Article in Compendium of continuing education in dentistry (Jamesburg, N. J.: 995) · October 2011 Source: PubMed citations 46 reads 3,359 authors: Some of the authors of this publication are also working on these related projects
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| Probing Depths
Most studies concluded that a lack of KG was not associated with increased probing depths (Table 2) 4,11,51
; however, one study re- ported contradictory data. 53
Several clinical trials concluded that the absence of KG was asso- ciated with a statistically significant increase in bone loss (Table 2) 4,41,51 or attachment loss 53 when sites with and without KG were compared, but others did not corroborate this finding. 11,55
The study by Chung et al 11 also noted that there was no association between bone loss and absence of KG and these data pertain to different implant surface configurations (eg, smooth, textured). Several other factors need to be considered when interpreting these data. It should be noted that the mean differences between control and test groups with respect to bone loss reported by Kim et al
51 and Bouri et al 4 were only 0.34 mm 51 and 0.28 mm, 4 respec-
tively. Furthermore, in all of the previous studies, assessments of bone loss were done on nonstandardized radiographs and the data tabLe 2 Statistically Significant differences in Humans: Amount of Keratinized Tissue Related to clinical parameters in the presence of < 2 mm vs. ≥ 2 mm of Keratinized Gingiva study N pi
gi pocket
bOp recession bone Length
(# implants)
Depth
(%) (mm)
loss (mm) Bouri et al 4
1.8 vs. 1.3* 1.5 vs. 0.91* ns 89 vs. 71* - 1.72 vs. 1.24* 4.1-4.9 yrs. Kim et al 51
100 (276) ns
ns ns
- 0.72 vs. 0.32* 0.65 vs. 0.41* 13 m Wennström et al 20 39 (171) NMD NMD
NMD NMD
- - 5 yrs. Chung et al 11
69 (339) 1.51 vs. 1.26* 0.94 vs. 0.76* ns ns
- ns
3 yrs. Bengazzi et al 54
- - - - ns
ns 2 yrs.
Zigdon et al 53
32 (63) - - 3.2 vs. 2.6* 0.36 vs. 0.23†* 0.90 vs. 0.27* 3.3 vs. 2.6‡* 3.52 m < 1 mm vs. ≥ 1 mm Schrott et al 50
58 (307) 0.24 vs. 0.25B - - 0.05 vs. 0.07B 0.69 vs. 0.08B* - 5 yrs.
0.67 vs. 0.40L*
0.22 vs. 0.13L* N = number of patients; PI = plaque index; GI = gingival index; BOP = bleeding upon probing; * = statistically significantly different; ns = not significant; - = not reported; NMD = no major differences-multiple regression analysis; † = bleeding scored 0 for absence and 1 for presence; ‡ = attachment loss, bone loss not recorded; B = buccal; L = lingual continuing education 2
between clinical parameters and absence/presence of KG, a pos- sible explanation for inconsistency in the literature is that with good oral hygiene, peri-implant soft-tissue health can usually be maintained if keratinized tissue surrounding implant/restoration is absent. 5 However, if there is less than good oral hygiene, it may be advantageous to have KG. 5 Use of the “good hygiene” criterion is complicated by the fact that defining a threshold that would be considered less than “good hygiene” is problematic. After reviewing the literature, Yeung 5 suggested that a case could be made for augmenting keratinized tissue around implants to facilitate plaque control by reducing mobile mucosal tissue. To bolster this contention, he referred to a consensus of opinions ex- pressed by authors who participated in a debate as to whether KG was needed around implants. The authors supported the practice of augmenting keratinized tissue around implant restorations when practical to minimize complications. 71 In contrast, Esposito et al 72 concluded in a systematic review that there was insufficient evidence to recommend increasing KG to maintain peri-implant health. Since publication of that systematic review several clinical trials were published. 4,11,50,51,53 They provided mixed results with respect to the necessity of augmenting keratinized tissue when comparing studies, and within the same investigation the absence of KG may or may not have an effect on certain clinical param- eters. Perplexingly, the data can be interpreted opposite ways. It could be concluded that a strong case cannot be made for routine augmentation of keratinized tissue around dental implants when there is dearth of KG, because there is inconsistency between studies to indicate that it is detrimental to restore implants when there is a lack of KG. Furthermore, when there were differences in the response of clinical parameters at sites with or without KG, the mean differences were usually small. In contrast, it could be contended that recent investigations indicated additional bone 4,51
or attachment loss 53 was associated with a dearth of keratinized tissue. While the increased mean bone loss was usually small (Table 2), there may be sites where bone loss was substantial. However, frequency distributions were not provided; therefore, it is not possible to distinguish how often and to what extent this occurred or if the data was skewed by a few sites that had extensive bone loss. It could also be asserted that short-term data (Table 2) may not reflect the possibility that an inflamed site may continue to deteriorate and compromise a restoration. Apparently, for some patients a lack of KG may be a risk factor for one or more issues: plaque accumulation, tissue soreness while brushing, increased gin- gival inflammation, recession, and bone loss. In this regard, studies are needed to provide predictive values with respect to how often spe- cific types of biological problems occur when KG is lacking. Ultimately, when there is a lack of keratinized tissue, clinicians need to make and others where it is unnecessary, and this may vary in different patients and sites within the same mouth. However, defining spe- cific situations adjacent to implants (eg, clefting of gingiva, reces- sion, shallow vestibule, frenum pull) or for particular patients (eg, thick or thin biotypes) that may benefit from gingival augmenta- tion has never been investigated. Instead, studies consistently employed test and control groups with respect to either a dearth or an adequate band of KG. To provide a perspective as to what information can be derived from studies and clinical experience, the impact of a lack of keratinized tissue on peri-implant health is discussed from several points of view: periodontal response to plaque adjacent to crown margins on teeth and implants, overall statistical significance of study findings, and interpretation and practical application of data to patient management. In general, subgingival crown margins on teeth predispose pa- tients to increased plaque accumulation and greater amounts of gin- gival inflammation than teeth without crowns. 25,62-65 Hypothetically, the inflammatory reaction around implant restorations may be worse than around teeth, because tissues surrounding dental im- plants may be more susceptible to inflammation due to the altered structure of connective around an implant. 1,26,30 However, this hy- pothesis is based upon animal studies that assessed the peri-implant response when hygiene is ceased for months or if ligatures were placed. These artificially created situations can provide some proof of principle concepts, but these data cannot be directly extrapolated to patient management. Furthermore, it needs to be noted that indi- vidual thresholds of plaque necessary to trigger signs of disease may vary between patients. 66 Most importantly, investigators reported that the response of tissues to plaque in patients was similar around teeth and implants, 67,68 and tissue response around implants was not problematic even when there was dearth of KG. 20,51,52
Based on these studies and the above clinical trials relating the level of plaque to the amount of KG, it cannot be concluded that all patients are more prone to plaque accumulation due to a lack of KG. Assessment of the clinical trials relating clinical parameters to the amount of KG can provide a perspective concerning trends that have been observed. Inspection of data in Table 2 suggests that in some studies there is a tendency to find increased inflammation, recession, and bone loss associated with diminished amounts of keratinized tissue. However, it is important to note that statisti- cally significant findings only indicate that the event did not oc- cur by chance. It does not mean that the outcome was large or important. 69 Therefore, clinicians need to decide whether findings in Table 2 are clinically signifi- cant. Unfortunately, the definition of clinical significance varies depending on the following factors: specific clinical field being addressed, size of the effect, measurement used to evaluate a therapy, and, ultimately, the clinical importance of the findings. 70 With respect to the relationship reLateD cOntent:
Learn more about implants at dentalaegis.com/go/cced27 29 www.dentalaegis.com/cced October 2011 compendium a decision to augment or not to increase the band of KG at a site for that particular individual based on data in the literature, the patient’s dental history, the unique characteristics of the site being treated, and the clinician’s experiences. The literature does not clearly define a patient’s susceptibility to deterioration in the absence of KG; however, there are situations where it seems logical that augmentation of KG would be beneficial: • Chronically inflamed sites, despite oral hygiene instruction and periodontal therapy. Sometimes it is necessary to alter the gingival topography to make hygiene easier. • Locations with ongoing recession or continued loss of clinical attachment or bone, regardless of periodontal therapy and good oral hygiene. • Sites where the patient complains of soreness when brushing, despite the appearance of gingival health. • Dental history suggesting predisposition to periodontitis or recession. • Patients noncompliant with periodic professional maintenance. • To improve esthetics. abOut the authOrs Yüklə 0,61 Mb. Dostları ilə paylaş:
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