J Clin Periodontol 2000; 27: 354–360 Copyright C Munksgaard 2000Printed in Denmark . All rights reserved

ISSN 0303-6979

Case ReportsH. De Vree, K. Steenackers andJ. A. De BoeverPeriodontal treatment of rapidDepartment of Periodontology, Dental School,University of Gent, Belgiumprogressive periodontitis in

2 siblings with Papillon-Lefevresyndrome: 15-year follow-upDe Vree H, Steenackers K, De Boever JA: Periodontal treatment of rapid progress-ive periodontitis in 2 siblings with Papillon-Lefevre syndrome: 15-year follow-up.J Clin Periodontol 2000; 27: 354–360. C Munksgaard, 2000.

AbstractAims: This paper reports the treatment of the periodontal component of thePapillon-Lefevre syndrome in 2 siblings (case A, born 1974; case B, born 1976).Method: The initial treatment, in 1982, consisted of extraction of all primaryteeth, scaling and rootplaning of the erupted permanent teeth and systemicantibiotic therapy. During 15 years, continuous and intensive periodontal treat-ment consisted of chlorhexidine 0.2% rinses, bi-weekly professional prophylaxis,scaling and rootplaning or surgery if indicated. Systemic antibiotics often ac-companied mechanical therapy after bacteriological analysis.Results: In case A, a favourable number of permanent teeth could be maintained,but in case B, all permanent teeth were lost in spite of the intensive treatment.Darkfield microscopy at different intervals revealed high numbers of spirochetesand motile rods in both siblings. Only in case A were they temporarily reducedto zero after scaling and rootplaning combined with metronidazole. Anaerobiccultering revealed high numbers of Actinobacillus actinomycetemcomitans (A.a) inboth patients. In 1994, 2 years after combined amoxicillin/metronidazole therapy,no A.a could be detected in case A. In case B, A.a could still be detected andwas found to be resistant to metronidazole. One year after extraction of all per-manent teeth, could no A.a be detected in case B.Conclusion: Intensive periodontal treatment combined with antibiotic therapywas not able to prevent complete tooth loss in case B. In case A, the treatment was

Key words: Papillon-Lefevre syndrome; earlymore effective, resulting in preserving a number of permanent teeth in a stableonset periodontitis; periodontal therapy; caseclinical situation. In these 2 cases, no attempt was made to create an edentulous report

period between the periodontally-diseased mixed dentition and the eruption ofthe remaining teeth, which may have contributed to treatment failure. Accepted for publication 19 May 1999

Most forms of inflammatory peri-odontal disease can be succesfullytreated and controlled, but some typesof disease in particular patients do notrespond well to treatment. One of theseis the Papillon-Lefevre Syndrome(PLS). This syndrome is believed to bea rare autosomal recessive disease witha prevalence of 1–4 per million (Gorlinet al. 1964). Up to 1994, over 200 cases

have been reported (Hart & Shapira1994). Characteristic symptoms are dif-fuse palmar and plantar hyperkeratosiscombined with a rapidly progressiveperiodontal breakdown affecting bothdentitions, resulting in premature lossof deciduous and permanent teeth (Pa-pillon & Lefevre 1924, Haneke 1979,Preus & Gjermo 1987). Increased sus-ceptibility to other infections has been

reported in approximately 25% of the130 cases described in 1975 (Haneke etal. 1975). Diagnosis is made on thepresence of concomitant symptoms, be-cause no pathogonomic disease markerexists to allow a definitive diagnosis.Therefore, it is not clear whether all re-ported cases are actually Papillon-Le-fevre syndrome or rather represent anetiologically diverse group of con-

Periodontitis with Papillon-Lefevre syndrome 355

ditions sharing similar clinical diseasemanifestations. Etiology and patho-genesis of PLS are still unknown, butintensive work during the past 15 yearshas suggested 2 main factors as beingresponsible for the initiation and pro-gression of PLS. Firstly, the presence ofvirulent gramnegative anaerobic patho-gens such as Porphyromonas gingivalis(P.g), Capnocytophaga, Spirochetes andActinobacillus actinomycetemcomitans(A.a) (Newman et al. 1977, Jung et al.1981, Preus 1988, Tinanoff et al. 1990,Kleinfelder et al. 1996). The elevatedantibody titers to A.a support the in-volvement of this bacteria in the peri-odontopathy associated with PLS (VanDyke et al. 1984, Bimstein et al. 1990).Secondly, defects in immune-mediatedmechanisms including impairment ofneutrophil chemotactic, phagocytic andbactericidal activities (Preus & Gjermo1987, Preus 1988, Diawari 1978, VanDyke et al. 1984), reduced lymphocyteresponse to pathogens (Haneke 1978,Dwari 1978), depression of helper-to-suppressor T-cells ratio (Lu et al. 1987),deficient monocytic function (Preus &Gjermo 1987, Bimstein et al. 1990), el-evation of serum immunoglobulin (Ce-lenligil et al. 1992) and degenerativechanges of plasma cells (Sloan et al.1984).

It is well-known that the generally ac-cepted periodontal treatment is not ef-fective to treat the periodontal compo-nent of PLS, at least in most cases andon a long term basis. Preus & Gjermo(1987) report that stringent plaque con-trol and professional non-surgical ther-apy retard the periodontal breakdown.An edentulous period inbetween theaffected deciduous and permanent den-tition seemed to have a positive influ-ence on the treatment outcome (Tinan-off et al. 1986, Tinanoff 1995). But thisapproach is not always successful(Glenwright & Rock 1990).

The symptoms, long-term treatmentand results after 15 years of intensiveperiodontal treatment of 2 siblings di-agnosed for PLS in 1982, will be de-scribed and discussed.

The patients

In July 1982, a 7 1/2-year-old girl (caseA, born November 1974) and heryounger, almost 6-year-old sister (caseB, born August 1976), were referred tothe department of Periodontology,Dental School, University of Gent, bytheir family dentist. An acute, early on-

set periodontitis was diagnosed (Figs. 1,2, 4–6). All standard therapeutic pro-cedures, such as oral hygiene instruc-tions, chlorhexidine rinses and pro-fessionally delivered profylactic pro-cedures did not have any influence onthe clinical aspects of the disease.Dermatologic examination revealed abilateral and symmetrical hyperkera-tosis of the palms and soles, in bothgirls (Figs. 3, 7). The condition was di-agnosed as Papillon-Lefevre syndrome.Medical examination in the PediatricDepartment did not reveal any otherdisorder. They were completely healthyand did not suffer from other infectiousdiseases.

A thorough oral examination wasperformed on both parents and oldersisters. None of them had or have anysimilar cutaneous or periodontal abnor-malities. Only a mild gingivitis was di-agnosed in the mother. The rapidly pro-gressive periodontal disease started atapproximately the same time in bothsisters, in spite of the difference inchronological age.

Clinical and microbiological status atthe start of the study (1982)

Oral and dental examination of the 2sisters revealed an acute gingival in-flammation with initial signs of ne-crosis. The oral mucosa was normal incolor and consistency. The gingivaltissues were swollen and displayed darkred granulomatous proliferations.Hypermobility of several deciduousteeth was observed and at several sitesthe probing depth was up to 7 mm. Thenumber of teeth and eruption patternwas normal. Upon slight pressure pusexuded from the periodontal pocketsand periodontal abscesses. The amountof supragingival plaque was low, al-though subgingival scaling showedabundant plaquedeposits. This subgin-gival plaque, as analysed by darkfieldmicroscopy, consisted of high pro-portions of spirochetes and motile rods.The flora cultured from these samplescontained high numbers of black pig-mented bacteroides, Eikenella corrodensand Capnocytophaga. At that time(1982), we did not have adequatemethods for sampling A.a.

Radiographic examination revealedsevere bone loss around all deciduousteeth. Several permanent teeth werepresent at different stages of develop-ment. In case A, the permanent maxil-lary and mandibular central incisors,

the mandibular lateral incisors and allfirst molars had erupted (Figs. 1, 2).The gingival tissues at the lower incisorswere oedematous and red, but no boneresorption was observed on any of thepermanent teeth. Case B had the per-manent mandibular central incisors andtwo 1st mandibular molars erupting. Amild inflammation, but no bone resorp-tion was observed on the lower incisorsduring eruption (Figs. 4–6).

Initial treatment

In the initial phase, the treatment was di-rected at altering the oral flora by extrac-tions, local mechanical therapy and anti-biotics, thereby allowing teeth to erupt inan oral environment with minimal in-flammation and with bacterial plaquecontaining low proportions of anaerobicbacteria. Therefore, after initial exami-nation and diagnosis, all remaining de-ciduous teeth were extracted under localanaesthesia. Metronidazole (250 mg, 4¿a day) was given immediately followingextractions for a period of 5 days. Allsubgingival pockets were irrigated with0.2% chlorhexidine solution.

Then, the 2 children started a thera-peutic phase with bi-weekly sessions ofprofessional oral hygiene. During eachsession plaque index was scored, fol-lowed by repeated oral hygiene instruc-tions.The supragingival plaque of theremaining permanent teeth was re-moved with a rotating brush, Eva-tipsand polishing paste. Scaling and root-planing of the exposed rootsurfaces wasperformed.

Long-term treatment and follow-up(1984–1997)Case A

The intensive prophylactic proceduresonly temporarily retarded disease pro-gression. In case of active progressingperiodontal pockets (bleeding on prob-ing, increased attachment loss andprobing depth), conventional subgingi-val scaling and rootplaning were per-formed with or without flap surgery. In1984, all permanent 1st molars and thelower left lateral incisor were extractedbecause of extensive bone loss. Duringthe eruption of the other permanentteeth, the gingival tissues could be keptin a clinically healthy condition by bi-weekly prophylaxis. The periodontiumwas free from clinical signs of inflam-mation for a period of several weeks tomonths after tooth eruption. Then,

356 De Vree et al.

Fig. 2. Case A: radiographic situation at the start of the study (1982).

Fig. 6. Case B: radiographic situation at the start of the study (1982).

Fig. 9. Case A: radiographic situation in 1997.

Fig. 11. Case B: radiographic situation in 1996, just before full-mouth extraction.

without any change in the oral hygieneregimen or the presence of any illness,an extremely rapidly progressing peri-odontitis in localised areas developed,with the formation of deep gingivalpockets and accompanied by multipleperiodontal abscesses. This resulted inan almost complete loss of periodontalattachment within a few weeks. Teethbecame extremely mobile and drifting.During the first treatment period (be-tween 1982 and 1986), mechanical treat-ment was accompanied by metronida-zole for 5 periods of 5 days, mainlyduring periods of exacerbations. Micro-biologically, exacerbations were char-acterized by elevated proportions ofspirochetes and motile rods as observedby darkfield microscopy. Darkfieldmicroscopic observations of samplestaken 1 week after the last intake of me-tronidazole showed a significant reduc-tion of the number of these bacteria.

However, this result was short-lived(Table 1). In March 1986, several per-manent teeth were extracted under gen-eral anaesthesia and the remainingerupted permanent teeth thoroughlyscaled. Again, metronidazole was givenimmediately after this procedure. Den-tures were made to replace the extractedteeth. Candida infection was often seenunder the upper dentures, and was dif-ficult to treat.

Anaerobic cultering data (October1986) revealed high levels of A.a. at dis-eased sites. Therefore, it was decided tocombine mechanical treatment withsystemic doxycycline (150 mg first day,75 mg for 6 days) during exacerbations.Unfortunately attachment loss con-tinued. A.a. could not be eliminatedcompletely, as revealed by new culturingof subgingival plaque. Further on, an-aerobic culturing was performed onceevery year. In 1992, a combined amoxi-

cillin/metronidazole therapy (375 mg/250 mg, 3¿ a day for 1 week) was suc-cessful in eradicating A.a. In 1995, froma series of possibly involved peri-odontopathogens including Porphyro-monas gingivalis, Prevotella intermedia,Actinobacillus actinomycetemcomitans,Bacteroides forsythus, Peptostrepto-coccus micros, Fusobacterium nucleatumand Campylobacter rectus only Fuso-bacterium nucleatum could be cultured(0.3% of the CFU). Darkfield micro-scopy of the same samples revealed onlysmall percentages of spirochetes andmotile rods and elevated proportions ofcurved rods and cocci. Case A is A.afree from 1992 until present. Since herpuberty in 1986, only two upper perma-nent molars were lost. 4 canines, 2 lower2nd premolares, 2 lower 2nd molars and4 3rd molars are present in a more orless stable clinical periodontal con-dition (Figs. 8, 9).

Periodontitis with Papillon-Lefevre syndrome 357

Fig. 1. Case A: clinical situation at the start of the study (1982).

Fig. 3. Case A: hyperkeratosis of the palms (1987).

Fig. 4. Case B: clinical situation at the start of the study (1982).

Fig. 5. Case B: clinical situation at the start of the study (1982).

Fig. 7. Case B: symmetrical hyperkeratosis of the palms (1986).

Fig. 8. Case A: clinical situation in 1997.

Fig. 10. Case B: clinical situation in 1996, just before full-mouthextraction.

358 De Vree et al.

Table 1. Darkfield microscopy in case A

Morphotype 12–85* 1–86 2–86

spirochetes 29 0 0motile rods 58 1 54curved rods 0 18 6straight rods 5 47 18filaments 8 1 0fusiforms 0 0 0cocci 0 33 22

* Metronidazole given immediately aftersampling.

Table 2. Darkfield microscopy in case B

Morphotype 12–85* 1–86 2–86

spirochetes 52 43 17motile rods 31 13 42curved rods 0 3 1straight rods 9 24 12filaments 6 1 0fusiforms 0 0 0cocci 2 16 28

* Metronidazole given immediately aftersampling.

On the suggestion of the dematolo-gist, etretinate therapy was installed inMarch 1990, but ended within the sameyear on request of the patient becauseof the side-effects. This seemed not tohave had any clinically remarkablechange in disease progression.

Case B

In the younger sibling, the same inten-sive treatment was performed. Spon-taneous exfoliation of the mandibularincisors occurred in 1985, due to severeand acute inflammation and extremelyrapid bone resorption. In 1986, all peri-odontally involved teeth were extractedunder general anaesthesia in order todecrease the pathogenic flora. Metroni-dazole accompanied mechanical treat-ment during exacerbations (250 mg, 4¿a day for 5 days) from 1982 until 1986.Analysis of the subgingival plaque withdarkfield microscopy, before and aftermetronidazole treatment, revealed al-most no reduction of the number ofSpirochetes (Table 2).

Bacteriological testing in 1986,showed elevated proportions of A.a.,which could only be reduced tempo-rarily by doxycycline (150 mg 1st day,75 mg until day 7). Later on, as in theolder sister, combined amoxicillin/me-tronidazole (375 mg/250 mg, 3¿ a dayfor one week) therapy was preferred. 2years after the last antimicrobial ther-

apy, A.a. was still present (90% of theCFU) and found to be resistant to me-tronidazole.

On the suggestion of the dermatol-ogist etretinate therapy (25 mg a day)was started in March 1990 to treat theskinlesions. It was ended in August1990, on request of the patient becauseof the adverse effects on the lips. Dur-ing this 5 month period, no additionalclinical effect on the gingival status wasobserved.

In spite of the continued bi-weeklymaintenance care and conservativeperiodontal treatment, all the maxillarypermanent teeth had to be extracted(except for the upper, non-erupted thirdmolars) between 1991 and 1992. Den-tures were made to replace the extractedteeth. No Candida infection was seen.Only 2 canines and 2 premolars in themandible were left (Figs. 10, 11).

Even after her puberty severe andrapid periodontal breakdown con-tinued. Since we were not able to elim-inate A.a. from the active sites, we de-cided in December 1996 to extract allremaining permanent teeth. On erup-tion, the upper third molars were alsoextracted to eliminate A.a. and to pre-vent further vertical alveolar bone lossby possible periodontal breakdown. 1year after full-mouth extraction, noA.a. could be detected on the oral mu-cosa, tongue or denture.

Discussion

In spite of intensive research in the pastdecade the etiology and the patho-genesis of the periodontal componentof the PLS are still unknown. Severalgenetic studies focused on mapping tocertain chromosomes and on mutationsin genes linked to cytokeratines (Fischeret al. 1997, Hart et al. 1997).

Consanguinity has been reportedseveral times, however this was not thecase in our two siblings (Soskolne et al.1996). Other studies tried to explain thepathogenesis by changes in the activityof lymphocytes and a depressed chemo-taxis of neutrophils (Firatii et al. 1997a,b,c). This decreased host response toinfection would then result in havinggeneralized infectious diseases more fre-quently. Even an increase in pyogenicliver abscesses has been reportedamongst PLS patients (Oguzkunt et al.1996). However, our two siblings werehealthy during all those years and hadno more minor illnesses (eg. measles,

flu, etc.) than any other child and thenon-affected sisters. Other studies in-vestigated the microbiological compo-nent focusing on the presence of A.a.(Ishikawa et al. 1994, Stabholz et al.1995, Kleinfelder et al. 1996). However,a wider range of pathogens cannot beexcluded (Clerehugh et al. 1996).

The treatment failure of our patientsis in agreement with previous reports,indicating that local, mechanical ther-apy and systemic antibiotics are rela-tively ineffective in halting periodontitisin this syndrome on a long-term basis(Rateitschak-Pluss & Schroeder 1984,Shikawa et al. 1994). In spite of inten-sive treatment, periodontal destructionprogressed rapidly in both girls between1982 and 1986. During this period, asjudged by darkfield microscopy, thesubgingival plaque responded well tometronidazole in case A. In case B,micro-organisms were already resistantto metronidazole or the drug had notbeen taken properly, since the numberof spirochetes did not change after ther-apy. No other antimicrobial treatmentin combination with scaling and root-planing was able to eliminate A.a. andcontinuous treatment was only tempo-rarily retarding disease progression. Re-tardation of the disease progress hasbeen reported on a short term basis butshould not lead to premature early con-clusions (D’ Angelo et al. 1992). Case Ahowever, was A.a. free after combinedantibiotic therapy and a more or lessstable clinical situation was obtainedsince 1987.

In recent years, a different thera-peutic approach has been proposed.This involves elimination of periodontalpathogenic flora, by extraction of allprimary teeth several months before theeruption of the permanent teeth, com-bined with antibiotic treatment to re-duce any possible infection of the per-manent dentition (Tinanoff et al. 1986,Preus & Gjermo 1987, Preus 1988). Thepermanent teeth subsequently erupting,remained periodontally healthy up to15 years after therapy (Tinanoff et al.1995). These authors suggested that anedentulous period between the peri-odontally diseased mixed dentition andthe eruption of the remaining teeth,along with systemic antimicrobial ther-apy, appear to be the key elements ofthe treatment of the periodontal com-ponent of Papillon-Lefevre syndrome.Such a radical, clinical approach elim-inates the number of bacteriologicniches in the mouth and most likely re-

Periodontitis with Papillon-Lefevre syndrome 359

duces the possibility of reinfection. Al-though transmission of pathogens incases of PLS has been reported (Pre-us & Olsen 1988, Petit et al. 1993).

In another case, however (Glen-wright & Rock 1990), an edentulousperiod between the clearance of all de-ciduous teeth and the premature erup-tion of the 1st permanent molars, didnot prevent subsequent development ofperiodontal disease. In this case, noantimicrobial treatment followed theextractions and can probably explainthe treatment failure.

On the advice of a dermatologist, ashort period of etretinate therapy wasinstalled in our patients, mainly to in-fluence the hyperkeratosis on hands, el-bows and feet. As with other anti-psori-atic medication, the medication had noeffect on the periodontal health. The 2children refused to continue this medi-cation, because of the side-effects. Themedication period was therefore not ex-tended enough to observe any improve-ment. This confirms the observationsreported in the literature (Blanclet et al.1991, Lundgren et al. 1996). Thoroughand intensive periodontal treatmentcombined with antibiotic and antiseptictherapy was not able to prevent com-plete tooth loss in case B. In case A, thetreatment was more effective resultingin a relatively stable situation and in atleast saving a number of permanentteeth. The treatment of our 2 patientswas directed primarily at altering theoral flora by conventional mechanicalmethods and antibiotic therapy. In thetreatment approach no attempt wasmade to create a complete edentulousperiod between the periodontally dis-eased mixed dentition and the eruptionof the remaining teeth. Now, upon fail-ure, it was directed at transient elimin-ation of the ecologic niche of the impli-cated organisms in case B.

Aknowledgment

The authors like to thank Dr. P.A. Ad-riaens, T. Seynhaeve, H. De Backer whoduring these 15 years were also involvedin the treatment of these 2 siblings.

Zusammenfassung

Parodontalbehandlung schnell fortschreiten-der Parodontitis bei 2 Geschwistern mit Pa-pillon-Lefevre-Syndrom: Nachuntersuchunguber 15 JahreDieser Artikel berichtet uber die Behandlungder parodontalen Komponente des Papillon-

Lefevre-Syndroms bei 2 Geschwistern (FallA: geboren 1974; Fall B: geboren 1976). DieInitialbehandlung im Jahre 1982 bestand ausder Extraktion aller Milchzahne, Scaling undWurzelglattung aller bleibenden Zahne undsystemischer Gabe von Metronidazol. Wah-rend 15 Jahren bestand die regelmaßige in-tensive parodontale Therapie aus Spulungmit 0.l2%igem Chlorhexidin, professionellenZahnreinigungen mit Scaling und Wurzel-glattung und ggf. chirurgischer Therapie in14-tagigen Abstanden. Nach bakteriologi-schen Untersuchungen wurde die mechani-sche Therapie haufig durch die systemischeGabe von Antibiotika unterstutzt. Im Fall Akonnte eine erfreuliche Zahl bleibender Zah-ne erhalten werden, wahrend im Fall B trotzder intensiven Behandlung alle Zahne verlo-ren gingen. Dunkelfeldmikroskopie zu ver-schiedenen Zeitpunkten ergab hohe Zahlenvon Spirochaten und beweglichen Stabchenbei beiden Geschwistern. Nur in Fall Akonnten diese Zahlen vorubergehend durchScaling und Wurzelglattung unterstutztdurch die Gabe von Metronidazol auf Nullreduziert werden. Anaerobe Kultivierung er-gab hohe Zahlen von Actinobacillus actino-mycetemcomitans (A.a.) bei beiden Patienten.1994, 2 Jahre nach kombinierter Gabe vonAmoxicillin und Metronidazol, konnte inFall A kein A.a. mehr nachgewiesen werden.In Fall B persistierte A.a. und stellte sich alsresistent gegen Metronidazol heraus. EinJahr nach Extraktion aller Zahne bei PatientB konnte A.a. nicht mehr nachgewiesen wer-den. In diesen Fallen wurde nicht der Ver-such unternommen eine zahnlose Phase zwi-schen dem erkrankten Wechselgebiß und demDurchbruch der verbleibenden Zahne zuschaffen. Dies konnte zu dem Mißerfolg derBehandlung beigetragen haben.

Resume

Traitement parodontal de la parodontite aprogression rapide chez 2 sœurs presentant unsyndrome de Papillon-Lefevre: suivi sur 15 an-neesOn trouvera dans cet article le compte rendudu traitement de l’element parodontal dusyndrome de Papillon-Lefevre chez deuxsœurs (cas A, nee en 1974; cas B, nee en1976). Le traitement initial, en 1982, aconsiste a faire l’extraction de toutes lesdents temporaires, detartrages et surfacagesdes racines des dents permanentes ayant faitleur eruption et traitement antibiotique sy-stemique. Pendant 15 ans, le traitement paro-dontal continu et intensif a consiste en bainsde bouche a la chlorhexidine a 0.2%, nettoya-ges dentaires professionnels toutes les 2 se-maines, detartrage et surfacage ou chirurgielorsque c’etait indique. Des antibiotiques sy-stemiques accompagnaient souvent le traite-ment mecanique apres analyse bacteriologi-que. Dans le cas A, un nombre satisfaisantde dents ont pu etre conservees, mais dans lecas B, toutes les dent permanentes ont eteperdues, en depit du traitement intensif. Parmicroscopie en fond noir a differents inter-

valles, on constatait un nombre eleve de spi-rochetes et de batonnets motiles chez lesdeux sœurs. Dans le cas A seulement, ces or-ganismes etaient reduits temporairement azero par detartrages et surfacages combinesau metronidazole. Par culture en anaerobio-se, on a mis en evidence des nombres ele-ves d’Actinobacillus actinomycetemcomitans(A.a.) chez les deux sœurs. En 1994, deux ansapres un traitement combine par amoxicilli-ne/metronidazole, on ne pouvait pas consta-ter d’A.a. chez le sujet A. Chez le sujet B,A.a. pouvait encore etre constate, et s’est re-vele resistant au metronidazole. Un an apresextraction de toutes les dents permanentes,aucun A.a. ne pouvait etre constate chez lesujet B. Dans ces deux cas, aucune tentativen’a ete faite pour creer une periode d’edenta-tion entre la denture mixte atteinte de paro-dontite et l’eruption du reste des dents, ce quipeut avoir contribue a l’echec du traitement.

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Address:

J. A. de BoeverUniversity of GentDental SchoolDepartment of PeriodontologyUniversity HospitalDe Pintelaan 1859000 GentBelgium