Oral Manifestations of the Nutritional Deficiency Diseases

Scurvy, Rickets, Pellagra and Beriberi Should be Recognized by Dentists

Dr. Mathew Podolin Discusses these Disorders in


                Scurvy is a nutritional deficiency disease and should be of considerable importance to the dentist for several reasons.

1st. Because scurvy has characteristic oral manifestations and the dentist has the opportunity to detect this disease long before the patient reaches the physician.

2nd. Because the oral symptoms although characteristic to this disease are nevertheless similar to many other oral disfunctions and in order to make a differential diagnosis a knowledge and ability to recognize scurvy is very helpful.

3rd. Because during the active process of scurvy especially in the advanced stages the patient develops a secondary anemia and becomes susceptible, both locally and systemically to infections and possible complications. Under such circumstances it is advisable to postpone dental surgery until the patient recovers.

Oral Symptoms

The oral symptoms are perhaps the most characteristic of scurvy. The swollen spongy bleeding gums, sometimes so swollen that they appear as double ridges, the crest of the swelling being at a level with the occlusal surface of the teeth. The tongue is usually clean, but injected and sometimes swollen. The teeth are usually carious, unclean, and become so loose that they frequently fall out. The breath is foul. The salivary glands may be enlarged. Spontaneous hemorrhages from the gums is quite common, but should not be confused with the various blood discrasias.

Generally the patient is anemic, very week and emaciated. Hemorrhages under the skin, (purpura) especially in the lower extremities can be readily observed in most cases. The purpura may be from a small single area to a generalized subcutaneous hemorrhage from hips to ankles. These symptoms are intensified with the progress of the disease. As the disease progresses, the patient may become so weak as to be unable to support his own weight and collapse.


Volume II, October, 1936.




Scurvy, not Rare

Scurvy in adults especially those living in the metropolitan centers is considered rare. Nevertheless we are reporting nine cases of adult scurvy that came under the observation of the Oral Surgery Department of Cook County Hospital, during the time of my residence on that service, January, 1930, to January, 1931. Scurvy in the adult, therefore, is by no means a rare disease and should be thought of more frequently when making a differential diagnosis in disease of the mouth.

True that both scurvy and rickets are common to infants. But the infant is likely to be seen by the pediatrician first, who is well acquainted with this malnutrition, where as the adult will frequently be quite unaware of the presence of this disease especially in its incipiency.

Scurvy is not a sudden disease. Its onset is slow and insidious. While the physician and dentist have no difficulty in recognizing advanced scurvy, it is quite the opposite with the “subacute”, or so called “latent” scurvy, when it is rather difficult of recognition.

Here is where the dentist is in a strategic position to render an invaluable service to the patient suffering from nutritional deficiencies.

In the “subacute” or “latent” scurvy there is only a partial avitaminosis, consequently the symptoms are relatively milder. Yet there are frequently apparent oral symptoms that may lead one to suspect this disease. These symptoms are likely to manifest themselves long before the patient registers any complaint.

The subacute scurvy is quite common. Undoubtedly many cases of the incipient and even advanced cases of scurvy have been diagnosed and treated as pyorrhea, only to make a spectacular recovery when orange juice in sufficient quantities is added to the diet.

The dentist should ever be on the lookout if he wishes to avoid such blunders. This author has had the opportunity to cure several cases of subacute scurvy that had been previously diagnosed and treated as pyorrhea.

Diagnosis of Advanced Stages

There is very little chance of not recognizing scurvy in the advanced stages by any competent physician or dentist, nevertheless we are prompted to cite a report on a case so as to emphasize the danger of not recognizing this disease. This case is reported by Dr. J. C. Diamond in the Canadian Medical Journal.

He was called in to see a child four years old. The mother gave a history that the child had been in perfect health until six months before, when the child became cranky on account of a tooth ache and was given a push by the mother. The child fell and could not use her legs again. She was taken to several doctors, who did not help her any. She next went to a chiropractor, who “set her spine” and “replaced her hips,”, but still the child refused to walk.

When Dr. Diamond was called in to see her, she was lying on her back with her knees acutely flexed, and the muscles of the thighs, legs and buttocks badly wasted, the child was in severe pain whenever her legs were touched. Her teeth had all been extracted because the doctor said, “that the painful legs and swollen gums were due to rheumatism caused by bad teeth.” The teeth were extracted but she was not any better. She was placed on orange juice, and was on her legs without pain three days after. Two weeks later she was completely cured.

Infantile scurvy is likely to be caused when the infant is on a proprietary food or condensed milk, that lack the antiscorbutic substance in the milk. Scurvy in infants may occur irrespective of good hygienic environment. Where teeth are present the oral symptoms are quite similar to adult scurvy. The characteristic lesions in infantile scurvy, however, is the very painful subperiosteal swellings and the epiphyseal softenings. To prevent scurvy in infants the food of the mother must contain sufficient antiscorbutic vitamins to produce a quality milk for a healthy infant. Likewise if the infant is not breast fed, its diet must contain the essential antiscorbutic vitamins.


Treatment can practically be accomplished on a diet of orange, lime or lemon juice, although a regular antiscorbutic diet is advisable. Local intra oral treatment consists of careful mouth hygiene and a suitable mouth wash. Cod liver oil and general ultra violet radiation may be of some therapeutic value.


Rickets had been called a calcium deficiency disease, probably because there is a definite lack of calcium in the growing bones. Essentially rickets is a metabolic disease affecting infants and is characterized by avitaminosis similar to scurvy. Like in scurvy there is a nutritional deficiency, but in addition there is a pronounced disturbance in the assimilation of lime salts. The calcium content of the bony tissues may be so low that it frequently causes a complete change in its composition, texture and form.

Rickets may develop during intra uterine life (foetal rickets) or may develop after birth (congenital rickets). The period of life at which rickets is most commonly seen is in the first and second year. Occasionally, however, this disease may be seen in a patient at the age of puberty. This, of course, being rare, nevertheless it should be thought of by the dentist when making a differential diagnosis.

The dentist has very little occasion to observe this disease, since it is so seldom seen after the age of three. But while he may not see the patient long after the recovery from rickets, the possible defect in the oral cavity left by this disease is quite obvious.

The eruption of teeth is disturbed, usually causing a definite retardation in the eruptive processes. The teeth may be small and badly formed. Frequently the enamel is partially or completely missing. The prevalence of caries in such a mouth would naturally follow. However, we question if these caries are a result of avitaminosis, or a low calcium content. The poorly developed tooth structure is just as likely to be the etiologic factor for caries in such a mouth. Although avitaminosis and a low calcium content are undoubtedly contributing factors and should be taken into consideration.

Spinal curvatures, bow legs and knock-knees are a common sequel to this disease

Rickets Recognized More Easily than Scurvy

Early symptoms of rickets are more easily recognized than that of scurvy. These symptoms are manifested by loss of appetite, restlessness and increased irritability. The child will cry at the slightest provocation. As the child grows the abdomen becomes prominent. Epiphyseal swellings are seen at the waist and ankle joints, and as the child begins to walk the shaft of the long bone will bend and sometimes may even fracture. The bow legs are almost characteristic to rickets and are the most destructive sign noticed by the parents.

Just like vitamin C, commonly known as the antiscorbutic vitamin, is important in the treatment of scurvy. So is vitamin D essential in the treatment of rickets. The difference, however, lies in the fact that vitamin d is the activator which enables the body to use calcium and phosphorous in building and maintaining normal bones and teeth. It seems that calcium and phosphorous are better assimilated when in a definite ratio.

Sunlight, Chief Factor in Treatment

Vitamin D, however, is not the only factor in the treatment of this disease. Sunlight is probably the chief factor, likewise the calcium phosphorous intake is to be considered. Exposure to sunlight, however, is the most important therapeutic measure in the treatment of rickets. Perhaps no other disease better illustrates the important role sunlight plays in the process of metabolism.

By feeding the cow a food containing vitamin A, at the same time exposing the animal to sufficient sunlight thus producing vitamin D. The milk produced will be definitely antirachritic. Where climatic or atmospheric conditions obscure the sun rays of for any other reason the sun rays are inaccessible, artificial sun rays or ultra violet rays may be resorted to.


Pellagra is a nutritional disease due mainly to lack of proper food balance. Insufficient intake and absorption of vitamins B and G. this disease is generally associated with malnutrition. People that voluntarily or involuntarily starve themselves are subject to this disease.

This includes the large group where the food deprivation is a result of poverty or where the patient starves for the purpose of reducing. Pellagra may occur at all ages and in all races, although it is more commonly found among the negro race.

Symptoms: A sore mouth is the first symptom to suggest pellagra. The oral mucosa may be hyperemic, very red at times and ulcerated. The tongue may be ulcerate or atrophic with a smooth red surface. There is an excessive salivation usually associated with an enlargement of the salivary glands.

The symptoms are further augmented with loss of appetite, digestive disturbances with possible slight diarrhea, headache, vertigo and insomnia. As the disease progresses eruptions on the back of the glands and other exposed parts of the body resemble an ordinary erythema from a sunburn. These symptoms may last for a few days or weeks and disappear in the acute stage, while in chronic pellagra these eruptions may continue for years with current manifestations in the spring or fall.

A diagnosis is easily confirmed with the presence of the symptoms of stomatitis, diarrhea, and dermatitis in the exposed surfaces of the body.


Treatment consists of a well balanced diet, rest in bed, brewers yeast and fresh liver are very helpful. Fowlers solution by mouth, sodium cacodylate hyperdermically and the administration of hydrochloric acid are the drugs that seem to be of real value.


Beriberi is the first nutritional disease that led to the discovery of avitaminosis. As a matter of fact our knowledge of vitamins started with the study of this disease. An epidemic of beriberi ravished tropical countries for more than two thousand years.

In 1897 Dr. Christian Eijkman, a Dutch physician discovered that the polished rice was the cause of beriberi among the natives, whose diet consisted chiefly of that food. Not that the polished rice contained an injurious element or toxin, but that the important vitamin or substance necessary to prevent beriberi was in the rice skins, that were discarded with the polishings.

Eijkman’s discovery was paralleled by many others, who were searching for the possible relationship of nutrition to disease.

In 1911 Casimir Frank separated the outside layer of the rice grains, a substance that would cure beriberi. This substance is known today as vitamin B. vitamin B is also present in the bran layer of cereals, in peas and beans, yeast, milk, eggs and some meats.

Symptoms: Beriberi is characterized clinically by multiple neuritis, edema, and cardiac weakness. The onset is insidious with malaise, loss of appetite, gastrointestinal disturbance. Palpitation of the heart and dyspnea. Definite neuritis soon  develops with parestesias, painful swelling of the legs.

One of the characteristic symptom of beriberi is the sense of heaviness in the legs. The muscles of the calf will be very tender and can be used as a test in the early stages of this disease. The reflexes are diminished so that the patellar reflex test is also of value in recognizing the disease. The reflexes are diminished so that the patellar reflex test is alsoof value in recognizing the disease in the early stages. In addition there is a shortness of breath due to cardiac weakness. Sudden heart failure may occur.



Oral Symptoms

The oral manifestations may be similar to scurvy with the exception of possible pain for which no local cause is apparent. This pain is probably a parestesia brought about by the general neuritis which is characteristic to this disease.


The treatment of this disease is entirely dietetic and symptomatic.

Case Reports

The case reports listed below illustrate adult scurvy typical to the disease with its local and general manifestations. The dentist is more apt to come in contact with this disease than he would with any of the other three diseases described. A careful study of the case histories and the illustrations in this paper should be of considerable value to the general practitioner.

Case I

PATIENT: J. S., Male, Widowed, age 45.

ADMITTED: 1-3-30.

No. 1148558.

DISCHARGED: 1-24-30.

HISTORY: Patient states that he had several attacks of swelling, redness and pain in the left leg and ankle joint, which later affected the right leg. First attack came February 1929, then April 1929, July 1929, and so on. Symptoms disappearing completely between attacks, only to reoccur with more intense pain. Three months ago he noticed a sore bleeding mouth with painful gums and loosened teeth which gave him considerable pain while chewing his food, while one tooth came out with a slight jerk of a string. The last attack persisted until admitted to hospital.

HABITS: Alcohol moderately, tea, coffee, bread and some meat. No Fresh fruit, occasional canned fruit.



No cardiac pain.

Shortness of breath on exertion.

No Cyanosis or Cough.



No Constipation.

No Belching.

No Gas.

No burning or pains in the abdomen.



No Nocturia.

No burning or frequency.



General weakness.

No loss of weight.



Slight appears O. K.

Hearing slightly impaired.





Scalp slightly bald.

No abnormalities or tenderness.



No strabismus.

Nystagmus, plosis.

Pupils are equal.

Left pupil larger than right.






NOSE: Normal, slightly purplish.



Pharynx injected.

Tongue coated, no deviation or tremor.

Teeth loose, carious covered with tartar.




Deep purple red.


Bleed on slight pressure.

Several spots of ulcerations.





Anterior Cervical adenopathy ++.

Thyroid just palpable.



Synimetrical inclination to high.

Narrow chest laterally with depressed sternum.

Normal expansion.



Normal expansion.

Normal resonance.

No dullness.



Reveals a fur sonorous basal rales.

Normal breath sounds.


HEART:   Apes beat not visible nor palpable.



Apes Systolic roughened sound.

Sounds both heard.

Base—Prominent pulmonic sound and Aortic

sound is pronounced near duplication of second sound.

Area—1” above nipple reveals rough systolic sound not transmitted further toward apes.

Radial pulses—Strong continued stroke, no corigan.

Base of sternum reveals impulse of right ventricle.

Palpation—No thrills felt.



Somewhat protuberant and obese.

Slight oedema in lower abdominal wall.

Liver—Not Palpable.

Spleen—Not Palpable.

Kidneys—Not Palpable.

No tenderness on deep or superficial pressure.



Sacral oedema ++.

No Defromity.



Right leg.

Oedema and slight varicosities of especially lower leg.

Redness in Retechial spots in blotchy areas over the foot and lower leg.

Larger areas are harder, darker, purple color, very tender.

Left leg is same as right but in a more advanced degree particularly around the ankle joint and over.

Lateral malleolus—with deep tenderness in muscle of calf and over tibial regions.

Arms essentially negative.








H. B.: 65%.



Ploymorphonuclear Neutrophiles—12.

Eosinophiles—                                        0

Basophiles—                                         0

Lymphocytes—                                    80

Mononuclear Lymphocytes—             8



Color—Straw Color.

S. G.—1.010.





Diacetic Acid—0.







WASSERMAN: Negative.


BLOOD CULTURE: Under aseptic conditions, inoculated over night, essentially negative.

Patient was placed on a scurvy diet, showed marked improvement and was discharged three weeks after admittance.



Case II


PATIENT: O. E., male, Age 47, single, Admitted 12-27-29, No. 1145688, Discharged 1-18-30.


TEMPERATURE, 98.6, Pulse, 120, Respiration, 28.


History: Patient states that he first noticed purplish discoloration of skin on the anterior surface of                 the right thigh near the knee, area became progressively extensive involving left leg also. Pain began   three days before discoloration, causing considerable difficulty to walk.


Patient’s diet consisted primarily of milk, cheese, meat and sandwiches. No fruit and very little vegetable.



Gastro Intestinal.

Appetite poor.

No nausea.

No vomiting.

No hematemesis.

No Melena.

No abdominal pain.

No constipation.

No parry stools.

Slight loss of weight.



No edema of feet.

Dyspnea on exertion.

No pericardial pain.



Cough occasionally.

No expectoration.

No hemoptysis.

No pain in chest.

G. U.:

No hematuria.

No dyspnea.

No polyuria.



Headache occasionally.

No paresthesias.

Few tremors of fingers.










TASTE: Impaired.



Medical—Colds occasionally.










Pupils equal and regular.

React to light and accommodation.

Conjunctive and sclera pale.



Marked palor of pharynx and tongue.

Teeth carious.

Gums swollen.


Bleeding upon slight pressure.

CHEST: Chest walk well formed, symmetrical, no deformities.



Apex beat not visible.

Palpable in fourth interspace, and clavicular line.

Soft systolic murmur, over apex, not transmitted.

Heart tones—rapid and regular.

Radial pulses equal and regular.



Expansion fair.

Tactile fremitus normal.

No impaired resonance.

Few rales at base of right lung.



Moderately distended.

No tenderness.

No rigidity.

No masses.

Liver, spleen, kidneys not palpable.

No fluids determinable.


BACK:  Negative.


GENITLIA:  Right incomplete inguinal hemia.



Marked palor of fingers.

Thigh reveals marked diffuse purpuric areas, edematous and tender with induration of left         Poplitial fossa.

Edema of left fore leg.

Purpuric areas in both fore legs.




H. B.: 65%


RED BLOOD COUNT: 2,250,000.






Polymorphonuclear Neutriphiles—64.

Polymorphonuclear Eosinophiles—  1.

Lymphocytes—                                    31.

Mononuclear Lymphocytes—            4.


Bleeding time—Three minutes.


Coagulation time (Howell) Fifteen minutes.




Specific gravity—1025.








WASSERMAN: Negative.


Patient was placed on a scurvy diet and was cured in a little over three weeks.


Case III


PATIENT:  K. M., male, Age 50, Single, No. 1179164.


Came to the Oral Surgery Department complaining of sore and frequent bleeding gums.


HISTORY: Patient states that about ten weeks ago he noticed many discrete pin head hemorrhages over medical aspect of left leg which rapidly coalesced. At the same time the patient noticed bleeding from his gums. His diet consisted chiefly of oatmeal and some milk. No fruit or vegetables were used for several months.









No nausea.

No vomiting.

Lost twenty pound during past month.

Bowels, O. K.


G. U.:  Essentially—Negative.







Physical examination reveals a white male about fifty years of age not acutely ill.

Essential pathologic findings: Marked hemorrhagic swelling of both upper and lower gums with many areas of ulcerations which bleed upon slight pressure. Marked discoloration of medial aspect of left leg.


RED BLOOD COUNT:                       2,900,000.

WHITE BLOOD COUNT:                          5,400.



Polymorphnuclear Neutrophiles—48.

Polymorphnuclear Eosinophiles—    0.

Polymorphnuclear Basophiles—        0.

Lymphocytes—                                    43.

Mononuclear Lymphocytes—             9.




S. G.—1012.









WASSERMAN:  Negative.




Patient was placed on a scurvy diet and was markedly improved. Sixteen days later he was discharged from the Hospital in good condition.


Case IV


PATIENT:  E. M., male, Age 29, Single, No. 1190221.


Was admitted to the Oral Surgery Department on the complaint of general malaise and markedly swollen and bleeding gums, also much pain in lower extremities.


HISTORY:  Patient states that he was operated upon for a gastric ulcer, and since then he maintained a diet of milk, bread and cheese, no fruit no vegetables and no meat fearing an acid reaction in his stomach. Several weeks ago he noticed that his gums started to bleed very readily, became markedly swollen and painful, simultaneously he noticed purpura hemorrhagic spots all over his right and left thigh which later extended clear down to the ankle. Fig. IV.








No nausea.

No vomiting.

Slight loss of weight.







Physical examination reveals a slightly under-nourished white male not acutely ill.



Gums, swollen, discolored and painful.

Gingival margin markedly swollen and bleed freely upon slight pressure. Extensive bridge work    rather unsanitary probably due to patient’s fear of pain. Generalized petechial skin eruption not elevated over both right and left thigh and tibial.


HEAD:  Eyes Pupils react to light and Acc. sluggishly.


NOSE AND EAR: Negative.






CHEST: Negative.


ABDOMEN: Scars due to heat burns.




RED BLOOD COUNT:                       3,850,000.


WHITE BLOOD COUNT:                         6,000.



Polymorphnuclear Neutrophiles—48.

Polymorphnuclear Eosinophiles—   0.

Polymorphnuclear Basophiles—       0.

Lymphocytes—                                   41.

Mononuclear Lymphocytes—         11.










Patient showed marked improvement on an anti-scorbutic diet and was sent home with the instructions to continue the diet prescribed.

Case V

PATIENT:  L. M., male, Age 39, Single, No. 1136595.

Came to Cook County Hospital because he was spitting blood. His history is very much similar to the ones described. His physical condition is that of a typical scurvy case. Continual oozing of blood at the gum margin. Teeth carious and unclean. Gums are swollen, spongy and ulcerated in spots.

Purpuric hemorrhages over the right and left legs.

Blood picture reveals a slight anemica.

Other findings were essentially negative.

Patient was placed on a scurvy diet and was cured.

Case VI

PATIENT:  J. Z., male, Age 41, Single, No. 110765.

Came to Cook County Hospital with the following history.

A year ago he received an injury to the right leg. Swelling of the leg below the knee occurred with           patches of hyperemia, later the leg became swollen and the edema of the right leg subsided.          Alternating from one leg to another. At present both legs are edematous.

Dyspnea has been present one month. He also complained of diarrhea for the past month. He has eight              to ten stools a day, watery and yellowish in color.

ESSENTIAL PATHOLOGY:  Mouth reveals the same picture previously described. That of a typical scurvy.                Gums purple, spongy, teeth loose with foul breath. Swelling and tenderness of both legs in l   lower third. Generalized adnopothy especially of cervical glands. Multiple acchymosis chiefly               around ankles.

Patient was placed on antiscorbutic diet and showed marked improvement in a relatively short time. Note: This case is suggestive of Beriberi.

Case VII

PATIENT:  J. B., male, Age 64, Widowed, No. 1110781.

Came to Cook County Hospital with the complaints of pains in both legs. Reddish discoloration of both   legs over posterior aspects and anorexia.

The History reveals that since his wife died he has been living on a very poor diet and subsides on a little              coffee and bread of milk and bread, no fruit, vegetable or even occasional meat. General   condition of patient is rather poor. He seems very much undernourished and debilitated.

Mouth reveals carious teeth, hygiene very poor, gums very spongy and inflamed bled   spontaneously. Tongue coated. No adnopothy palpable. Other findings were essentially relative              to the age of the patient.


Reddish discoloration along posterior aspect of both legs, and ecchymosis. Some bluish black     discoloration over medial aspect of left thigh and left knee.

The diagnosis of scurvy was made and patient placed on a scurvy diet. He improved rather slowly; was later transferred to Oack Forest.

Case VIII 

PATIENT:  Wm. K., male, Age 49, Single, No. 1105028.


Patient stats that he was well until about six weeks ago when he noticed pain in all hi teeth. This              continued and all his teeth became loose. His gums became swollen, spongy and bleed freely.            Simultaneously he noticed spots on his legs and thighs and his forearm. He became weak.

Dyspnea was especially noted, no walking or climbing stairs was possible. Patient had all the previously described symptoms of scurvy with a marked progressive anemia, with an increasing temperature. Patient died two weeks after admittance.

Case IX

PATIENT:  J. M., male, Age 40, Admitted 5-19-30, No. 1168484, Died 5-20-30.


History reveals that the patient has been frequenting restaurants for his meals and has not been eating               fresh fruit or vegetables.

A physical examination reveals a poorly nourished adult male with a marked palor.


MOUTH:  Gums of upper and lower jaw are spongy, ulcerated and bleed very easily. Teeth are very loose. Tongue appears smooth with atrophied papillae, no petechial hemorrhages noted in buccal mucosa. No adnopothy. Thyroid not enlarged.

CHEST:  Normal.

HEART:  Essentially negative.

No murmurs.

No thrills.



No tenderness.

No rigidity.

No masses.



H. B.: 50%

RED BLOOD COUNT:       2,690,000.

WHITE BLOOD COUNT:          3,450.

Diagnosis is that of a severe secondary anemia based on Scurvy.

AUTOPSY No. 437 reveals the following.

Gangrenous stomatitis (Scurvy).

Petechial hemorrhages of the pleura.

Slight coronary sclerosis.

Fatty degeneration of the myocardium and kidney.

Terminal bronchopneumonia.

Edema of the lungs.

Fibrous epicaritis.

Acute splenic tumor.

Bilateral hyrothorax.



Summarizing our findings from the reported case we find that

  1. Scurvy although easily cured with an antiscorbutic diet is not without its dangers.
  2. This disease manifests itself in the oral cavity in its initial stage, and the dentist is in a position to warn the patient of the consequences.
  3. Characteristic to scurvy these patients have been on a deficiency diet and all but the two, who developed complications, recovered when placed on an orange juice and vegetable diet.
  4. Adult scurvy is by no means a rare disease and should be thought of when making a differential diagnosis.
  5. That vitamins are essential to normal health, and constitute a definite substance found in foods, without which deficiency diseases occur.
  6. What part avitaminosis play in the production of caries is still a mystery. Further studies on the subject may definitely solve the problem.
  7. Anti Pellagra vitamins are found in many different foods, which probably account for the disease being generally limited to those who for one reason or another starve themselves.
  8. That mild or subacute cases of the deficiency disease are frequently mistaken for pyorrhea or other dental ailments and treated as such without success.
  9. That patients, whose health is not so good, and who manifest oral symptoms even though not true to the picture described in this paper, should be questioned about their diet just to make sure that they are getting an adequate ration of vitamins.
  10. That the dentist is more likely to suspect a deficiency disease long before the patient registers any complaint, consequently he is in a position to render a health service of considerable importance to that patient.



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