Drug-induced gingival enlargement

Introduction

Drug-induced gingival enlargement is classified by the American Academy of Periodontology as a dental plaque-induced gingival disease,  as evidence suggests that existing gingival inflammation may be necessary for its development and that proper plaque control and effective oral hygiene can lessen its severity or potentially prevent its occurrence altogether. 2 Currently, there are over 20 medications from three pharmaceutical categories including anticonvulsants, calcium channel blockers and immunosuppressants that are associated with gingival enlargement.4  It is the responsibility of the dental practitioner to recognize the potential of these medications to contribute to gingival enlargement and to provide the proper prophylactic care or appropriately refer the patient for periodontal therapy.  A team approach involving a consultation with a periodontist and the patient’s physician is a critical step in successful treatment.

Risk factors

During a course of treatment with a medication implicated in the pathogenesis of drug-induced gingival enlargement, poor plaque control is the most significant risk factor associated with its development.  The severity of enlargement is often proportional to the amount of gingival inflammation present and not the dosage of medication.  Overall, males tend to be affected three times as often as females and age is inversely correlated with likelihood of occurrence.

Medication

Prevalence of gingival enlargement with phenytoin (Dilantin®) use has been shown to be up to 50%, while other anticonvulsants such as valproic acid, Phenobarbital® and Tegretol® have been shown to be rarely associated with the disorder.  Of the calcium channel blockers, nifedipine (Adalat®, Procardia®) and diltiazem (Cardizem®) are the most likely to cause gingival enlargement (5-20%) while amlodipine (Lotrel®, Norvasc®), felodipine (Aggon®, Plendil®) and verapamil (Calan®, Covera®) are far less likely to be implicated.  Cyclosporin A, an immunosuppressant commonly used in organ transplant patients, has been shown to be associated in 25-30% of adult patients and over 70% in children, while tacrolimus has a significantly lower association at 14%.

Pathogenesis

While the physiology behind drug-induced gingival enlargement has not been definitively elucidated, histopathologic studies have shown that the gingival tissue volume increase is due to an excessive accumulation of extracellular matrix proteins including collagen and ground substance with a predominance of plasma cells.  Hence, the increase in tissue volume is primarily a connective tissue response and not epithelial.  Recent evidence suggests that this overgrowth could occur not from over-production of collagen, but rather through prolonged cell life of keratinocytes.  Another hypothesis is that fibroblasts in susceptible patients are sensitive to the medication in question, causing increased protein, and hence collagen, production.

Clinical presentation

Clinically, gingival enlargement frequently appears within 1-3 months of the initiation of treatment with the offending medication. The facial surfaces of the gingiva in anterior sextants are often most severely involved, and the patient may present with inflamed, fibrotic masses spreading from the interdental papillae to the attached gingiva that may interfere with mastication, speech and esthetics.  Due to discomfort secondary to inflammation and the physical topography of the enlarged gingiva, oral hygiene may be impaired and diet can be adversely affected.  This can lead to a host of other problems including caries, periodontal disease and immunosuppression secondary to malnutrition.

Treatment and prevention

Meticulous oral hygiene and plaque control combined with the removal of local factors are essential for any patient taking drugs associated with gingival enlargement.  A three-month periodontal maintenance interval is strongly recommended as well.  While excellent oral hygiene and professional plaque control can potentially prevent or lessen the severity of the condition, they often are insufficient for reversing the process once established.  It is therefore prudent to consult the patient’s physician to discuss potential drug substitutions that may result in regression of the lesions with proper supportive periodontal care and oral hygiene.  After drug substitution or withdrawal, evidence suggests that gingival lesions may resolve in 1-8 weeks in some patients.In transplant patients, however, drug substitution or cessation may not be an option due to the risk of transplant rejection.  Treatment of gingival enlargement in patients taking cyclosporin A should focus on their chronically immunosuppressed state.  In these patients, evidence suggests that topical antifungal treatment such as Nystatin lozenges, chlorhexidine rinses or a short course of azithromycin (3-5 days; 200-500 mg/day) can be effective.  There is evidence that systemic azithromycin remains effective in reducing gingival overgrowth from three months to two years after treatment, but this data is controversial.  A topical treatment including scaling and root planing in conjunction with an azithromycin-containing toothpaste used twice daily for one month has been shown to be effective in reducing gingival overgrowth as well, but the long-term efficacy of this treatment is unclear.

If the patient has gingival overgrowth and is currently taking:	Discuss the following substitution with the primary care provider:
Nifedipine (6-15%)	Isradipine, Amlodipine, Verapamil, Felodipine
Phenytoin (50%)	Carbamazepine, Valproic Acid, Vigabatrin, Phenobarbitone
Cyclosporin A (Adults 25-30%, Children >70%)	Tacrolimus

Note: incidence of gingival enlargement in parentheses.  Table adapted from Dongari-Bagtzoglou 2004.

While non-surgical therapy and, if possible, drug substitutions should be attempted first, surgery is often necessary to fully correct the esthetic and functional impairment encountered in this disorder.  Surgical excision has been successful in non-responding nifedipine cases when combined with good oral hygiene as well as in cases associated with verapamil and diltiazem, but it does tend to recur.A classic external bevel gingivectomy is an option to reduce redundant tissue.  An internal gingivectomy approach, however, has been advocated due to its ability to provide primary closure and reduce the incidence of postoperative bleeding, discomfort and infection.  Due to its technical difficulty, this procedure may be best referred to a periodontist.  Another surgical option is the CO₂ laser due to its decreased surgical time, rapid hemostasis and its compatibility with a host of underlying medical conditions.

Recurrence

Eighteen months after surgical therapy, the recurrence rate of gingival overgrowth in patients taking cyclosporin A or nifedipine was 34% in a study of 38 individuals.  Age, gingival inflammation and attendance at recall visits are all significantly related to recurrence.  To help prevent recurrence post-surgically, chlorhexidine rinse twice daily is recommended.

Conclusion

Drug-induced gingival enlargement is a common sequela to treatment with anticonvulsants, calcium channel blockers and immunosuppressants.  Evidence suggests that gingival inflammation is critical in its pathogenesis.  While it may be prevented through meticulous periodontal maintenance and home care, it is essential for the dentist to work together with the patient’s physician and periodontist in order to successfully treat this condition once it occurs.

Hand signs to commiunicate with the dentist during proceedure?

Most of the patients seeking dental treatments might be having a problem of how to communicate with the dentist during the dental procedure. That is because our main source of communication is verble communication which will be affected during dental procedure.
Here are some hand signs which you can use to communicate with the dentist during dental procedure. Please use these hand signals to communicate with the dentist during your dental procedure.

Dear Dentists, You can display this poster in your clinic in the waiting room.

How to Brush Your Teeth Properly

How to Brush your Teeth Properly Video

Efficacy of Root Planning

Definitions and Descriptions

Scaling: instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus and stains from these surfaces.

  

           Root Planing:

a) A treatment procedure designed to remove cementum or surface dentin that is rough, impregnated with calculus, or contaminated with toxins or microorganisms. (Amer. Acad. of Perio.)

b) A technique of instrumentation by which the “softened” cementum is removed and the root surface is made “hard” and “smooth” (Lindhe’s textbook)

c) American Academy of Periodontology Description:

    " Periodontal scaling is a treatment procedure necessary to remove hard and soft deposits from the tooth surface.  It is performed on patients with periodontal disease and is therapeutic, not prophylactic in nature.  Periodontal scaling may precede root planing.  Root planing is a meticulous treatment procedure designed to remove bacterial plaque and its toxins, calculus, and diseased cementum and dentin from the root surface.  The procedure may be a definitive treatment in some stages of periodontal disease, may be a part of pre-surgical procedures in others and an essential part of maintenance care.  Root planing is arduous and time consuming.  It may be done by quadrant(s) or full mouth (note: not allowed by insurance), may need to be repeated, and may require local anesthetic."

d) Root Preparation: Use of instruments or chemicals on root to eliminate irritants, prevent bacterial accumulation, and encourage wound healing.  (Amer. Acad. of Perio.)

e) Root Debridement:  The mechanical removal or disruption of

irritants to the periodontium: bacterial plaque, LPS (lipopolysacchirides), deposits and other plaque retentive factors to establish an environment favorable to the health of the periodontal tissues that will facilitate plaque control by the patient. The endpoint of debridement is recognizable by the color of the lavage and the feel of the tooth. Clinical endpoints are evaluated at various times post treatment. (Various sources)

Initial Therapy Procedures That Reduce Inflammation and Tooth Mobility  

            A). Periodontal

                        a) oral hygiene instructions

b) scaling and root planing

c) adult prophylaxis (scaling and tooth polish)

d) occlusal therapy

                                    1) occlusal adjustment

                                    2)  occlusal splints and bite planes.

            B)  Non-periodontal

                        a) removal of overhangs

b) caries control

c) extraction of hopeless teeth

d) provisional restorations

Biological Basis for Root Planing

A) The role of calculus and altered cementum

B)  Terms for periodontal healing:

a) Repair: Healing of a wound by tissue that does not fully restore the architecture or the function of the part.

b) Reattachment: To attach again. The reunion of connective tissue with a root surface on which viable periodontal tissue is present. Not to be confused with new attachment.

c) New attachment:

1) True new attachment: The reunion of connective tissue with a root surface that has been deprived of its periodontal ligament.  This reunion occurs by the formation of new cementum with inserting collagen fibers.

2) Long junctional epithelium (epithelial attachment): Adhesion of the junctional epithelium to a root surface that has been deprived of its periodontal ligament or connective tissue attachment.

d) Regeneration: Reproduction or reconstitution of a lost or injured part.

C) Objectives in root planing:

a)    restore gingival health by completely removing tooth surface factors that promote gingival inflammation

b)    make the root surface biologically acceptable to the soft tissues.

Limitations in root planing as part of non-surgical periodontal therapy.

Decision-Making Regarding Response to Initial Therapy

            A)  periodontal surgery

B) periodontal maintenance         

A)   initial therapy end point not reached

Summary of Recent Literature

PERIODONTAL SCALING AND ROOT PLANING

SUMMARY OF ISSUES CONTROVERSIES IN THE LITERATURE

In the past 30 years there have been numerous studies designed to test the effectiveness of scaling and root planing as a method of controlling periodontal diseases.  If there is one area in dentistry that is evidence based, it is periodontal instrumentation, because of the extensive studies and literature.  However, because many issues are controversial with support on each sides, conclusive evidence is lacking. Therefore, periodontal scaling and root planing remains as much an art as a science despite the literature.  Some of the important issues are listed below.  In the 1989 World Workshop in Clinical Periodontics, it was emphasized that in many of the studies, instrumentation was performed by experienced periodontists with unlimited time.  Extrapolation from carefully controlled experimental studies to real-life clinical situations should be done cautiously. 

Surgical Vs. Non-surgical Therapy

There is support that in non-surgical scaling and root planing the deeper the pocket is, the more difficult it becomes to instrument non-surgically.  Rabbini (1981) had results that “demonstrated a high correlation between percent of residual calculus and pocket depth”.  It was shown that pockets less than 3 mm were the easiest sites for scaling and root planing.  Pocket depths between 3 to 5 mm were more difficult to scale and pockets deeper than 5 mm were the most difficult.  Sherman  (1990) evaluated the ability of experienced clinicians to detect residual calculus following subgingival scaling and root planing.  She compared the clinical detection with the microscopic presence of calculus.  The results showed that "there was a high false negative response (77.4% of the surfaces with microscopic calculus were clinical scores as being free of calculus) and a low false positive response (11.8% of the surfaces microscopically free of calculus were clinically determined to have calculus)."  Her study indicates the difficulties in clinically determining the thoroughness of subgingival instrumentation.  Kepic (1990) found that complete removal of calculus from a periodontally diseased root, even with an open (surgical) approach is rare.  Rateitschak (1992) found that in non-surgical therapy, curettes could not reach the bottom of deep pockets.   It may be concluded from the above studies that in deeper sites, periodontal surgery may be required to gain direct access to the root surface for debridement. 

Ultrasonics Vs. Hand Instrumentation

    a. Calculus removal

Most studies have found both ultrasonic/sonic and hand instrumentation to be equally effective in calculus removal.  Gellin (1986) found that the combination of sonic instrumentation and hand instrumentation to be better than either method alone.

    b. Rough vs. smooth roots and cementum removal

There is little question that root surfaces which have become rough due to exposure to the oral environment and calculus promote bacterial adherence, increased surface area.  Several S.E.M. studies have shown that hand instrumentation is more effective than ultrasonics in cementum removal and may result in a smoother root, although a few studies show equal effectiveness.  Improperly used hand instruments, ultrasonics or rotary instruments may induce root surface roughness which may in themselves cause future periodontal problems.  It can be concluded that when root roughness is present, hand instruments are more effective in making a rough root smoother.  When improperly used, hand instruments or ultrasonic instruments may gouge the root surface.  When scaling and root planing is done as a closed procedure, the smoothness of the root is one of the best ways to determine if a suitable end point is being reached.   Quirynen and Bollen (1995) extensively reviewed the literature on rough roots and the relationship to adhesion and retention of oral microbes.  Most of the studies they reviewed show rough roots lead to high-energy surfaces, which collect and bind more bacteria.  

   c. Difficult to reach areas

O'Leary found the most difficult sites to instrument completely are furcations, grooves, CEJ's and line angles.  Ultrasonic instrumentation seems to be superior in accessing difficult to reach areas, especially furcations, although neither technique can completely remove calculus in this area.  The new modified ultrasonic  tip (e.g.: slimline® tips) has made deep pockets more accessible. 

   d. Resolving inflammation

Some studies have shown that ultrasonic and hand instruments are both equally effective in reducing inflammation.  Badersten (1983) when evaluating reduction of inflammation on single rooted found " no differences in results could be observed when comparing hand versus ultrasonic instrumentation".  She also found that there was no advantage to repeated root planing and that improvement occurred over a 9 month period of time.

   e. Overall conclusion on hand vs. ultrasonic instrumentation

There is evidence in the literature that it makes good clinical sense to use both types of instrumentation, whenever possible, because the two methods supplement each other.

Cementum Removal and Endotoxin (LPS)

Endotoxin is the potent inflammatory stimulator that is released by gram negative bacteria on cell death and thought to contribute to the progression of periodontal disease through its absorption into the root.  Jones and O'Leary (1978) showed that scaling diseased roots (without root planing) only partly reduced endotoxin but root planing "was able to render diseased root surfaces approximately as free of detectable endotoxin as were uninvolved, healthy root surfaces of unerupted teeth".  Nishimine and O'Leary 1979 found hand instruments to be more effective than ultrasonics in removing endotoxin in vivo. Several recent studies have shown that ultrasonic instrumentation is effective at removing adsorbed endotoxins, but these studies are in vitro.   There is clinical support for the removal of some of the cementum but not to the extent of removing all of the cementum.  Endotoxin, originally believed to require extensive instrumentation to be removed from the root surface, is now believed to be more weakly adherent than originally believed.  Several more recent studies have shown that ultrasonics is quite effective in removing cementum bound endotoxins.  Nyman (1988) compared scaling and root planing with scaling and polish (without cementum removal) and found the same degree of improvement following periodontal surgery.   It may be concluded that it is clinically sound to remove enough cementum to make the root surface smooth and clean, but removal of all the cementum is not justified.

Root Planing At Shallow Versus Deep Sites

A few studies have shown that root planing healthy sites tends to result in clinical attachment loss, while root planing at sites deeper results in clinical attachment gain. The critical probing is the average probe depth below which there is attachment loss and above which there is attachment gain for a particular procedure.  Lindhe (1982) found the critical probing depth for periodontal scaling and root planing to be 2.9 mm on average (shallower sites show attachment loss; deeper sites show attachment gain).  The important message here is that root planing should be directed at sites with disease and not performed at healthy shallow sites.

The Role of Calculus in Periodontal Disease

In a 1985 Review article on the pathogenesis of periodontal disease entitled "Calculus Revisited", Irwin Mandel states that "since the accepted scenario is that apical growth of supragingival plaque precedes the formation of subgingival calculus, there is no longer an issue of whether subgingival calculus is the cause or the result of periodontal disease.  Subgingival mineralization results from the interaction of subgingival plaque with the influx of mineral salts that is part of the serum transudate and inflammatory exudate.   This however should not be the basis for relegating calculus to the ash heap.  Morphologic and analytical studies point to the porosity of calculus and retention of bacterial antigens and the presence of readily available toxic stimulators of bone resorption.  When coupled with the increased build up of plaque on the surface of the calculus, the combination has the potential for extending the radius of destruction and the rate of displacement of the adjacent junctional epithelium.  The centrality of thorough scaling and root planing in the successful maintenance of periodontal health supports the view the subgingival calculus contributes significantly to the chronically and progression of the disease, even if it can no longer be considered as responsible for initiation".

Gingival Curettage and Root Planing

The American Academy of Periodontology Glossary states "gingival curettage is the process of debriding the soft tissue wall of a periodontal pocket".  It involves removal of ulcerated sulcular epithelium and some of the inflamed connective tissue ("granulation tissue").  Inadvertent curettage is done when the trailing edge of the curet removes some of the pocket wall during root planing.  Intentional curettage is accomplished when the cutting edge of the curet is directed toward the pocket wall.  Since teeth that are curetted are always root planed and inadvertent curettage occurs during root planing the two procedures cannot be separated.  Moreover, curettage is difficult to accomplish effectively in deep pockets.   At the current time gingival curettage, as a separate procedure, apparently has no justifiable application during active therapy for chronic adult periodontitis.

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Value of Coronal Scaling and Subgingival Debridement

TERMINOLOGY

Prophylaxis, Oral: The removal of plaque, calculus and stains from the exposed and unexposed surfaces of the teeth by scaling and polishing as a preventive measure for control of local irritational factors. In the clinic this procedure is selected in the treatment of gingivitis in the hope that the gingival will be returned to a state of health or at least will not develop into periodontitis.

Future preventive / recall cleaning will be termed prophylaxes as opposed to maintenance therapy.

Scaling: Instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus and stains from the teeth.

Root Planing: A treatment procedure designed to remove cementum or surface dentin that is rough impregnated with calculus, or contaminated with toxins or microorganisms. The term is in common usage but is not favored at the UW because it is restrictive, referring only to the root surface and not the adjacent soft tissues.

Root Curettage: Scraping or cleaning the walls of a cavity or surface by mean if a curet.

The procedure not only addresses the root surfaces but also focuses on the soft tissue of the periodontal pocket, especially when sharp, double-edged curets are used. In the patient with periodontitis (as opposed to gingivitis), the student and supervising Periodontics instructor will design a treatment plan consisting of from between 1 to 4 quadrant- equivalents of root curettage depending on the severity of the case. Once this treatment of periodentitis has been selected, then future recall treatment will be termed maintenance as attempts are made to maintain the status quo and prevent further breakdown of the periodontal support. Unfortunately this term is not widely used because many people consider it a surgical procedure.

Subgingival Debridement (SD): The removal of inflamed, devitalized, or contaminated tissue or foreign material from or adjacent to a lesion. This descriptive term for  “ subgingival cleaning” is favored by the UW Department of Periodontics.

Note:  A prophylaxis and quadrants root curettage cannot both be treatment planned on the same patient at the same time.

Benefits and Limitations

During the 1960s, it was shown that supragingival plaque accumulation led to gingival inflammation. It also is generally accepted that pathogenic subgingival plaque cannot develop in the absence of supragingival plaque. Furthermore, changes in supragingival plaque can induce changes in subgingival plaque. Successful periodontal therefore depends on meticulous daily removal of supragingival plaque by the patient and removal of plaque (and probably calculus) by debridement og the crown and root surfaces of the tooth by dental personnel. Both are fraught with problems. Patient compliance usually is not ideal and access to deep periodontal pockets and furcation invasions is difficult, if not impossible. Waerhaug (J Periodontol 49:119,1978) and Rabbani et al (J Periodontol 52:119,1981) demonstrated that SD was fairly effective in removing subgingival deposits in shallow pockets. In pocket depths between 3-5 mm the chances of failure exceeded the chances for success. When pocket depth surpass 5 mm or if significant furcation invasion existed, the chances for failure dominated.

All is not lost! In spite of these limitations there is ample evidence of benefit – at least short-term benefit.

Clinical Studies:

In a 4-week study Morrison et al (J Clin Periodontol 7:199,1980) looked at the effects of OHI, S/SD and occlusal adjustment performed on 90 patients each of whom had at least 20 teeth. The treatment took 4-6 visits. Importat results are illustrated in the following figures.

Results do depend on the degree of inflammation in soft tissue. After 4 week there was a decrease in probing depth and a decrease in periodontal attachment loss in moderate to deep periodontal pockets.  Of equal importance was the slight loss of attachment after instrumentation in shallow pockets. Let the tissues do the talking. In the absence of gingival inflammation, increased probing depths, and calculus, the clinician should be cautious and avoid subgingival instrumentation. “If it ain’t broke, don’t fix it!”

Histologic Studies:

In a clinical / microscopic study in 22 patients, Tagge et al (J Periodontol 46:527,1975) gave OHI and per formed SD and in a site that displayed the same amount of gingival inflammation clinically as another area in the same mouth which was not treated – i.e., the control site. A third similar site was treated by OHI alone. Eight weeks later all 3 sites were assessed clinically for inflammation and 66 biopsy specimens were taken. Clinically and microscopically there was less evidence of inflammation in the SD + OHI sites than in the other two. The data are presented graphically below.

Stahl et al (J Periodontal 42:678,1971) conducted a study to ascertain how long it would take the histologic improvement seen in gingival inflammation as a result of SD to return pre-treatment levels. Eighty suprabony pockets averaging 4.6 mm depth were curetted and then biopsied at appearing specimens from the same patient. By 8 weeks the inflammatory infiltrate was similar in distribution and degree to the control specimens.

Microbiological Studies:

Subgingival debridement has been shown to alter the subgingival microflora purportedly associated with the development of periodontal disease. But for how long? Magnusson et al (J Clin Periodontal 11:193,1993) studied the recolonization of spirochetes and motile rods following SD. The total counts and percentage of these organisms dropped immediately after treatment. By 4 weeks a gradual increase was noted and by the examinations conducted at 8,12, and 16 weeks post- treatment the motile segment of the subgingival microbiota had approached baseline. In a similar study by Handleman and Hess (J Dent Res 49:340,1970) repeated bacterial samples were evaluated after SD at day 3, 10, 30 and 60. There was an immediate increase in Gm + cocci and a decrease in the more complex organisms. The various bacteria studied returned to baseline levels by day 60. Interestingly probing depth was not correlated to the degree of inflammation.

Extended Studies:

(Ⅰ)  Badersten et al (J Clin periodontal 8:57,1981 and 11:63,1984) investigated the effect of SD on moderately advanced (4-7mm) and severely advanced (>7mm) periodontitis. In both studies only single-rooted teeth were treated and assessed. The common format included repeated OHI for at least 3 months followed by aggressive SD (with either hand instruments or ultrasonics) every three months until 1 year. The advanced study continued for a second year during which time OHI was given and the teeth received a coronal polish every 3 months. Plaque index, bleeding on probing, pocket depth all improved during the first few months and then remained stable. The results for periodontal attachment level were mixed. In the moderate study there were 106 sites that initially measured at least 6 mm. At 7 months there were 11 such sites and at 13 months there were 13. The advanced study had 305 sites initially measuring at least 7 mm; there were 43 such sites by 24 months. Thus the investigators were able to improve and maintain the periodontal status for 13 to 24 months. It took careful and repeated OHI in a motivated group of people. It took several rounds of thorough SD during the first year and in the second study periodic OHI and coronal polishing for the next 12 mouths. Not to be overlooked is the fact that all teeth were single-rooted. Molars, especially those with furcation invasions, really complicate treatment. May require surgical access to cope with problems.

(Ⅱ)  In an excellent long-term clinical study by Kalkwarf et al (J Periodontol 59:794,1988) a variety of surgical and non-surgical modalities were compared in teeth with furcation invasions. Regardless of the method used all sites tended to breakdown in the second year of maintenance.

(Ⅲ)  Fleischer et al (J Periodontol 60:402,1989) demonstrated that in molars with furcation invasions and probing depths of at least 7 mm, the percent  of attachment loss in the furcations was over 3 times the percent of loss on external root surfaces. That’s ugly!

Summary:

In spite of the limitations of access, especially in the posterior of the mouth and in the presence of furcation invasions, careful SD will lead to clinical, histologic and microbiologic improvement in moderate to severe periodontal disease – at least over a 2-3 month period. The better the patient’s plaque control efforts, the better the results, and the longer they will last.

Subgingival debridement is not advised in healthy sulci.

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