Many techniques have been developed over the years for managing gingival recession and preventing it from progressing. These techniques have been shown to be very successful (Chambrone et al. 2010), provided proper diagnosis has been made.
Proper diagnosis of a mucogingival deformity relies on clinical assessment of the recession present and soft tissue assessment, specifically the presence of ‘adequate’ zone of attached gingiva. Lang and Löe suggest in their classic paper from 1972, that a minimum of 2mm of attached gingiva is required to maintain periodontal health. The zone of attached gingiva can be calculated by subtracting the probing depth from the width of keratinized gingiva on the buccal of the tooth in question (Figure 1). Lack of adequate attached gingiva could lead to gingival inflammation ranging from rolled gingival margins to chronically edematous tissue manifesting in gingival bleeding and patient discomfort (Figure 2). Dorfman et al. in a series of publications from 1980-1985 studied a group of patients with bilateral areas of minimally attached gingiva. One side was treated with a free gingiva graft to increase the zone of attached gingiva, and the contralateral side was left untreated. A group of patients who did not present for routine dental care until the sixth year of follow up demonstrated increased recession in the untreated side. In variance, the patients who received regular dental care including scaling, and thus exhibited less gingival inflammation, did not demonstrate increased recession in the untreated side. These results suggest that the control of inflammation plays an important role in the prevention of gingival recession.
In addition to the surgical management of recession defects and lack of attached gingiva, it is important to identify and manage etiological factors. Improper tooth brushing techniques and high frequency of tooth brushing is implicated with the development and progression of gingival recession. This should be managed with oral hygiene instruction. Not all etiological factors can be managed, such as thin gingival biotype11 or severe crowding where the roots of the teeth extend through the buccal plate. Patients should be informed of all etiological factors, including those that pose risk for further progression of existing recession. Sites that are at high risk should be treated. Those at moderate risk should be assessed regularly and managed as the need develops.
One etiological factor that is poorly understood and described in the literature, perhaps due to the lack of accurate clinical methods for assessment, is the thickness of the buccal plate. There is strong evidence from the implant literature that the presence of thick buccal plate is crucial for preventing mid-buccal recession next to the implant restoration. Determining the thickness of the buccal plate next to an implant fixture is accomplished at the time of implant placement by inspection. We can even control the thickness of buccal plate by controlling the implant’s position and angulation. If required, bone grafting can increase the thickness of the buccal plate.
When assessing gingival recession around teeth, one should recognize that in some cases it is combined hard and soft tissue defect due to loss of the buccal plate adjacent to the exposed root. When extrapolating the implant literature to predict development and progression of recession around natural teeth, the thickness of the buccal plate should perhaps play a role, in addition to the presence of adequate attached gingiva and inflammation. This could also explain why recession does not always develop in areas with minimal attached gingiva. Such examples are the mandibular second and third molars where the buccal plate is thick due to the presence of the buccal shelf. Factors such as the position of the teeth in the alveolar trough and buccal tipping secondary to crowding could also compromise the thickness of the buccal plate, thus increasing the risk for recession developing.
Correcting gingival recession, similarly to preventing progression of recession, depends on proper diagnosis. Miller’s classification (Miller 1985) of gingival recession has been introduced in 1985, and is used to predict whether root coverage is possible. Class I Miller recession refers to recession defects that do not extend beyond the mucogingival junction (keratinized tissue is still present), and there is no loss of interproximal bone height. Class II Miller recession is similar, with the exception that the recession does extend beyond the mucogingival junction. 100% root coverage is possible with Miller I and II recession defects. Class III Miller recession defects extend beyond the mucogingival junction, and there is some loss of interproximal bone height. Only partial root coverage could be achieved in these type of recession. Class IV Miller recession is characterized by significant bone loss, and root coverage procedures are not indicated.
TREATMENT
Sullivan and Atkins (Sullivan and Atkins 1968) introduced the free gingival graft in 1968. The procedure involved preparing a periosteal bed by split thickness dissection extending apically from the mucogingival junction. The graft is harvested from the keratinized palatal tissue, and secured over the recipient site by means of multiple sutures. The periosteal bed has rich blood supply, enabling the grafted tissue to survive. Plasmic circulation is established in the early healing stages, allowing exchange of nutrients and waste products between the graft and the recipient site. The ingrowth of capillaries will ensure vitality of the graft. The free gingiva graft is still widely used today to augment the zone of attached gingiva in non-aesthetic areas and where root coverage is not planned (Figures 3-6).
Raetzke (Raetzke 1985), and in a separate publication in the same year, Langer and Langer (Langer and Langer 1985) described the free subepithelial connective tissue graft technique aiming at root coverage (Figures 7-10). Similarly to the free gingiva graft, a split thickness dissection is carried out to prepare a periosteal bed. The difference is that the split thickness dissection starts at the gingival margin, creating a supra-periosteal ‘pocket’. The donor connective tissue is harvested from the palate, with or without an epithelial collar depending in the harvesting technique used. Because this procedure is indicated primarily for root coverage, the exposed root must be scaled and root planed, followed by root conditioning, typically with tetracycline, in order to remove the smear layer and promote better attachment of the graft to the root surface. The connective tissue is secured over the root by sutures. Since the root is avascular, it is important that the donor tissue extends laterally and apically to lay over the periosteal bed. The mucosal flap is coronally positioned to either fully or partially cover the donor connective tissue. This ensures additional blood supply to the graft, which is particularly critical to the area of the donor tissue positioned over the exposed root. The flap should remain passive in its position, and is secured with sutures. As mentioned earlier, complete root coverage can be achieved in Miller I and II situations. It is important to note that this isn’t a regenerative procedure. Although seemingly the recession defect is covered and a band of keratinized tissue is restored, the buccal bone, periodontal ligament and cementum do not regenerate. The donor tissue establishes connective tissue attachment to the exposed root at the coronal portions and long junctional epithelium attachment at the apical segment.
CONCLUSION
The risk for gingival recession can be reduced by identifying and controlling associated risk factors, where possible. Behavioral risk factors can be addressed through patient education. Biological risk factors, such as minimally attached gingiva associated with gingival inflammation and hist
ory of recession can be managed surgically through a free gingival graft procedure to augment the attached gingiva. Many procedures have been developed for correcting gingival recession. The Miller classification is of great help in establishing the predictability of root coverage.OH
Dr. Shelemay maintains a private practice in Ottawa limited to periodontics and implant surgery. Dr. Shelemay is a Fellow of the Royal College of Dentists of Canada in Periodontology. He obtained his DDS from the University of Toronto in 1996, and subsequently completed a one year internship at Mount Sinai Hospital. Dr. Shelemay completed his MSc degree and specialty training in Periodontology at the University of Toronto in 2002. Dr. Shelemay can be reached at avishelemay@me.com.
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