orthodontic therapy. This thesis is based on 6 studies: • Paper I was designed as a cross-sectional study to determine accuracy and reproducibility of four different methods for assessing gingival thickness. • Paper II comprised an ex-vivo study assessing how well transgingival probing represents the true value of soft tissue thickness. The aim of this study was to assess differences and variation in gingival thickness when measured with transgingival probing or scanned with an intraoral device in porcine cadavers. • Paper III evaluated in a prospective manner if bone remodeling can befollowed through the bone turnover markers (BTMs) in orthodontic patients. Aim was to record the fluctuation of an osteoclastic and an osteoblastic BTM [C-terminal telopeptide of type I collagen (CTX) and N-terminal pro-peptide of type I pro-collagen (PINP), respectively] in both the gingival crevicular fluid (GCF) and the serum of orthodontic patients before and after the initial application of orthodontic forces. • Paper IV assessed in a prospective process the impact of fixed orthodontic appliances on blood Count and High-Sensitivity C-Reactive Protein Levels. Aim was to elucidate the magnitude of alterations in systemic blood counts in healthy individuals and identify possible inflammation status during the first period after fixed orthodontic appliance placement. • Paper V was a prospective controlled study aimed to assess whether incisor inclination change during orthodontic treatment with fixed appliances affects gingival thickness and the width of keratinized gingiva at mandibular incisors, compared with an untreated group of participants. • Paper VI was a prospective controlled study to assess whether orthodontic treatment with fixed appliances, compared to no treatment, has an effect on the development of gingival recession up to one year after treatment. The following conclusions were drawn: Paper I• The results demonstrated the differences between the tested methods (a.transgingival probing with a standard periodontal probe, b. transgingival probing with a stainless-steel acupuncture needle, c. ultrasound and d. color-coded periodontal probe), as far as accuracy and reproducibility were concerned. • Based on the reproducibility, the transgingival probing with the periodontal probe as well as the ultrasound determination seem to present an adequate choice for everyday practice. Paper II • Transgingival probing with a standard metal periodontal probe for assessing gingival thickness is a reliable method, with values very close to the true gingival thickness, and it can thus be considered as the clinical gold standard. Paper III • This was the first time PINP and CTX have been evaluated in the GCF and serum of orthodontic patients with fixed appliances. • No statistically significant alterations of CTX and PINP levels in the GCF and the serum of patients were recorded over time during the initial stages of orthodontic treatment. Paper IV • Orthodontic fixed appliances led to a limited and transient change in WBC and Hb levels during the first days after bracket placement. • The fluctuation of hs-CRP levels was not significant, demonstrating a lack of association between systemic inflammation and orthodontic treatment. Paper V • Mandibular incisor proclination during orthodontic treatment does not appear to significantly alter gingival thickness and width of keratinized gingiva, but orthodontic treatment, overall, leads to reduction of the width of keratinized gingiva. • Whether this limited reduction of width of keratinized gingiva during orthodontic therapy has an impact on the development of gingival recessions, especially on the long-term, still remains to be elucidated Paper VI • Evolution of recessions varied during orthodontic treatment: in some patients recession developed over time, but in several cases orthodontic treatment resulted in a reduction in the number of gingival recessions. The most affected teeth were the canines and the first premolars. • Orthodontic therapy exerted a negative impact on the development of gingival recession at 1-year posttreatment. The adjusted incidence rate was 67% higher for the intervention group versus the control; however, the severity was limited since most recessions were up to 1mm. • A long-term follow-up (5 years or more) after orthodontic treatment is necessary to provide data on whether orthodontic treatment is a major risk factor for the development of gingival recession. Key Conclusions and Clinical Implications • Transgingival probing with the periodontal probe as well as the ultrasound determination present an adequate choice for gingival thickness evaluation. • No statistically significant alterations of CTX and PINP levels in the gingival crevicular fluid and the blood serum of patients were recorded over time during the initial stages of orthodontic treatment. Moreover, a lack of association between systemic inflammation and orthodontic treatment during the first days after bracket placement was demonstrated. • Mandibular incisor proclination during orthodontic treatment does not appear to significantly alter gingival thickness and width of keratinized gingiva, but orthodontic treatment, overall, may lead to reduction of the width of keratinized gingiva. • Evolution of recessions varied during orthodontic treatment: in some patients recessions developed over time, but in several cases orthodontic treatment resulted in a reduction in the number of gingival recessions. The most affected teeth were the canines and the first premolars. • Orthodontic therapy exerted a negative impact on the development of gingival recession at 1-year post treatment. The adjusted incidence rate was 67% higher for the intervention group versus the control; however, the severity was limited, since most recessions were up to 1mm. • A detailed 3D analysis of the movement of the involved teeth presenting recession after orthodontic movement could provide further insights on the effect of orthodontic tooth movement on the development of gingival recession. • A long-term evaluation will show whether orthodontic treatment is a major factor for the development of gingival recession.