The sample consisted of 13 women (93%) and 1 man (7%). The tooth that presented most biologic width invasion was the first molar, in both groups. It were evaluated 122 sites, being 30 mesial (49%) and 31 distal (51%) sites in test group, and 29 mesial (47.5%) and 32 distal (52.5%) sites in the control group (Table
1). Gingival recession was observed in 18 teeth in test group and in 5 teeth in control group.
Table 1Prevalence of biologic width invasion, according to teeth, to dental site and to the group
Tooth |
First Molar | 19 | 31.1 | 18 | 29.5 |
Second Molar | 8 | 13.1 | 11 | 18.0 |
First Pre-molar | 11 | 18.0 | 10 | 16.4 |
Second Pre-molar | 18 | 29.5 | 16 | 26.2 |
Canine | 3 | 4.9 | 4 | 6.6 |
Incisor | 2 | 3.3 | 2 | 3.3 |
Site |
Mesial | 30 | 49.2 | 29 | 47.5 |
Distal | 31 | 50.8 | 32 | 52.5 |
Table
2 shows the descriptive statistics for test and control groups. A statistically significant difference was observed between bone crest level (
p < 0.001), bone defect level (
p = 0,005), vertical (
p < 0.001) and horizontal components (
p = 0.001).
Table 2Average of the parameters related to the sites probed
Probing depth | 2.5 | 1.4 | 2.1 | 1.1 | 0.080 |
Clinical attachment level | 2.7 | 1.4 | 2.3 | 1.3 | 0.095 |
Height of gingival recession | 2.3 | 1.0 | 2.3 | 0.6 | 0.655 |
Width of gingival recession | 4.0 | 1.6 | 2.7 | 1.3 | 0.180 |
Keratinized gingiva height | 3.2 | 1.7 | 2.7 | 0.6 | 0.089 |
Keratinized gingiva thickness | 1.4 | 0.4 | 1.4 | 0.6 | 0.691 |
Level of bone defect | 0.9 | 1.3 | 0.2 | 0.9 | 0.005 |
Bone crest level | 1.4 | 0.6 | 2.4 | 1.2 | < 0.001 |
Intrabony component | 0.6 | 0.7 | 0.1 | 0.2 | < 0.001 |
Horizontal component | 0.3 | 0.5 | 0.1 | 0.2 | 0.001 |
The correlation between the clinical and radiographic parameters of the test group is observed in Table
3. In test group, it was observed a statistically significant correlation between BOP with the intraosseous component (
p < 0.001) (
r = 0.618), and GRW with the intraosseous component (
p = 0.030) (
r = − 0.602); and, between the KGH and the bone level (
p = 0.037) (
r = − 0.267). In the control group, the correlation occurred between PI and BCL (
p = 0.027) (
r = − 0.283); and between KGT and BCL (
p = 0.034) (
r = − 0.273) and also of the intraosseous component (
p = 0.042) (
r = 0.226), (Table
4).
Table 3Correlation of clinical and radiographic findings for test group
Plaque index | 0.025 | 0.850 | 0.184 | 0.156 | 0.032 | 0.845 | 0.062 | 0.635 |
Bleeding on probing | −0.013 | 0.919 | −0.012 | 0.929 | 0.618 | < 0.001 | 0.001 | 0.991 |
Probing depth | −0.010 | 0.940 | −0.035 | 0.788 | −0.037 | 0.821 | 0.033 | 0.802 |
Clinical attachment level | 0.131 | 0.315 | −0.084 | 0.519 | 0.294 | 0.069 | 0.128 | 0.325 |
Height of gingival recession | 0.271 | 0.277 | −0.104 | 0.682 | 0.355 | 0.234 | 0.420 | 0.083 |
Width of gingival revession | −0.127 | 0.616 | 0.292 | 0.240 | −0.602 | 0.030 | −0.266 | 0.287 |
Keratinized gingiva height | −0.267 | 0.037 | −0.069 | 0.595 | 0.034 | 0.840 | −0.266 | 0.080 |
Keratinized gingiva thickness | −0.072 | 0.580 | 0.101 | 0.436 | −0.172 | 0.294 | −0.072 | 0.580 |
Table 4Correlation of clinical and radiographic findings for control group
Plaque index | 0.166 | 0.201 | −0.283 | 0.027 | 0.156 | 0.231 | 0.231 | 0.073 |
Bleeding on probing | −0.122 | 0.348 | −0.063 | 0.629 | −0.131 | 0.314 | −0.014 | 0.915 |
Probing depth | −0.107 | 0.411 | 0.222 | 0.086 | −0.123 | 0.343 | 0.100 | 0.444 |
Clinical attachment level | −0.126 | 0.333 | 0.233 | 0.071 | −0.141 | 0.277 | 0,075 | 0.564 |
Keratinized gingiva height | −0.065 | 0.620 | 0.088 | 0.498 | −0.080 | 0.541 | 0.101 | 0.438 |
Keratinized gingiva thickness | 0.247 | 0.055 | −0.273 | 0.034 | 0.262 | 0.042 | 0.052 | 0.688 |
Discussion
Periodontal health is a basic requirement for both the longevity of restoration and the aesthetics, as well as, function and maintenance of dentition. However, dental restorations presenting width invasion are a frequently problem in clinical practice and are capable of inducing gingival inflammation, loss of connective tissue and unpredictable bone loss [
19,
20]. Also, the invasion of the biologic width may cause periodontal pocket which does not imply the diagnosis of periodontal disease.
It was observed that the first molar, in the test and control groups, showed greater invasion of biological space. According to Vacek et al. [
5], there are variations in the dimensions of the supracrestal gingival tissue between teeth, as well as in their sites, with the average molar measurements being greater than in the other groups of teeth.
The gingival recession and inflammation were clinically observed in this study, in addition to the correlation between the presence of width invasion and the decrease in the level of the bone crest observed radiographically, these findings similar to those reported by Douglas-de-Oliveira et al. [
17].
The relationship between width invasion and bleeding on probing found in the literature and in the present study can be explained by the fact that the placement of restorative margins within the width space often leads to gingival inflammation, loss of clinical attachment and bone loss. This is probably due to the destructive inflammatory response of the microbial located deeper into the gingival sulcus. These alterations were justified by studies that evaluated the histological and clinical response of periodontal tissues to the position of the restoration margins within the biologic width [
21,
22].
In the present study, the negative correlation between keratinized tissue height and bone level was observed in the test group, which means that the higher the keratinized tissue, the lower the level of bone defect. In fact, according to Stetler and Bissada [
23], teeth with subgingival restorations and narrow keratinized gingiva have worse gingival inflammation compared to a wide range of keratinized tissue.
A negative correlation was found between plaque index and bone crest level in teeth with biologic width invasion in the control group. This can happen due to the biofilm retention in the rough surface areas of restoration that was brought into the gingival sulcus, where the patient is unable to properly cleaning his/her tooth, aggravating biofilm accumulation [
24]. Consequently, this condition could lead to progressive gingival inflammation followed by periodontal destruction with greater pocket depth, attachment loss and gingival recession, increasing vertical bone resorption and increasing the horizontal component [
17].
A negative correlation was also found between the thickness of the keratinized gingiva and the level of the bone crest in the control group. This result is in agreement with studies that evaluated gingival phenotype [
9] in which a greater distance from the supracrestal gingival tissue was found in thin phenotype compared to the thick phenotype.
Thus the use of radiographic data is important to diagnose the biologic width invasion. Interproximal radiographs are the most used one for this purpose, since it presents less distortion than the other techniques [
25]. In addition to this technique, a recent study [
26] has shown an innovative parallel-profile radiography technique for gauging the dimensions of biological space on the labial sites of anterior teeth.
In a patient with preserved biologic width, the measure up to the bone crest has an average of 3 mm [
12]. Furthermore, in the comparison between clinical and radiographic parameters in patients with invasion of the biologic width, association was observed between bleeding on probing, gingival recession and bone defects. This association was not found in the teeth of the control group, confirming the deleterious aspect of overlap restorations. These findings corroborate the concept that apically placed restorations within the supracrestal connective tissues may be harmful to periodontal health [
27,
28].