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Reactive inflammatory papillary hyperplasia of the palate
Reactiveinflammatorypapill$ry h‘ yperplasia.of{thepalate Lou.&H. Guernsey, Liew?en.w$ Colonel, DC; U&4*
R
ecently the English-languageliterature has reflectedan increased:intere+ in the often misnamedmultiple papillary excrescences, so-f$equently.&ed in denture-bearingareasof the.palate. Fisher and RzEshi$,aindY’r astor+~~kon&der the fundamental processto be .of an inflammatory n.aur& whereas.‘B echtp Robinson4and Waite5include,t.hese excrescences amongthe prema~igna+&ons of t.heoral cavity. Furthermore,s$&the lesionsa%:frequently assod+&dwith someform of palate-covering.@rosthesis, and since a. p‘ p;i(lelyquoted a&cleby Hobaek”reportedfifty-eve casesof carcinoma.ofthe.bar&palate ArkI’impl&&d denture irritation in t‘ wenty-one out. of thirty:three’ denture-wearing:pat$&s; it was thought that reactive papillary hyierplasia of-the palates‘ hould’ be studied in an attempt to resolvethe d$3iotcmythat now es&s. .‘ I‘ -. REVIEW OF THE LITERATURE
__. Becauseof the great variation in their appearanceand cfinical,characteris&.& numerousterms have been.used to. describethese iesions.~~SHe~ht,,!~ in I$ -eajly qa$er, describedthe lesion as a‘ “.. . . .painless~prol.&ratiori of’ the e$th&al tissue . . . made up of numerous.con&t& papiilomas,:.mi&erry.:rei in color, and generally confined to the tissue. under the relief ,. area f’ of. the .va&um . chamber.” Risher and Rashid emphasizedthe.degreeof &dness’ and related .it[ to;the degreeof inflammation present. Surface,plceratian,.~ho~~~er; .was-absentin all of the elevencasesthat they described.They also noted that the .&ll extentof the.papillary hyperplasiacould-bestbe.demonstrated by a stream.of&$ &*&&I perpendicularly to the patatal surface which causedthe -papillary &ass&~ to ., !..i,‘ .~ ._ ,‘ .:: L X%ief.. of the Orarl Surgery gqd Dentai C ‘ l’i&c~ $7th G&wk!E&pitkl; _.. .: 09757.
814
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separate from one another, t.hus dispelling the consolidating effect of viscid saliva and pressures from the denture base. An obliquely directed blast of air IXOduced a rippling mot,ion similar to that. of a vheat field in ELbreeze. Waite5 emphasized the sessile nature of the lesion and stated t,hat the papillary elevations vary as to surface area and depth. He further described food a.ccumulations, ora. secretions, and unhygienic debris trapped at t.he base of the papillae. These lesions are located on the palate, usually -under the relief area of the denture, although Fisher and Rashid’ note t1ia.t any area covered by a. denture flange may become inrolved. Waite5 points out that the hyperplasia was found to encompass the entire palatal vault to the soft palate, even inr-olving the lingual aspect of the alveolar ridge. All authors have generally agreed that the specific cause and predisposing factors of the hyperplasia. were olxt~~re but that. the tissue change was associated with some form of irritation. Treatment yecommended varies from simply removing the denture from the oral cavity for extended periods of time until t,he pathologic condition has been resolvedl. ’ to radical excision of the lesion, including the periosteum down to the palatal bone”, 5 with fulguration of the hone if malignant change is involred. Electrosurgical treatment is mentioned bs Waite, who emphasizes increased postoperative pain over the technique of excision wit,h the scalpel. Vaite5 reviews the role of tissue irritation as a cause of carcinoma. specificallp the role of denture irritation as pointed out b;\- Hohaek” and the spec.ific malignant potential of reactive papillary hyperplasia. of the palate as cited by Robinson.” He then aptly concludes that diagnosis 1~~ biopsy x-aries with the malignant potential of the biopsy specimen. CLINICAL
INVESTIGATION
A ciinieal investigation was made of ninety-nine cases of reactive papiilar) hyperplasia of the palate which were seen and t.wated at Walter Reed Genera1 Hospital from December, 1959. to June, 1961.. The first part of t.his study was directed toward determining the incidence of reactive papilla,ry h:-perplasia of the palate. Since the United States Arm>De&al. Corps has maintainecl a complete permanent. dental record on all actireduty military personnel since Jan. 1, 1957, 4:617 s~wh records at. Walter Reed General Hospital were reviewed to establish this incidence of reactive papillary hyperplasia. Furthermore, since t.he attire-duty military population is usualll\ of a younger age group and co~hl not. be expected to contain a. great number of denture wearers, 564 records of retired military personnel were also screened. In addition, records of a group of 711 retired personnel and dependents cohere reviewed to give a general sampling of all types of patients. No attempt IV:%S made to examine t.he patients Ivhose rec.ords were screened. The second part of the study inrolved the examination and surgical treatment of a larger series of casest.han had previously heen r8:port,ecl. This xv-asdone in order to study the condition closely, and to this end outlying dental cl.inics at camps, posts! and stations near Walter Reed General Hospital were requested
1. Xu2nmar~- of findings 5,899 dental records reviewed
fable
of reack-e
papillary
h;-perp?:a.sia, of the palate in
Reactive
papillary
hyperplasia
of palate
817
Fig.
Fig. d
Fig. 1. Typical Fig. 2. Typical tient. Note narrow
midpalatine midpalatine vault form
vault loeation vault loeation with tendency
of reactive papilhry hyperplasia of palate. of lesion in dentulous non-denture-%rearing toward outfolding of tissue.
pa
The extent and size of the lesions varied with the irritative factors and the length of time of their influence. Thus, an early reactive hyperplasia generally involved only a small area, of the palate and a,ppeared as a reddened but not raised spost,whereas one which had progressed through the wearing of several sets of dentures sometimes covered the entire palate. Such a case was reported by Thomas (his Fig. 1202). Two types could be distinguished. In one there was complete absence of inflammation while others showed pronounced inflammatory changes. In addition, one can recognize a diffuse papillary type, varying from slight to complete coverage of the palate (Fig. 3)) and a nodular or polypoid type which is more commonly found in the posterior palatine vault and often extends onto the soft palate (Fig. 4). On the basis of clinical findings and history, the following agents appear to be of etiologic importance: 1. Ill-fitting prosthetic devices, full or partial dentures. 2. Mechanical irritation, such as perpetration of the lesion in successive denture bases (Fig. 5). 3. Day and night wearing of the prosthesis.
Fig.
Fig.
Fig. 3. Diffuse papillary 1Cypeof reactive liyperplasia. Fig. 4. IC’odula r or polypoid type of reactive h.yperplnsia.
Pig. 5. Inder kat .ions in denture base from~pre-e&king
pa$&&y
4. Lack of oral hygiene or poor oral hygiene. 5. Denture cleansing habits, the use of proprietary to Ch~mica1 irritation. 6. Putrefaction of food. ‘1. Decreased salivary fiow. 8. Smoking. 9. Allergy. 10. Predisposing factors.
hgperplasia.
solutions leading
In dentulons patients who did not have the irritative presence of a. prosthesis, the shape of the palatal vault, seemed to be significant. It tended to prerent the normal cieansing of t.he palate with the tongue. A high, narrow s-anlt with a tenc1enc.y toward outfolding of tissue seemed. most, likely to de\-elop the condition (Fig. 2). X study of the age distribnt,ion revealed that reactive papillay hyperplasia is most frequently fol,uld between the ages of 20 and 50 years, with the sing7le highest incidence in the second decade (Table II) _. Thus, t,he condition is not found in older denture-wearing patients only. Although reactive papillary hq’perplasia of the palate has a quite typical appearance, part~icularly under a blast. of compressed ai!:, it must. be differentiated from certain lesions which ilax-e a similar appearance. especially ill dentulous mouths. Some of the conditions which mimic the appearance of reactive in&mmatory papillary hypePplasia are midpalatine p;-oTertic granulomas. the fnngal gra.nulomas (,histoplasmosis. blastomgcosisJ and coccidiomycosis) , capillary hemangioma, and allergic lesions. Of more serious importance is the yecognition of exophytic. squamons-cell eafciiioma, either priniar>- or metastatie. In suspicious cases it is of paramount importance that a specimen of tissue be s~xbmit.t.ed for histologic study. Treatment
Three methods of therapy have been recommended. The conserratire met,l:od, which advocates removal of the denture for an extended period of at, least, 7 months, is obviously impractical, in view of the essential nature oi’ the appliance and the quest,ionable regression of the lesion. excision of the periosteum! is Full-thickness pal&al excision, including acceptable in the ca,se of small lesions involving only t,he hard palate itself. However, full-thickness removal in very extensive cases would certainly jeopaydize the blood supply if both the posterior palatine and nasopalatine x-essels were sacrificed needlessly. Estensis-e exposure of palatal bone to the oral secretions and flora would also tend to increase the irxidence of pain and osteomyelitis, although the use of protect.ive dressings as recommended by Thoma (his Fig. 1194) woulld minimize this danger of infection. This treatment reqnires a prolonged healing period of 6 to 9 weeks.
Table
patients
II. Age distribution among denture-mcaring and non-delltllve-~vea~ing with reactive papillary hvperplasia of the palate
10 20 30 10 50 60 so SO
to to to to to to to
to
19 29 39 49 59 69 79 89
3 35 “3 19 8 5 1
1
3 “0 12 13 4 3 0 0
0 0. 2 1 0 1
0”
Electrosurge~y has been advocated for oral surgical procedures for many years. This method has been the subject. of comprehensive papers by Cnshing,” Asgis,lo Ogus,ll and Maeth,l’ and 1 ha-ve found it to be the method of choice. In the present study, a portable &vie unit was employed. A loop eiectmde, 1 em. in diameter, was used as the active electrode, and a. thin lead plate was rolled into a cylinder to act as the passive electrode. The patient heId this in thus completing the circuit (Fig. 6). his hand throughout the pr~ee&xe, The unit was used on eautery current, with a, current-intensity setting of 35 to 40 units. The intensity was, varied according to the amount of tissue requiring removal, but it was always set lower if extensive dehydrat.ion of the tissues resulted. In all. but one of the cases profound anesthesia x%-asobtained by means of 2 per cent. lidocaine with 1 :lOO,OOO epinephrine infiltrated- swb~~ucosa~ly in the palate and into the mucobueeal fold. A posterior-t,o-anterior sweep of the autting loop to a, depth off approximately tissue in strQs~ 1 to 2 cm. in 1 to 1.5 mm. was used to remove the hyperplastie length before the loop was removed from the mouth. The~patient was instructed to exhale so as to expel the smoke generated bmythe eha,rring of the tissues. This proeedure was repeated until removal of all the inflamed hyperp!astic tissue was completed. (Complete removal can be ascertained by the .yellow-gray appearance of the underlying tissue.) The charred tissues were wiped away by the assistant, using moistened 2 by 2, inch sponges made into a ball and clamped on a curved hemostat. Tissue from a represent,ativc area was removed for pathaiogic study,
‘ig. 6. Portable and cutting)
Bovie unit, passive used throughout for
electrode (rolled lead eleetrosurgical removai
sheet), axid of tissues.
active
~$eetic
Volume Number
20 6
Reacthue pq&ary
hyperplasia
of palate.
821
usually twothirds of the way through the procedure. Bleeding could be reduced somewhat by removal of the denture for 48 hours preoperatively so that the inflammatory process could abate and by cauterization of the bleeders with the loop. A zinc ‘bacitracin-hydrogenated fat periodontal dressingI was then softened in nearly boiling water and spread over the denture base or surgical splint. The patient was instructed to moisten the operated area with s,aliva and the denture
4
Pig. 7. Photographic summary of operative technique. 8, Marked relief chamber in denture. B, Preoperative reactive hyperplasia. C, Appearance after electrosurgery; darkened areas are sites of biopsy and bleeders which have been cauterized. I), Zinc bacitracin periodontal pack. E, Healed case.
which takes :3 to 4 weeks. Occasionally\: a become denuded because of the slo~xgh of the mill usually recorer it if the heat has not Occasionally a small sequestrum will form epithelization takes place.
small area of palatal bone will thin overlyi-lg tissue. Granulation damaged the bone beyond repair. and is sloughed out before final
Histopathoiogy
The microspcopic findings are summarized in Table III. Since the tissue specimens were examined by several resident pathologists, a lack of uniformiQ7 in the final histopathologic diagnosis resulted. The histologic findings were fairly consistent 1 however. They showed t.he numerous papillary excrescences i Fig. S) corered usually b- nonkeratinized hyperplastic epit.helium. the rete pegs of which may be acanthot.ic or show growth into the submucosa to form a psencloepitheliolllatons hyperplasia. Not infrequently these rete pegs are cut tan$entiall.v. thns giving the appearance of islands of epithelinm below the basement membrane ( F-g. 9 ) . The snbmucosal connective tissue shows a dense plasma-cell and lymphoc>-tic infiltra.te. FOLW cases &on-ed hyperkeratosis (Fig. 101. and t.wo cases of ulceration were also noted. In none of the cases reriexed n-as there evidence of dyskeratosis. Recurrence
Cases treated by means of a. Ml-thickness palatal excision required a postoperative healing period of 8 to 10 weeks until comp1et.e regeneration of the tissnes occurred. The use of a clear acrylic splint was adrocat,ed to protect the surgical site. Althongh the original protocol called for a. determination of recurrences, t,his study did not cover sufficient time .to permit any specific conclnsions to be drawn. DISCUSSION
Ill-fitting full upper acrylic and vlucanite dentures with relief chanlbe~s ha-c-e general157 been blamed for the formation of reactive papillary hperplasia of the palate. In a recent study, howes-er, Yra.storza’ points out. that acrylic dent.ures without relief chambers are also frequently a.ssociated with the condition. We agree with these findings. In the present series of cases, however, an almost equal nnmber vere found under partial dentures, part.icularlthe temporary acrylic t:-pe replacing anterior teeth, which are usually inserted relatively earl>- in life. A nnmber of c.ases also were associated x-it11 partial dentures of cast chrome st.eel metal. Although most, commonly- found in the midpalatine vault, in the relief chamber area, the lesion is freqnently located la.terall;.- on the paIate, over the crest of the alveolus. and bnccally under the denture flange. In spite of the long- list of cont,ribnt,ory factors enumerated. I am inclined to agree with YrastorzaY that a. predisposing factor is present as a ma.jor etiologic agent, for an unaccountabie nmnber of patients wear ill-fitting prostheses? have poor oral lggiene and are free of lesions. Although it, is difficult to determine the onset. of a lesion when there a.re no subjectiT-e symptoms, the condition has been noted as early as 9 months
8
Pig. Fig.
8. Photomierograph showing papilkq nature 9. Submucosa shows inflammatory infiltrate.
of lesion.
atid as k&e as 33 years after the insertion of dentirres. Of ~pa&kular ~~~~~~a~~e, however, was the high incidence of oecurrwm in the second dee~de -of life. This fact has not been brought out in any of the previous, stndies -review&l and the present finding is direct1.y attributable to the nakxre of the patient population treated in &Mary dental facilities. Biopsy is of particular importance in, the case 6f dentulous pa&mtsm’as the lesions can mimic other diseasesof a nmre serious natme.
Volume
20
Number
6
Fig.
IO. Pliotomicrograph
Reactive
showing
papillary
pseudoepitl~eliomatous
hypevplmia
hyperplasia
of palate
and
825
ulceration.
Since no ‘dyskeratosis wa,s reported by the twenty-two pathologists who have reviewed the microscopic specimens, I agree with Bhaskarl” and with Shafer, Hine and LevyI” that the lesion is benign and devoid of any premalignant potentiality. Since chronic irritation of epithelial tissue has been universally recognized as one of the leading etiologic agents in cancer, the incider,ee of squamous-cell carcinoma of the palate has been reviewed in an attempt to establish a, possible relationship between the existence of a reactive papillary hyperplasia of the palate and the subsequent development of carcinoma. Few studies or reports concerning the rela.tionship of the wearing of dentures to squamous-cell carcinoma of the palate are available. They are primarily found in the European literature. ThomaJ6 makes reference to cases of Shneider, Rhenwald, and Voss and concurs with their statement that they cannot say empirically that the effect of the prosthesis is the cause of the carcinoma in every case. However, ThomaP reports a case of extensive benign papillomatosis in which, 14 years; after ra.dical electrosurgical excision, extensive carcinoma of the palate with involvement of the sinuses was found t.o have developed. Ackerman and de1 R.egato17 consider carcinoma of the hard palate to be very rare. They quote New, who found only twenty-five cases of epidermoid carcinoma of the .hard palate among approximately 5,000 cases of cancer of the oral cavity, an incidence of 0.05 per cent. Hobaek,G in his extensive study of 560 cases of oral carcinoma, was able to demonstrate a “casual connection between irritation caused b,y prosthesis and cancer development in 86 of these cases.” Of particular interest was the finding of sixty-one cases in women (70 per cent) I twelve of whom (‘20 per cent) presented :marked Plummer-Vinson syndrome. The demure-base material in
2. The lesion was found mdev a.11sorts of pl.ostl~eses--~)oth frill and partial, acrylic or cast. base metal-and was not necessarily limited to the palatal 111Wosa >YOpT.
3. The lesion was found most frequently in denture weare.rs between 20 and 50 years of age, n-it,11 the highest single incidence of occurrence in the second decade. 4. Eight. cases were detected in non-denture x-earers. 5. Two general types are recognized: (a) DSfnse papillary and (1)) nodular or polypoid. 6. Etiology was discussed. No single. cause-and-effect ~elat~ioaship is noted. 5 predisposition factor is thought to c&t.. 7. Eled.rosnrgical removal is recommended as the preferred treatment. 8. The clinical and microsc.opic appeara.nce of the lesion was described. The lesion is considered to be benign, reactive? inflammatory in natnre. and essential.ly desoid of any premalignant potent.ialit.:+-. In the litepatwe reriexwd, no stud,~ has definitel>- shoxn a significant Pelationship between reactive papillar:hyperplasia of the pala.te and the occwrcnce of epiderroid carcinoma of’ the palate. 9. Prevention of recurrerxe of the lesion has been discussed.. Illustration Services of Walter Reed Grateful acknowledgment is given to the SIedical Army Hospital, Fort Eenning, Georgia, General Hospital, Washington 12, D. C., and Martia for the photographs and photomicrograpl~s in this paper. The a.uthor gratefully acknowledges the encouragement and asaistawe of Colonel Ii. B. Shira, Chief of Oral Surgerp ani\ Dental Rw-ice? Walter Reed General Hospital. Washington, D. C. REFERENCES A. I<., and Rashid, 1. Fisher: ~JIucc~sa~ ORAL SGRG., OPAL 2. Trastorzs, J.: Inflammatory
I'. MED.
J. : hfktmmatory & ORAL
PATH.
Papillary 5:
191-198,
H;,yerplasia
of
the
Palatd
1952.
Papillary Hypexplasia of the Palate, J. Oral Surg.: Anesth. D. Sel-v. 21: 3.31-336, 1963. Sm.S.: Chronic Irritation of the Eyithelial Tissues of the DIonth hssocinterl TYith Dentures. Am. J. Orthodontics & Oral Surg. 25: 574-565, 1939. Xohinsou. H. B. C.: Neoplaams axd “Precaurerous” Lesiolls of the Oral Regions, D. Clin. Korth America, p. 621, November. 11157. Waite? D. E.: Inflammatory Papillar>Hyperplada, J. Oral Surg., dnesth. S- Hosp. D. Serv. 19: ‘7111-214. 1961. Kobaek, A.: Dental Prosthesis and Intraoral Epirlermoid Carcinoma., leta rarliol. 32: 259-27.3. 1919. Walter: J.: Prosthet.ic Mucosal Hypertroph>in the Xouth Simulating Malignancy? Writ. M. J. 1: l&29-1431, 1953. Thoma, K. H.: Oral Surgery, eA. 4, St. Louis, 1963, The C. 5’. hJIosb~Cornpan-. pp. & Hosp.
-I3. He&t, 4. -5. 6. 7. Y.
91%9'1. 9. Cusbing. 10. Il. 1”. 13. 14.
H.: Eleetrosurqery as an lid to the Removal of Intracranial Tumors~ Surg. Qpec. & Obst. 47: 751-+84, 1928. Asgis: A. J.: Clinical Oral Elec,trosurger>-> X. Rec. 141: ?S7-^?90 193.5. @us. 51:. I.: Electrosurgcry, Am. J. O+thodonties & Oral Furg. i7: 83.P9. Feb.. 194-1. 1Iaeth, H.: Complications of ElectrosurgeqanIl Their Treatment, .J. ‘Oral Surg. I: L’os-209, 1943. Baer, P. S., Sumner. C. I?.: III. and Seigliano, J.: Studies on a Hydrogenated Fat-Zinc Bacitracin Periodontal Dressing, ORAL SGRG., ORAL AIED. S; ORAL P9TH. 13: 494.498, 1960. Bhaskar, S. N.: Synopsis of Oral Pathology. St.. Louis, 1961, The C. V. XosbCornpan>-. pp.
15. 16. 17. 18.
340-342.
Shafer, TV. G.. Hine, Al. K.? and Lery, B. M.: h Tedbook of Olal Pathology, Pldadeluhia. 1958. W. B. Saunders Comxjanr-. uu. 422-424. Th&~a,‘K. g., and Goldman, H. S%: d;rai LPatllologyj ed. 5, St. Louis, 1960, The C. 1’. JUosby Companr, pp. 972-975. Ackerman, L. ez:-c: a.nd de1 Regato, J. h.: Cancer-Diagnosis, Treatmeut, and Prognosis, ed. 2, St. Louis, 1954, The C. 5’. DIosb~ Company, pp. 313-315. TYaidron, C. A.: Personal Communica.tlon.
R
ecently the English-languageliterature has reflectedan increased:intere+ in the often misnamedmultiple papillary excrescences, so-f$equently.&ed in denture-bearingareasof the.palate. Fisher and RzEshi$,aindY’r astor+~~kon&der the fundamental processto be .of an inflammatory n.aur& whereas.‘B echtp Robinson4and Waite5include,t.hese excrescences amongthe prema~igna+&ons of t.heoral cavity. Furthermore,s$&the lesionsa%:frequently assod+&dwith someform of palate-covering.@rosthesis, and since a. p‘ p;i(lelyquoted a&cleby Hobaek”reportedfifty-eve casesof carcinoma.ofthe.bar&palate ArkI’impl&&d denture irritation in t‘ wenty-one out. of thirty:three’ denture-wearing:pat$&s; it was thought that reactive papillary hyierplasia of-the palates‘ hould’ be studied in an attempt to resolvethe d$3iotcmythat now es&s. .‘ I‘ -. REVIEW OF THE LITERATURE
__. Becauseof the great variation in their appearanceand cfinical,characteris&.& numerousterms have been.used to. describethese iesions.~~SHe~ht,,!~ in I$ -eajly qa$er, describedthe lesion as a‘ “.. . . .painless~prol.&ratiori of’ the e$th&al tissue . . . made up of numerous.con&t& papiilomas,:.mi&erry.:rei in color, and generally confined to the tissue. under the relief ,. area f’ of. the .va&um . chamber.” Risher and Rashid emphasizedthe.degreeof &dness’ and related .it[ to;the degreeof inflammation present. Surface,plceratian,.~ho~~~er; .was-absentin all of the elevencasesthat they described.They also noted that the .&ll extentof the.papillary hyperplasiacould-bestbe.demonstrated by a stream.of&$ &*&&I perpendicularly to the patatal surface which causedthe -papillary &ass&~ to ., !..i,‘ .~ ._ ,‘ .:: L X%ief.. of the Orarl Surgery gqd Dentai C ‘ l’i&c~ $7th G&wk!E&pitkl; _.. .: 09757.
814
&‘b :
N$;V&& :$X:.x, . .‘.I _I.*.. ,‘ .. .
: .
~__
separate from one another, t.hus dispelling the consolidating effect of viscid saliva and pressures from the denture base. An obliquely directed blast of air IXOduced a rippling mot,ion similar to that. of a vheat field in ELbreeze. Waite5 emphasized the sessile nature of the lesion and stated t,hat the papillary elevations vary as to surface area and depth. He further described food a.ccumulations, ora. secretions, and unhygienic debris trapped at t.he base of the papillae. These lesions are located on the palate, usually -under the relief area of the denture, although Fisher and Rashid’ note t1ia.t any area covered by a. denture flange may become inrolved. Waite5 points out that the hyperplasia was found to encompass the entire palatal vault to the soft palate, even inr-olving the lingual aspect of the alveolar ridge. All authors have generally agreed that the specific cause and predisposing factors of the hyperplasia. were olxt~~re but that. the tissue change was associated with some form of irritation. Treatment yecommended varies from simply removing the denture from the oral cavity for extended periods of time until t,he pathologic condition has been resolvedl. ’ to radical excision of the lesion, including the periosteum down to the palatal bone”, 5 with fulguration of the hone if malignant change is involred. Electrosurgical treatment is mentioned bs Waite, who emphasizes increased postoperative pain over the technique of excision wit,h the scalpel. Vaite5 reviews the role of tissue irritation as a cause of carcinoma. specificallp the role of denture irritation as pointed out b;\- Hohaek” and the spec.ific malignant potential of reactive papillary hyperplasia. of the palate as cited by Robinson.” He then aptly concludes that diagnosis 1~~ biopsy x-aries with the malignant potential of the biopsy specimen. CLINICAL
INVESTIGATION
A ciinieal investigation was made of ninety-nine cases of reactive papiilar) hyperplasia of the palate which were seen and t.wated at Walter Reed Genera1 Hospital from December, 1959. to June, 1961.. The first part of t.his study was directed toward determining the incidence of reactive papilla,ry h:-perplasia of the palate. Since the United States Arm>De&al. Corps has maintainecl a complete permanent. dental record on all actireduty military personnel since Jan. 1, 1957, 4:617 s~wh records at. Walter Reed General Hospital were reviewed to establish this incidence of reactive papillary hyperplasia. Furthermore, since t.he attire-duty military population is usualll\ of a younger age group and co~hl not. be expected to contain a. great number of denture wearers, 564 records of retired military personnel were also screened. In addition, records of a group of 711 retired personnel and dependents cohere reviewed to give a general sampling of all types of patients. No attempt IV:%S made to examine t.he patients Ivhose rec.ords were screened. The second part of the study inrolved the examination and surgical treatment of a larger series of casest.han had previously heen r8:port,ecl. This xv-asdone in order to study the condition closely, and to this end outlying dental cl.inics at camps, posts! and stations near Walter Reed General Hospital were requested
1. Xu2nmar~- of findings 5,899 dental records reviewed
fable
of reack-e
papillary
h;-perp?:a.sia, of the palate in
Reactive
papillary
hyperplasia
of palate
817
Fig.
Fig. d
Fig. 1. Typical Fig. 2. Typical tient. Note narrow
midpalatine midpalatine vault form
vault loeation vault loeation with tendency
of reactive papilhry hyperplasia of palate. of lesion in dentulous non-denture-%rearing toward outfolding of tissue.
pa
The extent and size of the lesions varied with the irritative factors and the length of time of their influence. Thus, an early reactive hyperplasia generally involved only a small area, of the palate and a,ppeared as a reddened but not raised spost,whereas one which had progressed through the wearing of several sets of dentures sometimes covered the entire palate. Such a case was reported by Thomas (his Fig. 1202). Two types could be distinguished. In one there was complete absence of inflammation while others showed pronounced inflammatory changes. In addition, one can recognize a diffuse papillary type, varying from slight to complete coverage of the palate (Fig. 3)) and a nodular or polypoid type which is more commonly found in the posterior palatine vault and often extends onto the soft palate (Fig. 4). On the basis of clinical findings and history, the following agents appear to be of etiologic importance: 1. Ill-fitting prosthetic devices, full or partial dentures. 2. Mechanical irritation, such as perpetration of the lesion in successive denture bases (Fig. 5). 3. Day and night wearing of the prosthesis.
Fig.
Fig.
Fig. 3. Diffuse papillary 1Cypeof reactive liyperplasia. Fig. 4. IC’odula r or polypoid type of reactive h.yperplnsia.
Pig. 5. Inder kat .ions in denture base from~pre-e&king
pa$&&y
4. Lack of oral hygiene or poor oral hygiene. 5. Denture cleansing habits, the use of proprietary to Ch~mica1 irritation. 6. Putrefaction of food. ‘1. Decreased salivary fiow. 8. Smoking. 9. Allergy. 10. Predisposing factors.
hgperplasia.
solutions leading
In dentulons patients who did not have the irritative presence of a. prosthesis, the shape of the palatal vault, seemed to be significant. It tended to prerent the normal cieansing of t.he palate with the tongue. A high, narrow s-anlt with a tenc1enc.y toward outfolding of tissue seemed. most, likely to de\-elop the condition (Fig. 2). X study of the age distribnt,ion revealed that reactive papillay hyperplasia is most frequently fol,uld between the ages of 20 and 50 years, with the sing7le highest incidence in the second decade (Table II) _. Thus, t,he condition is not found in older denture-wearing patients only. Although reactive papillary hq’perplasia of the palate has a quite typical appearance, part~icularly under a blast. of compressed ai!:, it must. be differentiated from certain lesions which ilax-e a similar appearance. especially ill dentulous mouths. Some of the conditions which mimic the appearance of reactive in&mmatory papillary hypePplasia are midpalatine p;-oTertic granulomas. the fnngal gra.nulomas (,histoplasmosis. blastomgcosisJ and coccidiomycosis) , capillary hemangioma, and allergic lesions. Of more serious importance is the yecognition of exophytic. squamons-cell eafciiioma, either priniar>- or metastatie. In suspicious cases it is of paramount importance that a specimen of tissue be s~xbmit.t.ed for histologic study. Treatment
Three methods of therapy have been recommended. The conserratire met,l:od, which advocates removal of the denture for an extended period of at, least, 7 months, is obviously impractical, in view of the essential nature oi’ the appliance and the quest,ionable regression of the lesion. excision of the periosteum! is Full-thickness pal&al excision, including acceptable in the ca,se of small lesions involving only t,he hard palate itself. However, full-thickness removal in very extensive cases would certainly jeopaydize the blood supply if both the posterior palatine and nasopalatine x-essels were sacrificed needlessly. Estensis-e exposure of palatal bone to the oral secretions and flora would also tend to increase the irxidence of pain and osteomyelitis, although the use of protect.ive dressings as recommended by Thoma (his Fig. 1194) woulld minimize this danger of infection. This treatment reqnires a prolonged healing period of 6 to 9 weeks.
Table
patients
II. Age distribution among denture-mcaring and non-delltllve-~vea~ing with reactive papillary hvperplasia of the palate
10 20 30 10 50 60 so SO
to to to to to to to
to
19 29 39 49 59 69 79 89
3 35 “3 19 8 5 1
1
3 “0 12 13 4 3 0 0
0 0. 2 1 0 1
0”
Electrosurge~y has been advocated for oral surgical procedures for many years. This method has been the subject. of comprehensive papers by Cnshing,” Asgis,lo Ogus,ll and Maeth,l’ and 1 ha-ve found it to be the method of choice. In the present study, a portable &vie unit was employed. A loop eiectmde, 1 em. in diameter, was used as the active electrode, and a. thin lead plate was rolled into a cylinder to act as the passive electrode. The patient heId this in thus completing the circuit (Fig. 6). his hand throughout the pr~ee&xe, The unit was used on eautery current, with a, current-intensity setting of 35 to 40 units. The intensity was, varied according to the amount of tissue requiring removal, but it was always set lower if extensive dehydrat.ion of the tissues resulted. In all. but one of the cases profound anesthesia x%-asobtained by means of 2 per cent. lidocaine with 1 :lOO,OOO epinephrine infiltrated- swb~~ucosa~ly in the palate and into the mucobueeal fold. A posterior-t,o-anterior sweep of the autting loop to a, depth off approximately tissue in strQs~ 1 to 2 cm. in 1 to 1.5 mm. was used to remove the hyperplastie length before the loop was removed from the mouth. The~patient was instructed to exhale so as to expel the smoke generated bmythe eha,rring of the tissues. This proeedure was repeated until removal of all the inflamed hyperp!astic tissue was completed. (Complete removal can be ascertained by the .yellow-gray appearance of the underlying tissue.) The charred tissues were wiped away by the assistant, using moistened 2 by 2, inch sponges made into a ball and clamped on a curved hemostat. Tissue from a represent,ativc area was removed for pathaiogic study,
‘ig. 6. Portable and cutting)
Bovie unit, passive used throughout for
electrode (rolled lead eleetrosurgical removai
sheet), axid of tissues.
active
~$eetic
Volume Number
20 6
Reacthue pq&ary
hyperplasia
of palate.
821
usually twothirds of the way through the procedure. Bleeding could be reduced somewhat by removal of the denture for 48 hours preoperatively so that the inflammatory process could abate and by cauterization of the bleeders with the loop. A zinc ‘bacitracin-hydrogenated fat periodontal dressingI was then softened in nearly boiling water and spread over the denture base or surgical splint. The patient was instructed to moisten the operated area with s,aliva and the denture
4
Pig. 7. Photographic summary of operative technique. 8, Marked relief chamber in denture. B, Preoperative reactive hyperplasia. C, Appearance after electrosurgery; darkened areas are sites of biopsy and bleeders which have been cauterized. I), Zinc bacitracin periodontal pack. E, Healed case.
which takes :3 to 4 weeks. Occasionally\: a become denuded because of the slo~xgh of the mill usually recorer it if the heat has not Occasionally a small sequestrum will form epithelization takes place.
small area of palatal bone will thin overlyi-lg tissue. Granulation damaged the bone beyond repair. and is sloughed out before final
Histopathoiogy
The microspcopic findings are summarized in Table III. Since the tissue specimens were examined by several resident pathologists, a lack of uniformiQ7 in the final histopathologic diagnosis resulted. The histologic findings were fairly consistent 1 however. They showed t.he numerous papillary excrescences i Fig. S) corered usually b- nonkeratinized hyperplastic epit.helium. the rete pegs of which may be acanthot.ic or show growth into the submucosa to form a psencloepitheliolllatons hyperplasia. Not infrequently these rete pegs are cut tan$entiall.v. thns giving the appearance of islands of epithelinm below the basement membrane ( F-g. 9 ) . The snbmucosal connective tissue shows a dense plasma-cell and lymphoc>-tic infiltra.te. FOLW cases &on-ed hyperkeratosis (Fig. 101. and t.wo cases of ulceration were also noted. In none of the cases reriexed n-as there evidence of dyskeratosis. Recurrence
Cases treated by means of a. Ml-thickness palatal excision required a postoperative healing period of 8 to 10 weeks until comp1et.e regeneration of the tissnes occurred. The use of a clear acrylic splint was adrocat,ed to protect the surgical site. Althongh the original protocol called for a. determination of recurrences, t,his study did not cover sufficient time .to permit any specific conclnsions to be drawn. DISCUSSION
Ill-fitting full upper acrylic and vlucanite dentures with relief chanlbe~s ha-c-e general157 been blamed for the formation of reactive papillary hperplasia of the palate. In a recent study, howes-er, Yra.storza’ points out. that acrylic dent.ures without relief chambers are also frequently a.ssociated with the condition. We agree with these findings. In the present series of cases, however, an almost equal nnmber vere found under partial dentures, part.icularlthe temporary acrylic t:-pe replacing anterior teeth, which are usually inserted relatively earl>- in life. A nnmber of c.ases also were associated x-it11 partial dentures of cast chrome st.eel metal. Although most, commonly- found in the midpalatine vault, in the relief chamber area, the lesion is freqnently located la.terall;.- on the paIate, over the crest of the alveolus. and bnccally under the denture flange. In spite of the long- list of cont,ribnt,ory factors enumerated. I am inclined to agree with YrastorzaY that a. predisposing factor is present as a ma.jor etiologic agent, for an unaccountabie nmnber of patients wear ill-fitting prostheses? have poor oral lggiene and are free of lesions. Although it, is difficult to determine the onset. of a lesion when there a.re no subjectiT-e symptoms, the condition has been noted as early as 9 months
8
Pig. Fig.
8. Photomierograph showing papilkq nature 9. Submucosa shows inflammatory infiltrate.
of lesion.
atid as k&e as 33 years after the insertion of dentirres. Of ~pa&kular ~~~~~~a~~e, however, was the high incidence of oecurrwm in the second dee~de -of life. This fact has not been brought out in any of the previous, stndies -review&l and the present finding is direct1.y attributable to the nakxre of the patient population treated in &Mary dental facilities. Biopsy is of particular importance in, the case 6f dentulous pa&mtsm’as the lesions can mimic other diseasesof a nmre serious natme.
Volume
20
Number
6
Fig.
IO. Pliotomicrograph
Reactive
showing
papillary
pseudoepitl~eliomatous
hypevplmia
hyperplasia
of palate
and
825
ulceration.
Since no ‘dyskeratosis wa,s reported by the twenty-two pathologists who have reviewed the microscopic specimens, I agree with Bhaskarl” and with Shafer, Hine and LevyI” that the lesion is benign and devoid of any premalignant potentiality. Since chronic irritation of epithelial tissue has been universally recognized as one of the leading etiologic agents in cancer, the incider,ee of squamous-cell carcinoma of the palate has been reviewed in an attempt to establish a, possible relationship between the existence of a reactive papillary hyperplasia of the palate and the subsequent development of carcinoma. Few studies or reports concerning the rela.tionship of the wearing of dentures to squamous-cell carcinoma of the palate are available. They are primarily found in the European literature. ThomaJ6 makes reference to cases of Shneider, Rhenwald, and Voss and concurs with their statement that they cannot say empirically that the effect of the prosthesis is the cause of the carcinoma in every case. However, ThomaP reports a case of extensive benign papillomatosis in which, 14 years; after ra.dical electrosurgical excision, extensive carcinoma of the palate with involvement of the sinuses was found t.o have developed. Ackerman and de1 R.egato17 consider carcinoma of the hard palate to be very rare. They quote New, who found only twenty-five cases of epidermoid carcinoma of the .hard palate among approximately 5,000 cases of cancer of the oral cavity, an incidence of 0.05 per cent. Hobaek,G in his extensive study of 560 cases of oral carcinoma, was able to demonstrate a “casual connection between irritation caused b,y prosthesis and cancer development in 86 of these cases.” Of particular interest was the finding of sixty-one cases in women (70 per cent) I twelve of whom (‘20 per cent) presented :marked Plummer-Vinson syndrome. The demure-base material in
2. The lesion was found mdev a.11sorts of pl.ostl~eses--~)oth frill and partial, acrylic or cast. base metal-and was not necessarily limited to the palatal 111Wosa >YOpT.
3. The lesion was found most frequently in denture weare.rs between 20 and 50 years of age, n-it,11 the highest single incidence of occurrence in the second decade. 4. Eight. cases were detected in non-denture x-earers. 5. Two general types are recognized: (a) DSfnse papillary and (1)) nodular or polypoid. 6. Etiology was discussed. No single. cause-and-effect ~elat~ioaship is noted. 5 predisposition factor is thought to c&t.. 7. Eled.rosnrgical removal is recommended as the preferred treatment. 8. The clinical and microsc.opic appeara.nce of the lesion was described. The lesion is considered to be benign, reactive? inflammatory in natnre. and essential.ly desoid of any premalignant potent.ialit.:+-. In the litepatwe reriexwd, no stud,~ has definitel>- shoxn a significant Pelationship between reactive papillar:hyperplasia of the pala.te and the occwrcnce of epiderroid carcinoma of’ the palate. 9. Prevention of recurrerxe of the lesion has been discussed.. Illustration Services of Walter Reed Grateful acknowledgment is given to the SIedical Army Hospital, Fort Eenning, Georgia, General Hospital, Washington 12, D. C., and Martia for the photographs and photomicrograpl~s in this paper. The a.uthor gratefully acknowledges the encouragement and asaistawe of Colonel Ii. B. Shira, Chief of Oral Surgerp ani\ Dental Rw-ice? Walter Reed General Hospital. Washington, D. C. REFERENCES A. I<., and Rashid, 1. Fisher: ~JIucc~sa~ ORAL SGRG., OPAL 2. Trastorzs, J.: Inflammatory
I'. MED.
J. : hfktmmatory & ORAL
PATH.
Papillary 5:
191-198,
H;,yerplasia
of
the
Palatd
1952.
Papillary Hypexplasia of the Palate, J. Oral Surg.: Anesth. D. Sel-v. 21: 3.31-336, 1963. Sm.S.: Chronic Irritation of the Eyithelial Tissues of the DIonth hssocinterl TYith Dentures. Am. J. Orthodontics & Oral Surg. 25: 574-565, 1939. Xohinsou. H. B. C.: Neoplaams axd “Precaurerous” Lesiolls of the Oral Regions, D. Clin. Korth America, p. 621, November. 11157. Waite? D. E.: Inflammatory Papillar>Hyperplada, J. Oral Surg., dnesth. S- Hosp. D. Serv. 19: ‘7111-214. 1961. Kobaek, A.: Dental Prosthesis and Intraoral Epirlermoid Carcinoma., leta rarliol. 32: 259-27.3. 1919. Walter: J.: Prosthet.ic Mucosal Hypertroph>in the Xouth Simulating Malignancy? Writ. M. J. 1: l&29-1431, 1953. Thoma, K. H.: Oral Surgery, eA. 4, St. Louis, 1963, The C. 5’. hJIosb~Cornpan-. pp. & Hosp.
-I3. He&t, 4. -5. 6. 7. Y.
91%9'1. 9. Cusbing. 10. Il. 1”. 13. 14.
H.: Eleetrosurqery as an lid to the Removal of Intracranial Tumors~ Surg. Qpec. & Obst. 47: 751-+84, 1928. Asgis: A. J.: Clinical Oral Elec,trosurger>-> X. Rec. 141: ?S7-^?90 193.5. @us. 51:. I.: Electrosurgcry, Am. J. O+thodonties & Oral Furg. i7: 83.P9. Feb.. 194-1. 1Iaeth, H.: Complications of ElectrosurgeqanIl Their Treatment, .J. ‘Oral Surg. I: L’os-209, 1943. Baer, P. S., Sumner. C. I?.: III. and Seigliano, J.: Studies on a Hydrogenated Fat-Zinc Bacitracin Periodontal Dressing, ORAL SGRG., ORAL AIED. S; ORAL P9TH. 13: 494.498, 1960. Bhaskar, S. N.: Synopsis of Oral Pathology. St.. Louis, 1961, The C. V. XosbCornpan>-. pp.
15. 16. 17. 18.
340-342.
Shafer, TV. G.. Hine, Al. K.? and Lery, B. M.: h Tedbook of Olal Pathology, Pldadeluhia. 1958. W. B. Saunders Comxjanr-. uu. 422-424. Th&~a,‘K. g., and Goldman, H. S%: d;rai LPatllologyj ed. 5, St. Louis, 1960, The C. 1’. JUosby Companr, pp. 972-975. Ackerman, L. ez:-c: a.nd de1 Regato, J. h.: Cancer-Diagnosis, Treatmeut, and Prognosis, ed. 2, St. Louis, 1954, The C. 5’. DIosb~ Company, pp. 313-315. TYaidron, C. A.: Personal Communica.tlon.