some aspects of parodontal disease

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22 SOME ASPECTS OF PARODONTAL DISEASE. ~ BY ADRIAN COWAN H AVING been asked to speak about parodontal disease, I have decided in this short paper to deal with the development of simple pyorrhcea from the stage of gingivitis, and to touch on some of the points of interest in the hope of provoking a discussion. Of the innumerable theories on the origin of pyorrhcea, the simplest and most logical, to my mind, is that of Fish. ~ He bases his view on the fact that our gums do not nowadays receive enough frictional stimulus to enable them to form the keratinous layer which is their protection. In days of yore, when our ancestors used their teeth for more activities than eating, and before our so-called civilised foods were forthcoming, this stimulation was not lacking. As a result of this absence of stimulus the gum can be torn fairly easily by a sharp piece of crust or other food : this results in the formation of a series of tiny ulcers which bleed, with the production of marginal gingivitis. Before the ulcers can heal, they are again traumatised; soon the inevitable secondary infection is well established, by far the commonest organism being Str. viridans. The organisms are kept strictly in their place by a leucocytic barrier, first polymorph and later round- celled, and, unless they are driven down into the depths of the subjacent connective tissue by trauma, the area beneath the floor of the ulcer is sterile. The toxins from the bacteria, however, seep through, and affect the various cellular elements in the region. The more highly specialised a cell, the less stimulus is needed to make it grow, and so the epithelial and bone cells in the immediate neighbour- hood where toxin is most concentrated are killed, while those further away may be stimulated. The epithelium which survives tends to proli- ferate rapidly but incompletely, and undergoes premature degeneration. On the other hand, the fibroblasts (which are of a lower degree of specialisation) are stimulated to grow, except in the most concentrated toxic area; this explains why a loose pyorrhcetic tooth may be so hard to extract. Cementum on the root receives its nutrition from the lymph in which it is bathed, and when this is polluted by toxins there develops either a hypertrophic or absorptive change, depending on the concentration. But the parodontal membrane itself is composed chiefly of collagen laid down by the fibmblasts ; this is an inert substance, very strong, but coin- p]etely incapable of repair or resistance to toxins or lysins. That is why pus treks in body tissue, by breaking down collagen, and here, too, destruction of the membrane proceeds more rapidly as the collagen is attacked. As the tissue under the epithelium is gradually destroyed, the sulcus around the tooth deepens, and the tag of gum thus released begins to be moved about by food. As a result, the surface tends to heal, because the gum on which it lies is moving with the pressure, and the friction Com~nunication to the Section of Odontology, made on Oct. llth, 1950.

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22

S O M E A S P E C T S OF P A R O D O N T A L D I S E A S E . ~

BY ADRIAN COWAN

H AVING been asked to speak about parodontal disease, I have decided in this short paper to deal with the development of simple pyorrhcea from the stage of gingivitis, and to touch on some of the

points of interest in the hope of provoking a discussion. Of the innumerable theories on the origin of pyorrhcea, the simplest

and most logical, to my mind, is that of Fish. ~ He bases his view on the fact that our gums do not nowadays receive enough frictional stimulus to enable them to form the keratinous layer which is their protection. In days of yore, when our ancestors used their teeth for more activities than eating, and before our so-called civilised foods were forthcoming, this stimulation was not lacking.

As a result of this absence of stimulus the gum can be torn fairly easily by a sharp piece of crust or other food : this results in the formation of a series of tiny ulcers which bleed, with the production of marginal gingivitis. Before the ulcers can heal, they are again traumatised; soon the inevitable secondary infection is well established, by far the commonest organism being Str. viridans. The organisms are kept strictly in their place by a leucocytic barrier, first polymorph and later round- celled, and, unless they are driven down into the depths of the subjacent connective tissue by trauma, the area beneath the floor of the ulcer is sterile. The toxins from the bacteria, however, seep through, and affect the various cellular elements in the region.

The more highly specialised a cell, the less stimulus is needed to make it grow, and so the epithelial and bone cells in the immediate neighbour- hood where toxin is most concentrated are killed, while those further away may be stimulated. The epithelium which survives tends to proli- ferate rapidly but incompletely, and undergoes premature degeneration.

On the other hand, the fibroblasts (which are of a lower degree of specialisation) are stimulated to grow, except in the most concentrated toxic area; this explains why a loose pyorrhcetic tooth may be so hard to extract.

Cementum on the root receives its nutrition from the lymph in which it is bathed, and when this is polluted by toxins there develops either a hypertrophic or absorptive change, depending on the concentration. But the parodontal membrane itself is composed chiefly of collagen laid down by the fibmblasts ; this is an inert substance, very strong, but coin- p]etely incapable of repair or resistance to toxins or lysins. That is why pus treks in body tissue, by breaking down collagen, and here, too, destruction of the membrane proceeds more rapidly as the collagen is attacked.

As the tissue under the epithelium is gradually destroyed, the sulcus around the tooth deepens, and the tag of gum thus released begins to be moved about by food. As a result, the surface tends to heal, because the gum on which it lies is moving with the pressure, and the friction

Com~nunication to the Section of Odontology, made on Oct. l l th , 1950.

SOME ASPECTS OF PARODONTAL DISEASE 23

is reduced. A new ulcer develops instead at the base of the loose gum where it hinges on the normal tissue.

At this stage the condition has changed from chronic marginal gingi- vitis to what Fish calls "pyorrhcea simplex ", and because the ulcer is at the base of the pocket, bleeding occurs only when the flap of gum is bent. This means that bleeding is less frequent in the later stages of chronic marginal gingivitis and, of course, in pyorrhcea; this is a pitfall for the many investigators who have tried to grade severity of lesions ~ccording to the amount of bleeding from the gum.

As the underlying tissues are destroyed, the surface epithelium grows down over them, following the tendency of epithelium to cover a denuded surface; this epithelium becomes re-attached to the tooth at the highest level of healthy tissue which remains. This explains how the epithelium, which has no destructive powers, comes to be occupying the place previously held by the parodontal fibres.

The cementum exposed by the destruction of the parodontal membrane has now lost its nutritive supply, and is dead. Furthermore, it harbours organisms and contributes to the parodontal damage.

Cementum is very like bone in structure, and when it is dead it is sequestrated. But cemental sequestration is brought about by a biological sealing off, since it cannot be exfoliated.

In the denture, a layer of callus-like substance, which has been termed " eburnoid ", seals it off 2 from the vital pulp, while outside, as we have seen, the epithelium grows down to the first healthy cemental cell. Thus that section of cementum is isolated.

Clinically, at this stage, we find flattening of the alveolar crest, a deep pocket filled with debris forming around the tooth, and considerable loosening due to loss of parodontal attachment. But so long as the pulp o~ the tooth is alive, indicating that infection has not reached parodontal membrane at the apex from that source, the tissues under the lymphocytic barrier at the base of the pocket are sterile.

The organisms thus remain in equilibrium with the leucocytes unless they are thrust into the deeper tissues by trauma, and this, of course, can and does easily occur. In this event they are either destroyed by phagocytes, wafted down the lymphatic channels, washed into the blood stream to be destroyed, or else find temporary refuge in some necrotic nidus where they multiply to set up a parodontal abscess.

Okell and Elliott 3 found that in cases of severe gingivitis, 11 per cent. showed transient bacteri~emia on chewing, while the figure rose to 75 per cent. after extraction. In clinically normal gums, 34 per cent. showed bacteri~emia after extraction, the duration of blood infection persisting for periods of from 10 minutes to 8 hours.

What are the dangers of pyorrhcea? First, it is the chief cause of loss of teeth in adult life, and, since

progressive alveolar absorption occurs, it is the chief cause of headache for those of us who have to make lower dentures.

Apart from droplet infection, the patient is swallowing much pus and filth from the pockets; this must have a bad effect on the gastric mucosa and may be an etiological factor in the production of peptic ulceration.

Greatest danger to life, however, arises from baeteri~emia in those

24 IRISH JOURNAL OF MEDICAL SCIENCE

patients whose heart valves are weakened from previous rheumatic car- ditis, or by some congenital flaw. Subaeute bacterial endocarditis is a well-recognised entity which is almost invariably due to infection with mouth organisms. Selbie has proved this serologically, and the organism involved is practically always Str. viridans, the chief contaminant in pyorrhcea~ Thus, pyorrhcea is a much more potent source of this con- dition than the apical granulomata which have condemned so many teeth.

To-day, with the introduction of chemotherapy and antibiotics, and with the known sensitivity of Str. viridans to both sulpha drugs and penicillin, there is no need for even the comparatively rare cases which follow dental work to occur.

Extractions should be limited in number, consultation with the physi- cian should always take place, and the patient should be hospitalised, and given suitable chemotherapeutic prophylaxis.

T r e a t m e n t o f Pyorrho~a : For some time I have been interested in ascorbic acid as an adjunct

to treatment. I t is well known to be of value in the treatment of bleeding gums, but its use was purely empirical, and I was struck by a curious similarity in radiographs of early cases of pyorrhcea and certain changes described in experimental scurvy.

Crandon ' put himself on a vitamin C-free diet and carefully observed the changes which took place. He described an irregularity in the parodontal shadow as being the first radiographic change in the mouth.

Observing a group of gingivitis and pyorrhcea cases here, during and just after the war when citrus fruit was scarce, I noticed that many of them showed this change, too. A simple petechial test showed that the vast majority were mildly deficient in ascorbic acid, and treatment on that line was instituted, controlled by further petechial tests.

After 6 months' treatment, radiographs showed an improvement in the parodontal shadow, with obvious clinical improvement also. I hope to complete that work and discuss it in detail here.

The principles involved in treatment are: elimination of pockets and maintenance of healthy, hard epithelial attachment. One can arrest pyorrhcea only at the stage at which it is found it is not cured.

Pockets are eliminated by papillectomy (removal of the papilla in- volved) or, in wider eases, by gingivectomy, care being taken to select the cases so that the treatment will not fall into disrepute from being carried out on subjects whose teeth are--to coin a phrase--hanging on by the tips of their apices. This treatment is followed up by massage with wooden points to stimulate keratin formation and keep the inter-spaces clear.

Scaling is essential : it should be done before operation and at regular intervals. I t should be something between what Samson described (as only he can) as the bloody surgical operation called " deep scal ing", or the other extreme, " t a r t a r flicking "

1. Fish, E. W. (1944). Parodontat Disease. Eyre and Spottiswoodo. 2.-Fish, E. W. (1948). Surgiccd Pathology o! the Mouth. Pitman. 3. Okell and Ell iot t (1935). Lancet, ii, 869. 4. Crandon, Lund and Dill (1940). New Eng. J. Med., 222, 748.

SOME ASPECTS OF PARODONTAL DISEASE 25

~ise~ssibn. The PRESIDENT (Mr. G. YEATleS) : I am very glad indeed to see so many mem-

bers of our profession a t th i s i n a u g u r a l m ee t i ng of t he Sect ion of Odontelogy of the Royal Acade~ny of Medicine in I r e l and . I t is an auspicious and a n i m p o r t a n t occasion. Some years ago a g r e a t need was fe l t amongs t members of our profession for a t r u l y in s t ruc t ive and scientific cen t re a t which va r ious subjects concern ing our everyday work could be discussed: th is led to the founda t ion of the Odontological Society.

F r o m a very small beg inn ing , our mee t ings d u r i n g recen t years have been very well a t t e n d e d and m a n y subjects of g r e a t i n t e r e s t have been discussed. Our p resen t membersh ip is most sa t i s fac tory , bu t I would like to see i t grow in numbers . There are very def in i te reasons why i t shouM do so.

" G r e a t t h i n g s , " i t is said, " of ten beg in in a small way , " and so i t has been. wi th us. S t a r t i n g wi th a few or ig ina l members , our Odontological Society has shown a s teady growth, and las t yea r we had the honour of a n i n v i t a t i o n to form a Sect ion of Odontology in the Academy of Medicine in I r e l and , s im i l a r to t he Odontological Sect ion of the Roya l Society of Medicine in London. Th i s suggest ion, we consider, was a g r e a t honour , and one which adds g rea t ly to t he pres t ige and s t a tu s of our profession.

This is the first t ime, so f a r as I am aware, t h a t our profession has been ex te rna l ly and officially recognised as a body of scientific men. H i t h e r t o , all our societies and associat ions have been s t r ic t ly confined wi th in a na r row pro- feesional circle. We are now recognised as a b r a n c h of the medica l p rofess ion; as members and fellows of th i s Academy, we may t ake p a r t in i ts scientific mee t ings and b r ing our views and exper ience to bear on those subjects in which we find a common in te res t . The medica l members, too, may a t t e n d our meet ings and very probably l ea rn s~meth ing from us.

This is a very desi rable s i t u a t i o n ; as t he years go by, t he profession of d e n t i s t r y is more and more becoming i n t e g r a t e d in p rac t i ca l med ic ine - -we share in t he new anaesthetics, new sedat ives , t he use of v i t a m i n s and ant ib io t ics , t h e s tudy of co-rela ted diseases, and so on.

May I ask you for a m o m e n t to consider our suggested p r o g r a m m e for the coming session? I t deals wi th such subjects as the use in d e n t i s t r y of t r i l ene analges ia , t he s tudy of ant ib io t ics , t he cold cu r ing acrylics (which I believe will revolu t ionise fill ing mater ia l s ) , absorbable h~emostatics and t h e i r t h e r a p e u t i c ac t ion , a n d the rSle of d ie te t ic fac tors in den t i s t ry . M a n y of these subjects are- ~o t to be found in the tex tbooks as yet , and I ask you if any den t i s t who wishes to keep himself ab reas t of the modern advances in d e n t i s t r y can proper ly neglect a t t e n d a n c e a t these meet ings . I can assure you they will be of in tense in te res t r w i th up- to- the-~ninute i n f o r m a t i on on recen t advances and new techn ica l processes. A t our las t mee t ing of the Odontological Society two or t h r ee coun t ry members h a d t rave l led a very long d is tance indeed to be present . T h a t was a most encourag ing sign, and t hey are g e t t i n g o ther members in t h e i r dis- t r i c t s to jo in ; also all members of t he I r i sh D e n t a l Associat ion have been notified. So t h a t th i s new Sect ion should now become well known as a n in- tense ly prac t ica l , scientific and h ighly in s t ruc t ive body, where any member of t he profession can l ea rn the l a tes t theor ies and methods and hear discussions on m a t t e r s t h a t so closely concern h im. As your P r e s i d e n t , I will do my u t m o s t t ~ see t h a t t he pape r s and discussions we may have are ca r r i ed ou t on these l ines, t h u s ensu r ing mee t ings which no den t i s t can real ly afford to anise. You will a lways and a t all t imes be more t h a n welcome.

Two po in t s I mus t m e n t i o n : firstly, we owe a deep debt of g r a t i t u d e to t h e Hen . Sec re t a ry of t he Odontelogical Society, Mr . Donogh O 'Br ien , for t he immense a m o u n t of t roub le he has t aken , and his real ly h a r d work in g e t t i n g th i s Sect ion of the Academy u n d e r way. I know t h a t a t t imes m a n y difficulties arose, and he r ichly deserves f rom us all t h e pra ise t h a t is his due h a v i n g b r o u g h t i t to such a successful issue.

My second du ty is to t h a n k you all for t he honour you have confer red on m e in e lec t ing me as your f irst P re s iden t . I t is an honour which I ve ry m u c k apprec ia te , and I assure you I will do my u t m o s t to see t h a t the Sect ion tlourishes.

This has been a wonderful ly i n t e r e s t i n g open ing paper , r emarkab le u n d e r t h e c i rcumstances , since Dr . Cowan had only five days in which to p r epa re i t . We. have seen t h r e e very i n t e r e s t i n g slides of w h a t t akes place in the i n i t i a l s t a g e s of pyorrhoBa. I should l ike to know if pyorrho~a is a h e r e d i t a r y disease; we have of ten seen hea l thy people w i th pyor rhmic mouths . They reach a f a i r age, and t he p y o r r h e a has no t affected t h e m a t all. I ra ise t h a t poin t , as one wh~ has seen so m a n y p a t i e n t s whose t e e t h h a d been ex t rac ted . One wonders w h e t h e r i t is b e t t e r to give t he p a t i e n t s t he use of t h e i r pyorrhmie t e e t h for a l onger period. I would l ike to ask Dr . Cowan how he admin i s t e r s ascorbic acid,

2 6 I R I S H J O U R N A L O F M E D I C A I J S C I E N C E

whe the r by a d m i n i s t r a t i o n of v i t a m i n C or by oranges . There is a per iod when there are deep pockets• You may e l imina te t h e m surgical ly ,*but they will fo rm aga in . I t is difficult to ge t the p a t i e n t to keep t he pockets clear. I t is a problem we face every day of our lives• • Mr . COm~OLT.T: W h a t dosage is admin i s te red of su lpha d rugs and penic i l l in m bacter~vmia, a n d of ascoroic acid P

Mr. FRAmz DVNNB: I do no t t h i n k we could have found a be t t e r speaker here on this subject t h a n Dr. Cowan. The E a s t m a n Den ta l Clinic advise p r e v e n t i n g the onset of pyorrhcva in t he mouth• Very often when we scale the t ee th of ~lfildren we do no t thoroughly clean t h e month . W h e n we have thorough ly oleaned the mouth we should inves t iga te the chi ld 's chewing habi ts , and we ahould demons t ra te how to use a too thbrush . I n th is way we would check g ingiv i t i s . Dr. Cowan deal t wi th the advanced s tage of pa rodonta l disease. He would be the first to agree t h a t the opera t ion of gingivectomy is no t now used

much a s i t was. I t should become a n o u t m o d e d operat ion. I hope to see the day when i t will be unnecessary to per form t h a t operat ion.

Mr. DONAOH O'BR~ZN: Can Dr. Cowan give us a definit ion of pa rodon ta t diseaseP Is there a difference between pa rodon ta l disease and per iodont i t i sP I would say t h a t t r a u m a t i c occlusion is due to m a l n u t r i t i o n . A large pe rcen tage e f cases of pa redon ta l disease occurs in p a t i e n t s wi th long tee th . I n these emms you do not get the same ke ra t i n i s a t i on of t he gum marg in . I n pa rodon ta i • lisease we are occupied in cur ing the symptoms and no t the cause. I n most cases you will usually find some definite cause.

Dr . J . KEITH: Is i t no t wrong to e x t r a c t a t one s i t t i ng a n u m b e r of t ee th affected with pyorrhcea ? Should they no t be ex t r ac t ed one or two a t a t ime ?

Mr. MURPHY : AS to pyorrhcea be ing hered i t a ry , I have th ree p a t i e n t s - - f a t h e r , mother and son. They all developed pyorrhcea between the ages of 19 and 22. We seem to pay excessive a t t e n t i o n to the t r e a t m e n t of pyorrhcea ins tead of

• t epp ing i t f rom forming. Are nylon too th brushes de t r imen t a l to t he gums? Is pyorrhcea aggrava ted by diabetes, anaemia or by prolonged t r e a t m e n t wi th d rugs for o ther diseases?

Co~ndt. J . DELANEY: IS t r a u m a t i c occlusion a causal fac tor in pyorrheea ? If i t is, how can t r a u m a t i c occlusion lead to des t ruc t i on of pa rodon ta t membranes ? Will pyorrhoea spread to the r e m a i n i n g t e e t h ?

Dr. J . RYA~ : If a p a t i e n t has pa rodon ta l disease, as a rou t ine t r e a t m e n t I give a simple mouthwash con ta in ing iodine. W h e n scaling, i t is very difficult to ge~ r id of every t race of t a r t a r , and i t c anno t be done a t one s i t t ing . Where the pockets are deep in pa rodon ta l disease the t rouble has t h e n reached the bone. The only way to e l imina te deep pockets is to go r i g h t down, e l imina te t he in- fected bone, and pack these pockets. I do not believe in the use of eseharot ics for pyorrhcea or pa rodon ta l disease.

Dr. COWAN (in reply) : The quest ion of he red i ty is a difficult one. I believe t h a t only the gum and tooth fo rma t ion which can be the predisposing factors a r e hered i ta ry . I t is no t uncommon for ch i ld ren to i nhe r i t t he large t ee th of the f a the r and the small jaws of the mother .

The p a t i e n t whose res is tance is lowered is ce r ta in ly more suscept ible to pyorrhcea, as he is to any o ther disease.

The dosage of ascorbic acid in my expe r i m en t a l work was 500 mgm. da i ly for a week. I t was an in ten t iona l ly large dose, bu t the v i t a m i n is qu i te harmless .

When I am ex t rac t ing , I give penic i l l in abou t hal f an hour before opera t ing , in doses va ry ing f rom 200,000-500,000 uni ts , t he l a t t e r for surgical cases such as impacted lower t h i r d molars. Dosage can be con t inued wi th proca ine penici l l in la ter .

Scal ing is very i m p o r t a n t , b u t can be g rea t ly overdone. I have seen damage caused by so-called " deep scal ing " .

The subject of t r a u m a t i c occlusion is much too wide to discuss now. Suffice i t to po in t ou t t h a t any tooth receiving more t h a n i ts share of t he b i t i n g force may be subject to ver t i ca l or l a t e ra l stress, and the p a r o d o n t a l m e m b r a n e is t o r n o n the t r ac t ion side and th ickened on the pressure side. Deep pockets resu l t on the t r ac t i on side.

I be]ieve t h a t h a r d nylon too th brushes a re ha rmfu l , and avoid t h e i r use where possible.

All g ingivi t is , f rom wha teve r source, should be r ega rded as po t en t i a l pyorrhcea. I t is easy for a phys ic ian to miss the cond i t ion if i t is a t t he chronic m a r g i n a l

:gingivit is s tage. Escharot ics should only be used as a t e m p o r a r y measure to control t h e inf lamed

t issue. They should no t be necessary for more t h a n a few days a t a t ime. I d isagree t h a t the bone is infected in pyorrhcea, unless ac tua l ly exposed,

The changes which t a k e place in the a lveolar bone a re en t i r e ly t he r e su l t of ~oxins affect ing bone cells. In fec ted bone is dead bone.