Manifestations in the oral cavity diseases of the gastrointestinal tract and endocrine system in children. Chronic recurrent aphthous stomatitis. The clinic, diagnosis, tactics dentist.

 

 

 

 

The term “aphthous” is derived from a Greek word “aphtha” which means ulceration. Recurrent aphthous stomatitis (RAS) is one of the most common painful oral mucosal conditions seen among patients. These present as recurrent, multiple, small, round, or ovoid ulcers, with circumscribed margins, having yellow or gray floors and are surrounded by erythematous haloes, present first in childhood or adolescence.[1]

 

RAS is characterized by recurrent bouts of solitary or multiple shallow painful ulcers, at intervals of few months to few days in patients who are otherwise well.[2] RAS has been described under three different clinical variants as classified by Stanley in 1972.[3]

1.     Minor RAS is also known as Miculiz’s aphthae or mild aphthous ulcers. It is the most common variant, constituting 80% of RAS. Ulcers vary from 8 to 10 mm in size. It is most commonly seen in the nonkeratinized mucosal surfaces like labial mucosa, buccal mucosa, and floor of the mouth. Ulcers heal within 10–14 days without scarring.

2.     Major RAS is also known as periadenitis mucosa necrotica recurrens or Sutton’s disease. It affects about 10–15% of patients. Ulcers exceed 1 cm in diameter. Most common sites of involvement are lips, soft palate, and fauces. Masticatory mucosa like dorsum of tongue or gingiva may be occasionally involved.[4] The ulcers persist for up to 6 weeks and heal with scarring.

3.     Herpetiform ulceration is characterized by recurrent crops of multiple ulcers; may be up to 100 in number. These are small in size, measure 2–3 mm in diameter. Lesions may coalesce to form large irregular ulcers. These ulcers last for about 10–14 days. Unlike herpetic ulcers, these are not preceded by vesicles and do not contain viral infected cells. These are more common in women and have a later age of onset than other clinical variants of RAS.[5]

Predisposing factors

Genetics

A genetic predisposition for the development of apthous ulcer is strongly suggested as about 40% of patients have a family history and these individuals develop ulcers earlier and are of more severe nature.[2] Various associations with HLA antigens and RAS have been reported. These associations vary with specific racial and ethnic origins.

Trauma

Trauma to the oral mucosa due to local anesthetic injections, sharp tooth, dental treatments, and tooth brush injury may predispose to the development of recurrent aphthous ulceration (RAU).[1] Wray et al.[6] in 1981 proposed that mechanical injury may aid in identifying and studying patients prone to aphthous stomatitis.

Tobacco

Several studies reveal negative association between cigarette smoking, smokeless tobacco and RAS. Possible explanations given include increased mucosal keratinization; which serves as a mechanical and protective barrier against trauma and microbes.[7–9] Nicotine is considered to be the protective factor as it stimulates the production of adrenal steroids by its action on the hypothalamic adrenal axis and reduces production of tumor necrosis factor alpha (TNF-α) and interleukins 1 and 6 (IL-1 andIL-6).[10] Nicotine replacement therapy has been suggested as treatment for patients who develop RAU on cessation of smoking.[11]

Drugs

Certain drugs have been associated with development of RAU; these include angiotensin converting enzyme inhibitor captopril, gold salts, nicorandil, phenindione, phenobarbital, and sodium hypochloride. NSAIDS such as propionic acid, diclofenac, and piroxicam may also cause oral ulceration similar to RAS.[12]

Hematinic deficiency

Deficiencies of iron, vitamin B12, and folic acid predispose development of RAS. Deficiencies of these hematinics are twice more common in these individuals than controls. Contrary findings in various studies relating the association of hematinic deficiency and RAS have been explained as due to varying genetic backgrounds and dietary habits of the study population.[2,12]

Gluten sensitive enteropathy/celiac disease, inflammatory bowel disease

Gluten sensitive enteropathy (GSE) is an autoimmune inflammatory disease of small intestine that is precipitated by the ingestion of gluten, a wheat protein in susceptible individuals. It is characterized by severe malnutrition, anemia, abdominal pain, diarrhea, aphthous oral ulcers, glossitis, and stomatitis. RAS may be the sole manifestation of the disease. The use of gluten-free diet in the improvement of RAS is considered uncertain. It has been suggested that evaluation for celiac disease may be appropriate for RAS patients.[13] Inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis may present with apthous-like ulceration.[1]

Sodium lauryl sulfate – containing toothpaste

An increased frequency in the occurrence of RAS has been reported on using sodium lauryl sulfate (SLS)-containing tooth paste with some reduction in ulceration on use of SLS-free tooth paste. However, because of the widespread use of SLS-containing dentifrice, it has been proposed that this may not truly predispose to RAS.[1]

Hormonal changes

Conflicting reports exist regarding association of hormonal changes in women and RAU. Studies state association of oral ulceration with onset of menstruation or in the luteal phase of the menstrual cycle. Mc Cartan et al.[14] in 1992 established no association between apthous stomatitis and premenstrual period, pregnancy, or menopause.

Stress

Stress has been emphasized as a causative factor in RAU. It has been proposed that stress may induce trauma to oral soft tissues by parafunctional habits such as lip or cheek biting and this trauma may predispose to ulceration. A more recent study shows lack of direct correlation between levels of stress and severity of RAS episodes and suggests that psychological stress may act as a triggering or modifying factor rather than etiological factor in susceptible RAS patients.[15]

Micro organisms implicated in apthous ulcers

Several micro organisms have been implicated in the pathogenesis of RAS. Several contrary findings have been reported in the various studies published.

RAS and oral streptococci

Oral streptococci have been considered as microbial agents in the pathogenesis of RAS. They have been implicated as microorganisms directly involved in the pathogenesis of these lesions or as agents which serve as antigenic stimuli, which in turn provoke antibody production that cross-react with oral mucosa. It has been suggested that L form of α-hemolytic streptococci,Streptococcus sanguis; later identified as Streptococcus mitis was the causative agent of this disease. Hoover et al.[16] in 1986 demonstrated low levels of cross-reactivity of oral Streptococci and oral mucosal antigens and considered the reactivity to be non-specific and clinically insignificant.

RAS and Helicobacter pylori

H. pylori has been implicated as one of the organisms in the etiopathogenesis of RAS. H. pylori is a gram-negative, S-shaped bacterium that has been associated with gastritis and in chronically infected duodenal ulcers. H. pylori has been reported to be present in high density in dental plaque.[17] Porter et al.[18] in 1997 measured the levels of IgG antibodies againstH. pylori in patients with RAS and showed that no the frequency of anti-H. pylori seropositivity was not significantly elevated in patients with RAS and other ulcerative and non-ulcerative oral mucosal disorders.

Viruses as etiologic agents in RAS

Various viruses have been implicated in the etiopathogenesis of recurrent apthous stomatitis. There have been several suggestive, but as yet there exists inconclusive evidence toward a viral etiology. Characteristics of aphthous ulcers which are indicative of infectious etiology include recurrent ulceration, lymphocytic infiltration, perivascular cuffing, presence of auto-antibodies, inclusion bodies in case of herpetiform ulcers and similarity of RAU to viral ulcerative diseases in animals.[19] Virtanen et al.[17] in 1995 demonstrated the presence of human cytomegalovirus DNA (HCMV) in biopsies of oral mucosal ulcers, but they were unable to rule out the presence of this virus which may have existed as a super infection or co infection from existing HCMV in saliva. Sun et al.[20] in 1996 demonstrated the presence of HCMV genomes by polymerase chain reaction in pre-ulcerative oral apthous tissues. They postulated that when viral infection occurs in oral epithelial cells expressing major histocompatibility complex class II molecules (MHC-II), an intense T-cell response is elicited against virus containing oral epithelial cells. They concluded that HCMV may play role in perpetuating local immune response in genetically predisposed individuals.

Sun et al.[21] in 1998 demonstrated the presence of Epstein-barr virus (EBV) genomes by polymerase chain reaction in pre-ulcerative oral apthous tissues in RAU patients. They postulated a possible role of association of EBV in pre-ulcerative oral lesions in patients of RAU.

Role of tumor necrosis factor alpha in RAS

Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine and is one of the most important cytokine implied in the development of new apthous ulcers in patients. The association of TNF-α in the development of RAS gains credence due to the fact that immunomodulatory drugs such as thalidomide and pentoxifylline have been found effective in the treatment of RAS. Thalidomide reduces activity of TNF-α by degrading its messenger RNA and pentoxifylline inhibits TNF-α production.[22,23] Antigenic stimulation of oral mucosal keratinocytes results in the production of pro-inflammatory cytokines such as IL-2 and TNF-α. TNF-α also causes expression of class I major histocompatability complex, subsequently these cells are targeted for attack by cytotoxic T cells.[1]

Mumucu et al.[24] in 2009 proposed a composite index to monitor the clinical manifestations associated with oral ulcers in patients of RAS and Behcet’s disease. They proposed that such indices serve to provide important information regarding prognosis of disease and therapeutic effect of medication.

The index evaluated the oral ulcer activity, ulcer-related pain, and functional disability. Oral ulcer activity was recorded as number of ulcers in the past 1 month. This was scored zero if there were no ulcers and as one, if the number of ulcer was greater or equal to than one. The pain status was evaluated on a visual analogue scale (VAS). This is a 100-mm line with extreme values at either end. The patients have to mark the intensity of pain on the line.

Functional status evaluation

This involved the evaluation of effects of oral ulcers on tasting, speaking, and eating/chewing/swallowing. This was evaluated by both Likert-type scale and VAS scale. Scoring is done as 0, wheone of the time; 1, little of the time; 2, some of the time; 3, most of the time; 4, all of the time and VAS (0–100 mm).

Use of visual analog scale to evaluate the pain caused by ulcers is highly subjective and is ridden with interpersonal variation. This is a continuous scale with no discrete levels as would be suggested by grades such as none, mild, moderate, or severe. Further studies in different population and ethnic groups need to be carried out using this criteria to validate this index.

The microscopic picture of aphthous ulcer is non-specific, and diagnosis must be based on history and careful clinical examination. The mucous membrane of aphthous ulcer shows superficial tissue necrosis with a fibrinopurulent membrane covering the ulcerated area. The necrosis is covered by tissue debris and neutrophils. Epithelium is infiltrated by lymphocytes and few neutrophils. Intense inflammatory cell infiltration, predominantly neutrophils present immediately below the ulcer, mononuclear lymphocytes are seen in adjacent areas. Minor salivary glands commonly present in areas of aphthae exhibit focal periductal and perialveolar fibrosis and chronic inflammation.[12,25]

Diagnosis of RAS is based on history, clinical manifestations, and histopathology. Other causes of recurrent oral ulceration must be ruled out. Systemic diseases which present with recurrent oral ulcerations are summarized in Table 1. Diagnostic criteria for minor RAU were proposed by Natah et al.[12] in 2004. They proposed that a diagnosis of idiopathic RAU and secondary RAU (associated with systemic disease) is established when four major and one minor criteria are fulfilled. The major and minor criteria for diagnosis of minor RAU are illustrated in Tables ​Tables22 and ​and33.

Table 1

Systemic diseases with recurrent oral ulceration (modified from reference 1)

Table 2

Major criteria for diagnosis of RAU minor (Natah et al.[12] 2004)

Minor criteria for diagnosis of RAU minor

Management

There is no definitive curative treatment for RAS. Possible systemic association with RAS must be ruled out, especially in cases where there is sudden development of ulceration in adulthood.[2] Laboratory investigations such as complete blood counts, red cell folate, serum ferritin levels, and vitamin B12 recommended. Screening for GSE must be done in cases where associated systemic manifestations of GSE are present. Various topical and systemic agents used in treatment of RAS are summarized in 

DISEASES OF THE DIGESTIVE SYSTEM.

 

I. DISEASE OF THE MOUTH.

ACUTE STOMATITIS.

 

Definition.—An acute inflammation of the mucous membrane of the

mouth, occurring most frequently in children, though no age is exempt.

Etiology.—The causes that give rise to stomatitis are generally local,

though it may rise from gastric or intestinal derangements, chemical

and mechanical irritants being the most common, such as sharp edges of

broken or carious teeth; very hot drinks, such as tea and coffee; highly

spiced food; tobacco, both chewing and smoking; irritating dust inhaled

at certain work, such as lime, coal, marble, and workers in various

minerals; the corrosive acids or alkalies; and sometimes from the

decomposition of food lodged between the teeth, and fetid cavities. It

may also be caused by dentition, or follow the eruptive fevers.

 

Symptoms.

 

The inflammation is attended by the following symptoms: heat, pain, redness, and swelling. At first the mouth is dry and hot, with a burning, smarting sensation; but soon secretion is established, and mucus and saliva are found in excess. This condition is often called catarrhal stomatitis. Mastication is painful, and hot drinks, and coarse food give rise to pain. The tongue is coated, the breath is fetid, and the

child becomes peevish and cross. In a few days the disease loses its angry character, the inflammation becomes subacute, while the mouth is bathed in a ropy, offensive mucus.

 

Diagnosis.—The diagnosis is easily made. The red, inflamed character of the mucous membrane; the tenderness, the burning sensation, dry mouth, followed by hypersecretion of mucus, are symptoms which caot be mistaken for those of any other trouble.

 

Prognosis.—The prognosis is favorable, the disease usually giving way in a week or ten days.

 

Treatment.—This is simple and quite successful. After thoroughly cleansing the mouth with a weak solution of pyrozone, or a wash of comboracic acid, or, better still, a solution ofhydrastin and chlorate of potassium, we prescribe phytolacca ten drops, and water four ounces; a teaspoonful every hour. As a mouth-wash I know of nothing to equal the phosphate ofhydrastia and chlorate of potassium. If there are any gastric or intestinal complications, remedies should at once be used to correct these wrongs. If there should be fever, combine aconite with the phytolacca, and give every hour. The mouth should be kept sweet and clean. The diet should consist of liquid food; warm drinks are more agreeable than very cold or very hot fluids.

 

APHTHOUS STOMATITIS.

Synonyms.—Follicular Stomatitis; Disseminated Vesicular Stomatitis; Fibrinous Stomatitis.

Definition.—A variety of stomatitis, characterized by small, round, white patches upon the mucous membrane of the tongue, gums, and cheeks. Small vesicles appear upon an inflamed base, and later form small ulcers.

 

Etiology.—This variety usually occurs in children under three years of age, though it may occur at any period of life. It may accompany the acute infectious diseases, and occasionally occurs as an epidemic. An impoverished condition of the blood favors the disease, as well as poor hygienic surroundings; gastro-intestinal disorders also predispose to this lesion, whileStrumpell believes the milk from cows suffering from the hoof and mouth disease, is an exciting cause.

The time of the year may also be considered a factor in this disease, spring and fall being the seasons when colds prevail and intestinal disturbances are common.

 

Symptoms.—The mouth is exquisitely tender, and, wheursing or attempting to eat, a burning sensation follows. As a result, the child is peevish and fretful. The tongue is furred, the breath is fetid, and a slight fever is occasionally noted; there may be some gastric or intestinal disturbance.

On inspecting the mouth, small vesicles are seen on the inner surface of the lips, and along the sides of the tongue, and near the frenum; they may also be found on the cheeks; these rupturing, small, white patches, surrounded by a red base are observed, which may later ulcerate. There is a free secretion of saliva and mucus, which, in the infant, dribbles from the mouth, and in older patients necessitates frequent spitting.

There may be enlargement of the submaxillary glands.

 

Diagnosis.—The small vesicles upon the sides of the tongue and mouth, followed by white or yellowish patches, make the diagnosis plain.

 

Prognosis.—The disease usually yields to treatment in a week or ten days, though some cases prove very intractable, with a tendency to recur at intervals.

 

Treatment.—Cleanliness is of the greatest importance, and the mouth should be rinsed with lukewarm water after each feeding. In bottle-fed babies, great care must be taken that the bottle and nipple are kept sweet and clean, the nurse being instructed to scald out the bottle after each nursing, and lay in plain cold water, or in soda or lime water.

 

For a mouth wash, potassium chlorate and hydrastis, or boracic acid, will prove among the best. Painting the patches with equal parts of thuja and water is also frequently beneficial. Internally, specific phytolacca is the remedy par excellence. If there is fever, add aconite to the above. Where the tissues are bluish and the breath bad, echinacea will prove more effective. Where the tongue is coated with a moist, yellow, pasty coating, potassium chlorate and hydrastis one dram, to water four ounces, a teaspoonful every hour, will give relief and the best results. Where there is hypersecretion of saliva, specific belladonna ten drops, to water four ounces, will be indicated. Dr. Webster likes the action of jaborandi for this same condition. In the adult, where the ulcers persist, apply bluestone direct to the ulcers.

 

THRUSH.

Synonyms.—Parasitic Stomatitis; Stomatitis Mycosa.

 

Definition.—A specific fungous disease of the buccal mucous surfaces, characterized by whitish or yellowish deposits, in which are found the saccharomyces albicans.

Etiology.—Predisposing causes are such as furnish a soil suitable for the propagation of the thrush fungus; such as tuberculosis, congenital syphilis, or any disease whereby the blood is impoverished. In bottle-fed children, when cleanliness is not observed, and the bottle and tube contain sour milk; in adults, typhoid fever, diabetes, and carcinoma, are fruitful causes.

The specific cause is the fungus above mentioned (saccharomyces albicans), which thrives in the changed condition of the mouth secretions, fermentation having changed the normal alkaline secretion to acid.

 

Symptoms.—The child is fretful and peevish, the result of the burning pain, and frequently a diarrhea, with greenish stools, occurs. On inspecting the mouth, we find the mucous membrane dry and of a dusky red color, upon which are seen the thrush spots in the form of white patches, first upon the tongue, rapidly extending to the lips,

cheeks, pharynx, and sometimes to the esophagus and stomach.

When the extension is so general, a troublesome diarrhea exists. The saliva, after a few days, becomes profuse, but is acid in character; in fact, we find an acid saliva iearly all forms. of stomatitis.

 

Diagnosis.—The dryness of the mouth in the early stage, the white patches, which can be readily removed without bleeding, the absence of the yellow ulcers seen in aphthous stomatitis, makes the diagnosis comparatively easy. The presence of the fungus, revealed by the microscope, makes the diagnosis positive.

 

Prognosis.—This is favorable unless there is marked cachexia, in which case it may be quite stubborn.

 

Treatment.—Remembering that the fungi thrive in an acid medium, our mouth-washes will be selected to correct this condition ; hence the alkalies are used; bicarbonate of sodium, boracic acid, potassium chlorate, etc. After each feeding, the mouth is to be carefully washed, every particle of food being removed. Sweets of all kinds are to be avoided, as they favor fermentation. The general health is to be improved by adopting more favorable hygienic conditions. Plenty of fresh air and wholesome and easily digested food will be important factors in the cure.

Phytolacca, echinacea, nux vomica, rhus tox., and others of like character, will be used. Inunction of quinine and lard will improve the condition of the skin, and act as a tonic. In all these cases we are not to overlook the great fact that the impoverished condition of the blood furnishes the soil for the development of the parasite, and remedies are to be used which will give us a better blood, and consequently a more healthy body. When we fail in this respect, the local trouble persists in spite of local treatment.

 

ULCERATIVE STOMATITIS.

Synonyms.—Fetid Stomatitis; Putrid Sore Mouth.

 

Definition.—A stomatitis characterized by the formation of ulcers on the gums and cheeks, attended by an offensive breath.

Etiology.—This is a disease of childhood, though it is sometimes met with in the adult. The predisposing causes are similar to those of aphthous stomatitis and thrush; viz., poor hygienic conditions, bad air, light, and food; poor clothing, damp and filthy quarters, and all conditions that impoverish the blood. Neglect of the mouth, and bad teeth, also favor the disease. No doubt the infectious fevers favor the generation of the virus whatever that may be. It is most likely due to a specific germ; but, as yet, the specific cause has not been discovered.

 

Symptoms.— “On examining the mouth, we find the gums red, swollen, and spongy, and where the ulcer is situated, a grayish, pultaceous material, on removing which, the surface is raw and bleeding. It generally commences on the front part of the gums, but gradually passes between the teeth, affects the posterior surface; continuing, it destroys the gum both before and behind, and, passing to the lips and cheeks adjacent, forms irregular ulcerations, covered by the same material. If it continues long, the tongue is swollen, and is marked by the teeth; the saliva becomes thick and very offensive, often streaked with blood, the gums bleeding at the slightest touch. The stomach is usually deranged, the bowels irregular, the tongue covered with a dirty coat, and more or less febrile action.” (Scudder.)

 

Diagnosis.—The soft, spongy condition of the gums, the characteristic ulceration, the foul breath, the vitiated saliva, together with the cachectic appearance of the patient, render the diagnosis easy.

 

Prognosis.—The disease usually yields readily to treatment, and even in those cases due to impoverished blood a cure will result in a few weeks under specific medication.

 

Treatment.—After thoroughly cleansing the mouth with pyrozone, boracic acid solution, or listerine, and the removal of carious teeth, we put the patient on potassium chlorate andhydrastis, both for its local and systemic use. It will fit more cases than any other remedy. For the nasty, dirty, pasty coating upon the tongue, which tells of sepsis, use sodium sulphite. If the sub-maxillary glands are involved, phytolacca will prove our best remedy. When the tissues are dusky, baptisia or echinacea will prove the better agents.

The ulcers may be touched with thuja, or with nitric acid, applied on a pine pencil. The gastric and intestinal disturbance may call for nux vomica or small doses of Podophyllin. Drop doses of Howe’s acid solution of iron is a good tonic, as well as quinia and hydrastis. To harden the spongy gums, an application of tincture of myrrh and glycerin, three times per day, is useful. The diet should be nutritious and given in fluid form.

 

MEMBRANOUS STOMATITIS.

 

Synonym.—Croupous Stomatitis.

 

Definition.—An inflammation of the buccal mucous membrane, characterized by the formation of a false membrane.

 

Etiology.—There seems to be quite a difference of opinion as to the specific cause of this form of stomatitis. Some regard the Klebs-Loeffler bacillus as responsible for it, while others contend that gonorrheal or syphilitic infection in the new-born is the primary lesion that gives rise to the disease.

 

Symptoms.—This form of stomatitis appears in the shape of small, irregular patches, of a grayish white color, the parts surrounding being red, painful, and hot. Of this Scudder says:

“The breath is fetid, and the submaxillary glands enlarge. As the disease proceeds, the patches of membranous exudation extend, become more or less detached, and are succeeded by others, and the intervening surfaces are red and swollen. The tongue is swollen and the mouth continually open, allowing the escape of altered saliva. The enlargement of the lymphatic glands increases, the face swells, the breath becomes more fetid, and the pulse more quick and rapid, and generally soft, open. or full and weak.” “The disease sometimes extends back to the throat, and even involves the mucous membranes further, sometimes occasioning imminent danger. It may become chronic, and continue for weeks or months.”

 

Diagnosis.—This is made by the membranous character of the patches.

 

Treatment.— “With small doses of aconite we associate phytolacca, rhus, or baptisia, as indicated. When the tissues are full, the first; if contracted and hot, with vivid redness, sometimes fissured and bloody, the rhus; and if there is dusky discoloration, the baptisia. The remedies are used in the ordinary small doses, and the phytolacca and baptisia may also be used as washes. When the tongue is broad, pallid, and dirty—a rare case—sodium sulphite is the remedy.

 

‘As a local application, the hydrochloric acid with honey, one part to three, four, or six, will be found as good as anything; it should be applied with a small piece of sponge attached to a stick to the membranous exudations, being careful to reach them all. At the same time a saturated solution of potassium chlorate. with a small portion of glycerin, may be frequently used. An infusion of cinchona, acidulated with hydrochloric acid, has been recommended subsequently; but I would prefer the decoction of rumex, ainus, and quercus rubra.”

 

GANGRENOUS STOMATITIS.

 

Synonyms.—Cancrum Oris; Noma; Water Cancer.

 

Definition.—Gangrene of the cheek and gums, affecting delicate and sickly children, rarely the adult, and characterized by a rapid destruction of tissue. The disease is generally fatal.

Etiology. — Predisposing Causes. — Age. — The disease usually occurs between the ages of two and six years, and is more frequently found in girls than in boys.

 

Climate.—It prevails in low moist, countries, especially in Holland.

 

Infections Fevers.—While the disease may be primary, it frequently follows the infectious fevers, especially measles, scarlet fever, typhoid fever, typhus fever, and pneumonia. In fact, any disease that lowers the vitality, as well as poor hygienic conditions which impoverish the blood, predispose to noma.

 

The Exciting Cause.—Mercurialization has been thought, by many, to be responsible for this destructive disease, and from the similarity of symptoms of this and mercurial stomatitis, there are strong grounds for the belief. The microbic theory has its adherents, but as yet no specific germ has been discovered.

 

Symptoms.—The disease commences with an indurated swelling, usually near the angle of the mouth. On grasping the swollen mass between the finger and thumb, we get the sensation that the induration extends through the entire cheek. Externally the affected side is swollen, and presents a blanched, glassy appearance. Internally, there is a dusky redness, in the center of which the ulcer rapidly forms; phagedenic in character, it rapidly destroys tissue, and may perforate in three or four days, though rarely before seven or eight days. The entire cheek may be involved, the tissues melting awav like a snowball in the sun. From the ulcer an ichorous fluid is discharged, and shreds of tissue slough off and are mixed with the changed and vitiated saliva. The odor is peculiarly fetid and that of gangrene. The submaxillary glands are always swollen; usually there is but little pain.

 

As the disease progresses, the temperature rises to 104° or 105° ; the pulse, though feeble, is rapid. In swallowing, more or less of the ichorous fluid and shreds of the gangrenous tissue enter the stomach, and a troublesome diarrhea often follows, or the patient, poisoned by the inhalations from his owecrotic cheek, finds septic lobular pneumonia complicating the already overburdened system; the prostration increases, the mind wanders, or the patient sinks into stupor, and succumbs to general sepsis. Death may occur in a few days, or be delayed three or four weeks. In exceptional cases, the patient recovers, leaving great disfigurement from cicatrization of tissue; the disease is generally confined to one side.

Diagnosis.—When fully established, the diagnosis is not difficult. The hard, indurated nodule near the angle of the mouth, the phagedenic character of the ulcer, the gangrenous tissue and foul odor, and later the perforation, can hardly be mistaken for any other variety.

Prognosis.—This is a very grave disease, and the prognosis is decidedly unfavorable, principally due to the impoverished condition of the blood, and general sepsis.

Treatment.—The local treatment will consist of first cleansing the mouth thoroughly, trimming away the gangrenous sloughs and washing the ulcer with a five per cent solution of pyrozone, or a solution of potassium permanganate. The orifice should then be packed with cotton saturated in echinacea.

Internally, give echinacea three drams, water four ounces; teaspoonful one hour, alternating with a saturated solution of hydrastin or potassium chlorate. Where the tongue is covered with a nasty, dirty, pasty coating, sodium sulphite will be used. The mineral acids will replace the above remedies if the tongue be dry and brown and sordes appear on the teeth. The treatment will be antiseptic throughout.

 Chronic gastritis

 

The gastritis is an inflammation of a mucosa of a wall of a stomach. There are acute and chronic forms of it enough extended among children, diseases. Acute gastritis often meets among the children, especially among the children at preschool age. And chronic gastritises very often begin at younger school age. It is bound by that at entering in school the general and alimentary regimen of children sharply changes. Besides it is enlarged emotional and an exercise stress. But it often happens that the diagnosis “gastritis” is also put to one-year-old children.

 

Gastritis can be a brief and sudden illness (acute gastritis), a longer-lasting condition (chronic gastritis), or a special condition, perhaps as part of another medical illness.

An example of acute gastritis is stomach upset that may follow the use of alcohol or certain medications such as aspirin or nonsteroidal anti-inflammatory drugs.

Helicobacter pylori is a type of bacteria that infects the stomach. Infection with this bacteria may lead to chronic gastritis.

 

Gastritis is a common medical problem, with up to10% of people who come to a hospital emergency department with the complaint of abdominal pain being ultimately diagnosed with gastritis.

 

Gastritis can be classified on the basis of the underlying cause (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs , autoimmunity, or allergic response) and thehistopathologic pattern, which may suggest the cause and the likely clinical course (eg, H pylori –associated multifocal atrophic gastritis).

 

Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although some gastropathies, such as those associated with NSAID intake, exhibit minimal inflammation, these entities are discussed in this article because they are frequently included in the differential diagnosis of chronic gastritis.

 

Chemical or reactive gastritis is caused by injury to the gastric mucosa resulting from reflux of bile and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol. These chemicals cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia detectable as foveolar hyperplasia, and damage to capillaries, with mucosal edema, hemorrhage, and increased smooth muscle in the lamina propria.

 

Because inflammation is minimal or lacking in these chemical-caused lesions, gastropathy or chemical gastropathy is a more appropriate description than chemical or reactive gastritis, as proposed by the updated Sydney classification of gastritis. It is important to keep in mind that mixed forms of gastropathy and other types of gastritis, especially H pylori gastritis, may coexist.

 

No single classification provides an entirely satisfactory description of all types of gastritis.  However, an etiologic classification at least provides a direct target toward which therapy can be directed, and for this reason, such a classification is used in this article. In many instances, chronic gastritis is a relatively minor manifestation of diseases that predominantly manifest in other organs or manifest systemically (eg, gastritis in individuals who are immunosuppressed).

 

H pylori gastritis is a primary infection of the stomach and is the most frequent cause of chronic gastritis. Cases of histologically documented chronic gastritis are diagnosed as chronic gastritis of undetermined etiology or gastritis of undetermined type wheone of the findings reflect any of the described patterns of gastritis and a specific cause cannot be identified.

 

 

 

 

Symptoms

 

Gastritis in children symptoms do not always mirror what is happening in the stomach. They include the following:

·       Pain described as burning, aching, and gnawing in the center just below the rib cage where the stomach is located   The pain is usually in the upper central portion of the abdomen (the “pit” of the stomach). Sometimes gastritis pain occurs in the left upper portion of the abdomen and in the back. The pain seems to “go right straight through.” People often use the terms burning, aching, gnawing, or soreness to describe the pain. Usually, a vague sense of discomfort is present, but the pain may be sharp, stabbing, or cutting.

·       A sense of discomfort

·       Nausea and vomiting: The vomit may be clear, green or yellow, blood-streaked, or completely bloody, depending on the severity of the stomach inflammation.

·       Feeling of fullness or burning in the upper part of the belly ·       In more severe gastritis, bleeding may occur inside the stomach. Any of the following symptoms can be seen as well as those already mentioned.

·       The stomach lining when examined through a viewing instrument, the endoscope, will have minimal or no changes at all in severe cases.

·       Belching usually either does not relieve the pain or relieves it only briefly. ·       Bloating ·       The child may appear abnormally pale ·       Sweating ·       Stool may be dark red or black in color   Symptoms of gastritis in children is more or less the same. Ø Nausea Ø Vomiting Ø Weight loss Ø Loss of appetite Ø Poor growth Ø Heartburn Children are also seen to complain of severe pain in the abdomen. The problem with these symptoms is that they are common to so many other medical conditions.   The symptoms of gastritis in children may seem to be a lot worse, as compared to adults. This could be because a child’s digestive system is immature and therefore a bit weaker. Some of the most common gastritis in children symptoms include weight loss, diarrhea, heartburn, mild nausea, tarry stools, constipation, indigestion and pain in the stomach. Hence, as soon as any of these symptoms are seen in a child, it is important to consult a doctor. Children may need to undergo a physical exam or other tests, for a proper diagnosis. Some of the tests that may be required include x rays, blood tests, stool tests and an endoscopy.   Exams and Tests ·  Complete blood count (CBC) showing anemia ·  EGD (esophagogastroduodenoscopy) and biopsy showing gastritis ·  Stool guaiac test to check for blood in the stools

Gastritis Treatment

 

The methods used for gastritis cure may vary, based on the factors that have caused the condition. Hence, chronic gastritis treatment may vary a bit from acute gastritis treatment, since their causes are usually different. Since chronic gastritis is caused by H. Pylori infections, chronic gastritis treatment needs to focus on the eradication of the bacteria. On the other hand, acute gastritis is usually a result of alcohol abuse or excess use of NSAIDS. Therefore, acute gastritis treatment mainly includes elimination of such habits. Most health care providers advise people to take medication for treating stomach acids, so that the signs and symptoms of gastritis remain under control.

 

The medicines that are a part of gastritis treatment include:

Ø Antacids for neutralizing stomach acids

Ø Medication for blocking acids and promoting healing

Ø Antibiotics for destroying the H. Pylori bacteria

Ø Medication to reduce the production of acid

 

Unfortunately, the side effects associated with most of the medicines mentioned above can be quite strong, which is why most people prefer going in for gastritis treatment that is natural. This includes the use of simple home remedies, using natural ingredients such as fresh ginger, garlic, fennel seeds, grape leaves, licorice, carom seeds and potato juice, spinach juice and carrot juice.

 

Since weight plays an important part in the symptoms of this condition, it is also important for people to follow the right gastritis treatment diet plan. Foods like acidic foods, sweets, alcohol, fried food, spices, aerated drinks and fatty food should be avoided. Apart from choosing the foods that are right, it is important for people to eat small portions at frequent intervals and drink a lot of water.

 

Since gastritis is usually caused by poor eating habits in children, one of the main components of gastritis in children treatment includes making dietary changes. The child needs to follow a proper diet, where neither too much, nor too little food is consumed. Some of the recommendations include:

 

Ø Drinking coconut water often

Ø Eating a bowl of rice every day

Ø Getting a good amount of fresh fruits and vegetables

Ø Including many fiber rich foods in the diet

Ø Taking two glasses of milk

  

A peptic ulcer is a sore on the lining of the stomach or duodenum. A common cause of peptic ulcers is infection with the H. pylori bacterium, but a class of medications called non-steroidal anti-inflammatory agents (NSAIDs), like aspirin and ibuprofen, can lead to such ulcers as well.

 

Contrary to popular belief, stress and spicy foods do not cause ulcers, but can exacerbate existing ones. H. pylori leads to an ulcer by attacking the mucous shield that coats the stomach and duodenum, allowing digestive acid to get through to the lining beneath. The acid and the bacteria irritate the lining and cause an ulcer. H. pylori is a well known culprit in adult peptic ulcers but may not be as common in children. Peptic ulcers are unusual in healthy children. Children who have serious medical conditions may develop peptic ulcers as a secondary condition. Also, children may be more vulnerable to the effects of NSAIDs and therefore peptic ulcers in children may be caused by such medications more often than in adults..

 

The pathogenesis of peptic ulcer disease is multifactorial, but the final common pathway for the development of ulcers is the action of acid and pepsin-laden contents of the stomach on the gastric and duodenal mucosa and the inability of mucosal defense mechanisms to allay those effects. Abnormalities in the gastric and duodenal mucosa can be visualized on endoscopy, with or without histologic changes. Deep mucosal lesions that disrupt the muscularis mucosa of the gastric or duodenal wall define peptic ulcers. Gastric ulcers are generally located on the lesser curvature of the stomach, and 90% of duodenal ulcers are found in the duodenal bulb.

 

Symptoms

·       dull stomach ache or pain

·       abdominal discomfort that comes and goes

·       pain and discomfort that typically occur several hours after a meal or in on an empty stomach

·       pain, discomfort that may be relieved by eating

·       pain and discomfort that are usually relieved by antacid medications

·       bloating

·       gas

·       nausea

·       less commonly, vomiting

 

Diagnosis

Ø X-ray of the gastrointestinal tract

Ø Endoscopy, an exam of the stomach and duodenum with an endoscope, a thin, lighted tube with a tiny camera on the end

   

 

Ø Blood test or stool test for H. pylori

 

Treatment

Ø Eradication of  H. pylori (when present)

 

Ø Acid-suppressive drugs

 

Ulcers caused by H. pylori are treated with a course of antibiotics to eradicate the bacterium from GI tract, as well as with drugs to reduce stomach acid, and protect the stomach lining. Ulcers caused by NSAIDs are treated by stopping the medications that caused them and by taking drugs that promote healing of the stomach lining.

 

Complications

 

 Hemorrhage:  Mild to severe hemorrhage is the most common complication of peptic ulcer disease. Symptoms include hematemesis (vomiting of fresh blood or “coffee ground” material); passage of bloody stools (hematochezia) or black tarry stools (melena); and weakness, orthostasis, syncope, thirst, and sweating caused by blood loss.

 

Gastric Ulcer Perforation

 A peptic ulcer may penetrate the wall of the stomach. If adhesions prevent leakage into the peritoneal cavity, free penetration is avoided and confined perforation occurs. Still, the ulcer may penetrate into the duodenum and enter the adjacent confined space (lesser sac) or another organ (eg, pancreas, liver). Pain may be intense, persistent, referred to sites other than the abdomen (usually the back when caused by penetration of a posterior duodenal ulcer into the pancreas), and modified by body position. CT or MRI is usually needed to confirm the diagnosis. When therapy does not result in healing, surgery is required.

 

 Free perforation:  Ulcers that perforate into the peritoneal cavity unchecked by adhesions are usually located in the anterior wall of the duodenum or, less commonly, in the stomach. The patient presents with an acute abdomen. There is sudden, intense, continuous epigastric pain that spreads rapidly throughout the abdomen, often becoming prominent in the right lower quadrant and at times referred to one or both shoulders. The patient usually lies still because even deep breathing worsens the pain. Palpation of the abdomen is painful, rebound tenderness is prominent, abdominal muscles are rigid (boardlike), and bowel sounds are diminished or absent. Shock may ensue, heralded by increased pulse rate and decreased BP and urine output. Symptoms may be less striking in elderly or moribund patients and those receiving corticosteroids or immunosuppressants.

 

Diagnosis is confirmed if an x-ray or CT shows free air under the diaphragm or in the peritoneal cavity. Upright views of the chest and abdomen are preferred. The most sensitive view is the lateral x-ray of the chest. Severely ill patients may be unable to sit upright and should have a lateral decubitus x-ray of the abdomen. Failure to detect free air does not exclude the diagnosis.

 

Immediate surgery is required. The longer the delay, the poorer is the prognosis. When surgery is contraindicated, the alternatives are continuous nasogastric suction and broad-spectrum antibiotics.

 

 Gastric outlet obstruction:  Obstruction may be caused by scarring, spasm, or inflammation from an ulcer. Symptoms include recurrent, large-volume vomiting, occurring more frequently at the end of the day and often as late as 6 h after the last meal. Loss of appetite with persistent bloating or fullness after eating also suggests gastric outlet obstruction. Prolonged vomiting may cause weight loss, dehydration, and alkalosis.

 

If the patient’s history suggests obstruction, physical examination, gastric aspiration, or x-ray may provide evidence of retained gastric contents. A succussion splash heard > 6 h after a meal or aspiration of fluid or food residue > 200 mL after an overnight fast suggests gastric retention. If gastric aspiration shows marked retention, the stomach should be emptied and endoscopy done or x-rays taken to determine site, cause, and degree of obstruction.

 

Edema or spasm caused by an active pyloric channel ulcer is treated with gastric decompression by nasogastric suction and acid suppression (eg, IV H2 blockers). Dehydration and electrolyte imbalances resulting from protracted vomiting or continued nasogastric suctioning should be vigorously sought and corrected. Prokinetic agents are not indicated. Generally, obstruction resolves within 2 to 5 days of treatment. Prolonged obstruction may result from peptic scarring and may respond to endoscopic pyloric balloon dilation. Surgery is necessary to relieve obstruction in selected cases.

 

 Recurrence:  Factors that affect recurrence of ulcer include failure to eradicate H. pylori, continued NSAID use, and smoking. Less commonly, a gastrinoma (Zollinger-Ellison syndrome) may be the cause. The 3-yr recurrence rate for gastric and duodenal ulcers is < 10% when H. pylori is successfully eradicated but > 50% when it is not. Thus, a patient with recurrent disease should be tested for H. pylori and treated again if the tests are positive.

 

Although long-term treatment with H2 blockers, proton pump inhibitors, or misoprostol reduces the risk of recurrence, their routine use for this purpose is not recommended. However, patients who require NSAIDs after having had a peptic ulcer are candidates for long-term therapy, as are those with a marginal ulcer or prior perforation or bleeding.

 

 Stomach cancer:  Patients with H. pylori–associated ulcers have a 3- to 6-fold increased risk of gastric cancer later in life. There is no increased risk of cancer with ulcers of other etiology.

 

Gastroesophageal Reflux Disease

 ORAL HEALTH CONSIDERATIONS

Patients who experience gastric reflux disease complain of dysgeusia (foul taste), dental sensitivity, erosion and/or pulpitis. Dental sensitivity is generally due to the erosion of enamel by gastric acid. Erosion leads to dentin sensitivity and, at times, irreversible pulpal involvement. Patients who exhibit signs of reflux disease must be medically evaluated and referred appropriately. Patients who have a diagnosis of GERD may need to be treated in a semisupine position and premedicated with H2 receptor antagonists or antacids. Any medications that may cause nausea (such as narcotic analgesics) should be prescribed judiciously because of the increased likelihood of regurgitation and possible aspiration. Mild baking soda mouth rinses (one half teaspoon of sodium bicarbonate in 8 ounces of water) may be rinsed and expectorated to minimize dysgeusia due to acid reflux. Topical fluoride applications via a custom-made occlusive tray will ensure optimal dental mineralization. H2 receptor antagonists may cause central nervous system (CNS) effects in a continuum from fatigue and lethargy to confusion, delirium, and seizures. These effects are dose dependent; thus, they may be seen more commonly in elderly persons or in those with impaired kidney or liver function. Patients who are taking cimetidine may experience a toxic reaction to lidocaine if injected intravascularly. Cimetidine also has been shown to inhibit the absorption (and therefore, the blood concentration) of the systemic antifungal drug ketaconazole. Soft-tissue changes such as esophageal fibrosis and stricture may complicate intubation if the patient requires general anesthesia. Oral mucosal changes are minimal; however, erythema and mucosal atrophy may be present as a result of the exposure of tissues to acid.

DUODENAL ULCER DISEASE, PEPTIC ULCER DISEASE

 Oral Health Considerations.

 If a patient presents with symptoms of epigastric pain, as described previously, the dentist should refer this person to the primary care physician for diagnostic work-up. Oral manifestations of peptic ulcer disease are rare unless there is anemia from gastrointestinal bleeding or persistent regurgitation of gastric acid as a pyloric stenosis leading to dental erosion, typically of the palatal aspect of the maxillary teeth. Vascular malformations of the lip have been reported and range from a very small maculae to a large venous pool. The dentist will often see patients with a history of peptic ulcer disease. To prevent the aggravation of the disease in these patients, the avoidance of actions that increase the production of acid is essential. Thus, lengthy dental procedures should be avoided or spread out over shorter appointments to minimize stress. Also, dentists should avoid administering drugs that exacerbate ulceration and cause gastrointestinal distress, such as aspirin and other NSAIDs; acetaminophen products are preferable and are recommended. A patient who reacts to dental procedures in a particularly stressful way may be a candidate for sedation. Dentists should be aware that patients who are taking anticholinergic drugs often present with dry mouth. This may be particularly problematic for denture wearers.

Denture adhesives and artificial saliva may aid in the retention of these prostheses. There is an increased risk of dental caries if hyposalivation is prolonged and if the patient placessugarcontaining items into the mouth in an effort to stimulate saliva flow or uses sugar-ladened antacid lozenges. Therefore, artificial saliva and/or chewing sugarless gum to stimulate salivary flow may help prevent dental caries. Informing the patient of this side effect of anticholinergic drugs and stressing proper diet and oral hygiene are critical for these patients.Additionally, because many antacids contain calcium, magnesium, and aluminum salts that bind antibiotics such as erythromycin and tetracycline, the dentist should be aware that administration of one of these drugs within an hour of antacid therapy may decrease the absorption of the antibiotic by 75 to 85%.Consequently, antibiotics should be taken 2 hours before or 2 hours after ingestion of antacids. Exogenous steroid administration is likely to exacerbate the ulcer because of the increased production of acid caused by the steroid and should be avoided. Although it is generally good policy to prescribe penicillin V instead of penicillin G (because of the destruction of penicillin G by gastric acid), it is essential with patients who have peptic ulcers. Before extensive oral surgical or periodontal procedures are undertaken, it may be prudent to determine the patient’s red blood cell count, hemoglobin,hematocrit, and platelet count. If the patient has a history of ulcer perforation and subsequent hemorrhage, blood loss can result in anemia. Consequently, the associated risks of performing surgery on an anemic patient will be encountered. Delayed healing, risk of bacterial infection (particularly with anaerobic bacteria, due to tissue hypoxia), and grave side effects of respiratory depression by narcotic analgesics enhanced by a state of anemia are examples of such associated risks. Lastly, cimetidine and rantidine, drugs commonly prescribed for duodenal ulcer patients, have occasionally been associated with thrombocytopenia.

ULCERATIVE COLITIS

 Oral Health Considerations.

 Due to the symptoms of severe frequent diarrhea and abdominal pain or cramping, it is unlikely that a patient will be seeking routine dental care with undiagnosed ulcerative colitis. Nonetheless, should an undiagnosed patient attend a dental office for care, then the risks associated with anemia (such as delayed healing, an increased risk of infection, the side effects of narcotic analgesics, and depression of respiration) collectively contraindicate surgical treatment until the disease is under control. Obviously, following a history and a thorough examination, signs and symptoms of ulcerative colitis and/or anemia would warrant a referral to the patient’s primary care physician. More likely is the situation of a diagnosed and medically managed patient attending a dental office for routine or episodic oral health care. The following section addresses those issues a dentist must be knowledgeable about when treating patients who have ulcerative colitis. The oral changes that occur in ulcerative colitis cases are nonspecific and uncommon, with an incidence of less than 8%. Aphthous stomatitis of the major and minor variety has been reported in patients with active ulcerative colitis. There is nothing unique about these lesions, and it has been suggested that their appearance is coincidental. However, they may result from nutritional deficiencies of iron, folic acid, and vitamin B12 due to poor absorption in the gut and/or blood loss directly related to the ulcerative colitis. In addition, anti-inflammatory medications such as the 5-aminosalicylates which often represent the mainstay of therapy for IBD( inflammatory bowel disease) patients and which are excreted in saliva, are known to cause aphthous ulcers and RAU in some patients. In patients who are prone to develop aphthous ulcers, the appearance of a new crop of oral ulcers often heralds a flare-up of the bowel disease. Other nonspecific forms of ulceration associated with skin lesions have been reported. Pyoderma gangrenosum may occur in the form of deep ulcers that sometimes ulcerate through the tonsillar pillar. Pyostomatitis vegetans, a purulent inflammation of the mouth, may also occur. These oral lesions are characterized by deep-tissue vegetating or proliferative lesions that undergo ulceration and then suppuration. As the lesions disappear with a total colectomy, it is speculated that these manifestations are due to the effects of circulating immunocomplexes induced by antigens that are derived from the gut lumen or the damaged colonic mucosa. Lastly, ulcerative colitis patients also can develop hairy leukoplakia, a lesion more commonly associated with acquired immunodeficiency syndrome (AIDS). This lesion probably serves as a marker of severe immunosuppresionand may result from the use of corticosteroids or other immunosuppressive agents. Medical management for ulcerative colitis may necessitate alterations of dental therapy or special precautions. Sulfasalazine interferes with folate metabolism, and supplemental folic acid may be needed, especially if a macrocytic anemia is revealed in a complete blood count.

Many side effects are associated with the use of corticosteroids and ACTH. The development of hypertension and diabetes are serious side effects for patients who are taking these two drugs and the dentist must be aware of this. Obtaining a blood pressure reading and obtaining a blood glucose measurement by finger prick in the office and/or consultation with the treating physician to understand the patient’s current medical status is critical. Long-term corticosteroid therapy may cause osteoporosis and vertebral compression fractures; thus, carefully positioning the patient in the dental chair and encouraging the patient to take dietary calcium supplements may help prevent fractures. Long-term use of steroids can also result in adrenal suppression. Major operative procedures can precipitate adrenal insufficiency if the steroid doses are not adjusted properly. Patients undergoing surgery require increased doses of steroids before and after the procedure because their own adrenal response to stress is blunted. Patients who were formerly on steroid therapy may also experience adrenal suppression. For example, 20 mg of prednisone daily for 7 to 10 days can cause adrenal suppression, and adrenal activity may not return to normal for 9 to 12 months. Clearly, consultation with the patient’s physician is warranted prior to surgical procedures. Chronic bleeding can be associated with ulcerative colitis. Prior to dental procedures, blood studies that include hemoglobin, hematocrit, and a red blood cell count should be undertaken to rule out the presence of anemia. Further, patients on immunosuppressive agents such asazathioprine might be expected to have changes in white and red blood cell counts, and total and differential white blood cell counts should be ascertained before embarking on surgical procedures. Patients who have extensive bowel surgery may suffer from malabsorption of vitamin K, vitamin B12 , and folic acid. Again, before any surgical procedures are completed, these patients should be evaluated for both macrocytic and microcytic anemia and bleeding disorders from insufficient levels of vitamin K (fibrin clot formation). Clotting factors II, VII, IX, and X are all dependent on Vitamin K. Thus, a prothrombin time and a partial thromboplastin time should be obtained. Alternatively, an international normalized ratio (INR) will also provide critical information about the patient’s ability to form a blood clot. Finally, patients taking the immunosuppressive agent azathioprine may suffer from additional side effects that impact dental management. Suppression of the liver can be expected, and liver function tests should be completed in those patients who will receive dentist-prescribed medications thataremetabolized in the liver. Typically, patients taking an immunosuppressive agent like azathioprine are monitored by their primarycare physician with liver function tests. Consequently, consultation with the patient’s physician will help the dentist determine the patient’s liver function. Obviously, toxic doses of the same drugs may be reached if reduced drug metabolism is not taken into consideration.

 

CROHN’S DISEASE

 Oral Health Considerations

 Oral lesions, both symptomatic and asymptomatic, affect 6 to 20% of Crohn’s disease patients. Most oral manifestations of Crohn’s disease occur in patients with active intestinal disease, and their presence frequently correlates with disease activity. Recurrent aphthous ulcers are the most common oral manifestation of Crohn’s disease. It is not clear whether these oral manifestations are true expressions of Crohn’s disease, pre-existing and/or co-incidental findings, direct results of medical treatment, or manifestations of an associated problem such as anemia. Certainly, pyostomatitis vegetans, cobblestone mucosal architecture, and minor salivary gland duct pathology represent granulomatous changes that constitute the hallmark of Crohn’s disease. Biopsy specimens of these multiple small nonhealing aphthous ulcers reveal granulomatous inflammation. Less often, Crohn’s disease patients develop diffuse swelling of the lips and face, inflammatory hyperplasias of the oral mucosa with a cobblestone pattern, indurated polypoid taglike lesions in the vestibule and retromolar pad area, and persistent deep linear ulcerations with hyperplastic margins. Granulomatous lesions have also been observed in the salivary glands, where they may cause rupture of the ducts and localized mucocele formation. Numerous medications, including anti-inflammatory and sulfa-containing preparations that are commonly used to manage IBD patients, have been reported to cause oral lichenoid drug reactions. Superinfection with Candida albicans is often associated with IBD and may represent a primary manifestation of the disorder, a reaction to thebacteriostatic effect of sulfasalazine, or an impaired ability of neutrophils to kill this granuloma-provoking organism. Of interest is the possibility that oral lesions may precede theradiologic changes of the disease by up to 1 year. This underscores the sometimes subtle signs and symptoms of Crohn’s disease and the possibility that a dentist may encounter a patient with undiagnosed Crohn’s disease. Frequently, patients will complain of pain associated with ulcerative lesions in the oral cavity. Palliative rinses, ointment, and topical steroids may be helpful. There appears to be an increased risk of dental caries that is probably related to dietary changes in patients with IBD. The causes of the dental caries and increased incidence of bacterial and fungal infections are multifactorial but appear to be related to either the patient’s altered immune status or diet. Oral effects of malabsorption may also be seen.Pallor angular cheilitis, and glossitis, all oral manifestations of anemia, may occur, particularly in undiagnosed or poorly controlled disease. Nutritional deficiencies that are directly related to the section of the bowel affected by the disease can occur. Malnutrition is often a problem, and monitoring the patient’s compliance with dietary supplementation is essential. As with ulcerative colitis, the medical management of a patient with Crohn’s disease may alter his or her dental management. The following description of dental management is applicable to patients with a diagnosis of IBD. The underlying assumption of this management is that patients with IBD are at increased risk for the development of oral infections, including dental caries. Consequently, dental management of patients with IBD should include the following:

1. Frequent preventive and routine dental care to monitor oral health and to prevent the destruction of hard and soft tissue. If the patient is taking a systemic corticosteroid, monitoring of blood pressure and evaluation of blood glucose is necessary.

2. Evaluation of hypothalamic-pituitary-adrenocortical function, to determine the patient’s ability to undergo extensive dental procedures.

3. Diagnosis of oral inflammatory, infectious, or granulomatous lesions (including performance of a biopsy if necessary).

4. Treatment of oral manifestations of IBD, particularly symptomatic lesions. Palliative rinses and topical steroid therapy ( fluocinonide 0.05%) may be helpful. Topical steroid therapy should be short-term and monitored because of the side effect of mucosal atrophy and systemic absorption.

5. Consultation with the patient’s physician to completely comprehend the medical management of the patient. In particular, knowledge of the effects, side effects, and drug interactions of any medications the patient is taking is essential.

 

▼ORAL DISEASES AND DIABETES

Oral conditions that are seen in individuals with diabetes may include burning mouth, altered wound healing, and an increased incidence of infection. Enlargement of the parotid glands and xerostomia can occur; both are conditions that may be related to the metabolic control of the diabetic state. Medications that diabetic patients often take for related or unrelated systemic conditions may have significant xerostomic effects. Thus, the xerostomia seen in individuals with diabetes may result more from medications than from the diabetic condition itself. Neuropathy of the autonomic system can also cause changes in salivary secretion since salivary flow is controlled by the sympathetic and parasympathetic pathways. Dry mucosal surfaces are easily irritated and are associated with“burning mouth” syndrome; they also provide a favorable environment for the growth of fungal organisms. Some studies have shown an increased incidence of oral candidiasis in patients with diabetes whereas other studies have not. The effect of diabetes on the dental caries rate is unclear. Some studies have demonstrated increased caries in people with diabetes, which has been associated with xerostomia or increased gingival crevicular fluid glucose levels. Other studies have shown similar or decreased caries rates in people with diabetes. Since most diabetic individuals limit their intake of fermentable carbohydrates, the less cariogenic diet may limit caries incidence. In recent studies of type 2 diabetic patients and nondiabetic control subjects, no differences were seen in salivary flow rates, organic constituents of saliva, salivary counts of acidogenicbacteria, salivary counts of fungal organisms, or coronal and root caries rates. These findings suggest that diabetic individuals as a group are similar to nondiabetic people in regard to these oral conditions. Periodontal Health and Diabetes Strong evidence suggests that, unlike the conditions discussed above, diabetes is a risk factor for the prevalence and severity of gingivitis and periodontitis. Diabetes is associated with increased gingival inflammation in response to bacterial plaque, but the degree of glycemic control is an important variable in this relationship. In general, well-controlled diabetic individuals and nondiabetic people have similar degrees of gingivitis, with the same level of plaque. Conversely, poorly controlled diabetic subjects have significantly increased gingivitis, compared to either well-controlled diabetic or nondiabetic individuals. In large epidemiologic studies, diabetes has been shown to significantly increase the risk of attachment loss and alveolar bone loss approximately threefold when compared to nondiabetic control subjects. These findings have been confirmed in meta-analyses of multiple studies in various diabetic populations. Diabetes increases not only the prevalence and severity of periodontitis but also the progression of bone loss and attachment loss over time. Periodontitis is similar to the classic complications of diabetes in its variation among individuals. Just as retinopathy, nephropathy, and neuropathy are more likely to be seen in diabetic patients with poor glycemic control, progressive destructive periodontitis is also more common in those with poor control. However, some poorly controlled diabetic patients do not develop significant periodontal destruction, just as some do not develop the classic diabetic complications. Conversely, well-controlled diabetes places the person at a lower risk for periodontal disease, similar to the risk of nondiabetic individuals; yet,well-controlled diabetic patients may still develop periodontitis, just as nondiabeticindividuals do. Other risk factors for periodontitis, such as poor oral hygiene and smoking, play a similar deleterious role in both diabetic and nondiabetic individuals. Hyperglycemia results in increased gingival crevicular fluid glucose levels, which may significantly alter periodontal wound-healing events by changing the interaction between cells and their extracellularmatrix within the periodontium. Vascular changes seen in the retina, glomerulus, and perineural areas also occur in the periodontium. Theformation of AGEs results in collagen accumulation in the periodontal capillary basement membranes, causing membrane thickening. AGE-stimulated smooth-muscle proliferation increases the thickness of vessel walls. These changes decrease tissue perfusion and oxygenation. AGE-modified collagen in gingival blood vessel walls binds circulating LDL, which is frequently elevated in diabetes, resulting inatheroma formation and further narrowing of the vessel lumen. These changes in the periodontium may dramatically alter the tissue response to periodontal pathogens, resulting in increased tissue destruction and diminished repair potential. Diabetes results in changes in the function of host defense cells such as polymorphonuclear leukocytes (PMNs), monocytes, and macrophages. PMN adherence, chemotaxis, and  hagocytosis are impaired. Defects in this first line of defense against periodontopathic microorganisms may significantly increase periodontal destruction. Monocytes and macrophages in diabetic individuals are often hyper-responsive to bacterial antigens. This up-regulation results in a significantly increased production of proinflammatory cytokines and mediators. The net effect of these host defense alterations is an increase in periodontal inflammation, attachment loss, and bone loss. Collagen is the primary structural protein in the periodontium. Changes in collagen metabolism in diabetic individuals contribute to wound-healing alterations and periodontal destruction. The production of matrix metalloproteinases (MMPs) such as collagenase is increased in many diabetic patients. Increased collagenase production readily degrades newly formed collagen. Conversely, AGE modification of existing collagen decreases its solubility. The result of these changes in collagen metabolism is a rapid dissolution of recently synthesized collagen by host collagenase and a preponderance of older AGE-modified collagen. Thus, diabetes induces a shift in the normal homeostatic mechanism by which collagen is formed, stabilized, and eventually turned over; this shift alters healing responses to physical or microbial wounding of the periodontium. Tetracycline antibiotics and chemically modified tetracycline agents reduce host collagenase production and collagen degradation through mechanisms that are independent of their antimicrobial activity. These drugs may have benefits in managing conditions such a periodontitis, arthritis, diabetes, osteoporosis, and others in which collagen metabolism is altered.

DENTAL MANAGEMENT OF THE DIABETIC PATIENT

General Dental Treatment

Overall, diabetic patients respond to most dental treatments similarly to the way nondiabetic patients respond. Responses to therapy depend on many factors that are specific to each individual, including oral hygiene, diet, habits such as tobacco use, proper dental care and follow-up, overall oral health, and metabolic control of diabetes. For example, the diabetic patient with poor oral hygiene, a history of smoking, infrequent dental visits, and a high fermentable-carbohydrate intake is more likely to experience oral diseases such as caries andperiodontitis and to respond poorly to dental treatment than a diabetic patient without these factors. Glycemic control appears to play an important role in the response to periodontal therapy. Well-controlled diabetic patients with periodontitis have positive responses to nonsurgical therapy, periodontal surgery, and maintenance that are similar to those of people without diabetes. However, poorly controlled diabetic patients respond much less favorably, and short-term improvements in periodontal health are frequently followed by regression and by recurrence of disease. It is imperative that the dental practitioner have a clear understanding of each diabetic patient’s level of glycemic control prior to initiating treatment. Patients may present to the dental office with oral conditions that suggest an undiagnosed diabetic state. An example is severe rapidly progressing periodontitis that exceeds what would be expected given the patient’s age, habit history, oral hygiene, and level of local factors (plaque, calculus) (Figures 1 and 2).

 

FIGURE 1

Radiograph of area 18-19 in a 35-year-old male with a 4-year history of type 1 diabetes. The patient had generalized moderate plaque levels but minimal alveolar bone loss. He rarely used dental floss. Widening of the periodontal ligament (space 18) was due to occlusal trauma, which was treated by occlusal adjustment.

 

 

FIGURE 2

Radiograph of area 18-19 in the same patient shown in

Figure 21-1 at 39 years of age and with an 8-year history of poorly controlled

type 1 diabetes (HbA1c values were 10.2 to 11.3%). There is a rapid progression

of bone loss, the severity of which exceeds that expected from

plaque and calculus levels.

 

Other findings seen in some undiagnosed diabetic patients include enlarged gingival tissues that bleed easily upon manipulation and the presence of multiple periodontal abscesses (Figures 3, 4, and 5).

FIGURE 4

Palatal view of the maxillary right sextant in the same

patient shown in Figure 3. An abscess can be noted on the palatal aspect

of tooth 2.

 

FIGURE 3

Lingual view of mandibular incisors of a 60-year-old

female with poorly controlled type 2 diabetes. The HbA1c value at initial

examination was 13.9%. Multiple periodontal abscesses (teeth 22, 23, 25,

26, and 27) with severe inflammation and bone loss can be seen

 

.

FIGURE-5

Radiograph of the same sextant shown in Figure 4.

Severe bone loss can be noted on tooth 2.

 

 

If the clinician suspects an undiagnosed diabetic state, the patient should be questioned to elicit a history of polydipsia, polyuria, polyphagia, or unexplained weight loss (see Table 4).

TABLE 4 Signs and Symptoms of Undiagnosed Diabetes

Polydipsia (excessive thirst)

Polyuria (excessive urination)

Polyphagia (excessive hunger)

Unexplained weight loss

Changes in vision

Weakness, malaise

Irritability

Nausea

Dry mouth

Ketoacidosis*

*Ketoacidosis is usually associated with severe hyperglycemia and occurs primarily

in type 1 diabetes.

The patient should be questioned about a family history of diabetes. If diabetes is suspected, laboratory evaluation

and physician referral are indicated (see Table 5).

TABLE 5 Laboratory Diagnostic Criteria for Diabetes

 

Diagnosis is by any of the following three methods and must be confirmed on a subsequent day by any one of the same three methods.

1. Presence of diabetes symptoms plus casual (nonfasting) plasma glucose ≥ 200 mg/dL (casual glucose may be drawn at any time of day without regard to time since last meal)

2. Fasting plasma glucose* ≥ 126 mg/dL (fasting is defined as no caloric intake for at least 8 hours)

3. Two-hour postprandial glucose† ≥ 200 mg/dL during an oral glucose tolerance test using a glucose load containing the equivalent of 75 g of anhydrous glucose dissolved in water‡

*Categories of fasting plasma glucose are as follows: < 110 mg/dL = normal; ≥ 110 mg/dL and < 126 mg/dL = impaired; ≥ 126 mg/dL = provisional diagnosis of diabetes (must be confirmed on a subsequent day, as described above).

†Categories of 2-hour postprandial glucose are as follows: < 140 mg/dL = normal glucose tolerance; ≥ 140 mg/dL and < 200 mg/dL = impaired glucose tolerance; ≥ 200 mg/dL = provisional diagnosis of diabetes (must be confirmed on subsequent day, as described above).

‡This method is not recommended for routine use.

 A patient with previously diagnosed but poorly controlled diabetes may present with oral findings similar to those of the undiagnosed diabetic individual. The dental practitioner must establish the level of glycemic control early in the treatment process; this can be done by physician referral or by a review of the patient’s medical records. Patients who perform SBGM may be asked to bring their glucose log to the dental office for review by the dental team. The clinician should determine the patient’s recent glycated hemoglobin values since this test provides a measure of glycemic control over the preceding 2 to 3 months. HbA1c values of less than 8% indicate relatively good glycemic control; values greater than 10% indicate poor control.

Physician referral is appropriate any time glycemic control is in question. The issue of glycemic control should be addressed often by the dental team since dental treatment outcomes may be dependent partly on good metabolic control of the underlying diabetic state. Other key dental treatment considerations for diabetic patients include stress reduction, treatment setting, and the use of antibiotics, diet modification, appointment timing, changes in medication regimens, and the management of emergencies. Endogenous production of epinephrine and cortisol increase during stressful situations. These hormones elevate blood glucose levels and interfere with glycemic control.

Adequate pain control and stress reduction are therefore important in treating diabetic patients. Profound anesthesia reduces pain and minimizes endogenous epinephrine release. The small amounts of epinephrine in dental local anesthetics at 1/100,000 concentration have no significant effect on blood glucose. Conscious sedation should be considered for extremely anxious patients. Most practitioners who use intravenous sedation elect to use fluids without dextrose, such as normal saline. However, fluids such as D5W (a 5% solution of dextrose in water) in small amounts should not produce wide fluctuations in glycemia in most patients. Most diabetic patients can easily be managed on an outpatient basis in the dental office. Patients with very poor glycemic control, severe head and neck infections, other systemic diseases or complications, and dental-treatment needs that will require long-term alteration of medication regimens or diet may be considered for treatment in a more controlled medical environment. The use of systemic antibiotics for routine dental treatment is not necessary for most diabetic patients. Antibiotics may be considered in the presence of acute infection. Some clinicians prefer to prescribe prophylactic antibiotic coverage prior to surgical therapy if the diabetic patient’s glycemic control is poor. This usually applies to emergency situations since elective procedures are generally deferred until glycemic control improves. In patients with severe periodontitis, adjunctive use of tetracycline antibiotics in conjunction with mechanical periodontal therapy may have beneficial effects on glycemic control as well as on periodontal status. Dental treatment can result in postoperative discomfort. This may necessitate changes in the diet, especially in cases of extensive dental therapy. Because diet is a major component of diabetes management, diet alterations that are made because of dental treatment may have a major impact on the patient. Whereas some patients are very knowledgeable about their diabetic condition and can adjust for changes in diet, this may not be the case with others. The clinician may need to consult the patient’s physician prior to therapy, to discuss diet modifications and required changes in medication regimens. Another diet change occurs when patients are placed on orders to take nothing by mouth (NPO) before dental treatment, a common recommendation before conscious sedation. Consultation with the patient’s physician may be needed to adjust the dose of insulin or oral agents in this situation; however, some patients are able to make these adjustments themselves. Physicians often recommend reducing the insulin dose that immediately precedes lengthy or extensive dental procedures. Appointment timing for the diabetic patient is often determined by the individual’s medication regimen. Conventional wisdom holds that diabetic patients, like other medically compromised individuals, should receive dental treatment in the morning. While this may be true for some patients, it is not true for others. It is generally best to plan dental treatment to occur either before or after periods of peak insulin activity. This reduces the risk of perioperative hypoglycemic reactions, which occur most often during peak insulin activity. For those who take insulin, the greatest risk of hypoglycemia will thus occur about 30 to 90 minutes after injecting lispro insulin, 2 to 3 hours after regular insulin, and 4 to 10 hours after NPH or Lente insulin. For those who are taking oral sulfonylureas, peak insulin activity depends on the individual drug taken. Metformin and the thiazolidinediones rarely cause hypoglycemia. The main factor to consider in determining appointment times is the peak action of insulin and the amount of glucose being absorbed from the gut following the last food intake The greatest risk would occur in a patient who has taken the usual amount of insulin or oral agent but has reduced or eliminated a meal prior to dental treatment. For example, if the patient takes the usual dose of regular insulin before breakfast but then fails to eat or eats less than the usual amount, the patient will be at increased risk for hypoglycemia during a morning dental appointment. Patients with good long-term glycemic control and patients with a previous history of severe hypoglycemic episodes are at greater risk for future hypoglycemia. Often, it is not possible to plan dental treatment so as to avoid peak insulin activity. This is particularly true for patients who take frequent insulin injections. In these instances, the clinician must be aware that the patient is at risk for perioperative hypoglycemia. It is helpful to check the pretreatment blood glucose level (using the patient’s glucometer) and to have a source of carbohydrates readily available. When treating patients with a history of asthma or angina, dentists usually have the patients bring their inhaler or nitroglycerine with them to dental appointments. In the same way, diabetic patients should be encouraged to bring their glucometer with them to the dental office. Before dental treatment begins, the patient may check his or her blood glucose. If the level is near the lower end of the normal range, a small amount of pretreatment carbohydrate may prevent hypoglycemia during the appointment. Having the glucometer available also allows rapid determination of blood glucose levels should the patient experience signs and symptoms of hypoglycemia.

CONCLUSION

Diabetes mellitus is a metabolic condition affecting multiple organ systems. The oral cavity frequently undergoes changes that are related to the diabetic condition,

 

and oral infections may adversely affect metabolic control of the diabetic state. The mechanisms underlie the oral effects of diabetes share many similarities with the mechanisms that are responsible for the classic diabetic complications. The intimate relationship between oral health and systemic health in individuals with diabetes suggests a need for increased interaction between the dental and medical professionals who are charged with the management of these patients. Oral health assessment and treatment should become as common as the eye, foot, and kidney evaluations that are routinely performed as part of preventive medical therapies. Dental professionals with a thorough understanding of current medical treatment regimens and the implications of diabetes on dental care are able to help their diabetic patients achieve and maintain the best possibleoral health.

Diabetes mellitus presented with an ulcerating rash

 

A 63-year-old woman with a 4 1/2-year history of diabetes mellitus presented with an ulcerating rash, primarily on the shins, groin, and face (Panel A); cheilitis (Panel B); and glossitis. Her symptoms had been worsening for 4 years despite specialized wound care. In addition, she noted concurrent weight loss, depression, abdominal pain, and intractable nausea. She was taking 500 mg of metformin daily. Given her history of diabetes mellitus and the skin findings, abdominal computed tomography was performed, and glucagon levels were measured. An enhancing, lobulated mass measuring 7 cm in diameter was found in the tail of the pancreas, and the patient’s fasting glucagon level was elevated, at 890 pg per milliliter (normal range, 0 to 80). The mass was resected, and pathological examination of the specimen confirmed a diagnosis of glucagonoma. Glucagonomas are rare neuroendocrine tumors that can cause diabetes and a rash known as necrolytic migratory erythema, which has a characteristic annular pattern of erythema with central crusting and bullae. The prognosis correlates with the stage of tumor development and the potential for resection. In this patient, 1 day after resection, the rash had faded significantly. Four weeks after discharge, the patient had normal glucose levels (while taking no medication), and the necrolytic migratory erythemahad completely resolved