IMMUNOLOGY OF INFECTION

Immunology of infection. Immunology in acute and chronic odontogenic, paradontogenic and neodontogenic MFR inflammation and prevention of complications. Immunology of MFR specific inflammation (tuberculosis, actinomycosis , syphilis, AIDS).

 

SPECIFICAL INFLAMMATORY  PROCESSES OF THE MFA (ACTINOMYCOSIS, TUBERCULOSIS, SYFILIS), AIDS: CLASSIFICATION, CLINICAL COURSE, DIAGNOSIS, TREATMENT.

Cervicofacial Actinomycosis

Cervicofacial actinomycosis is a disease that is characterized by the formation of abscess, fistulae, tissue fibrosis and draining sinus tracts. This disease can mimic many other conditions such as granulomatous disease and malignancy. They show soft tissue swelling in the neck and head.Cervicofacial actinomycosis is caused by bacteria known as Actinomyces israelii. This type of bacteria is usually present in the mouth, however it is capable of causing disease once it enters the tissues from an injured portion of the body. Actinomyces israelii anaerobic meaning it dislikes oxygen and grows deep inside the tissues where oxygen level is low. Root canal treatment, tooth extraction, poor dental hygiene or jaw surgery are some of the reasons which allow access to Actinomyces israelii thus causing an infection.

 

 

Actinomycosis Actinomycosis – the chronic illness caused by various kinds of Actinomyces. It is characterised by a lesion of various organs and tissues with formation of dense infiltrates which then abscess with the advent of fistulas and an original lesion of a skin. Actinomycosis aetiology Originators – various kinds of Actinomyces, or radiant mushrooms. The cores from them is the following: Actinomyces israelu, Actinomyces bovis, Actinomyces albus, Ac. violaceus. Actinomyces well grow on nutrient mediums, forming colonys of the irregular form, is frequent with radiant edges. Are pathogenic for many kinds of agricultural and laboratory animals. In a pathological stuff meet in the form of druses which represent yellowish lumps in diameter of 1-2 mm. At microscopy in the centre of druses the clump of strands of a mycelium, and on periphery – flasklike inflations is found. At a coloration a hematoxylin – eosine the central part of druse is imbued in dark blue colour, and flasks in the pink. There are druses at which the border from flasklike cells is absent. Actinomyces are sensitive to a benzylpenicillin (20 Unit/ml), streptomycin (20 mkg/ml), Tetracyclinum (20 mkg/ml), Levomycetinum (10 mkg/ml) and erythromycin (1,25 mkg/ml). Actinomycosis epidemiology The actinomycosis is extended in all countries. With it humans and agricultural animals are ill. However cases of infestation of the human from sick humans or animals it is not described. Originators of an actinomycosis eurysynusic in the nature (hay, straw, bedrock, etc.). Actinomyces often find in healthy humans in an oral cavity, a debris, lacunas of tonsils, on a mucosa of a gastrointestinal tract. Matters both exogenous, and endogenous infestation means. Actinomycosis pathogenesis The most frequent is the endogenous path of an infection contamination. Actinomyces eurysynusic in the nature, in particular on plants, can get with plants to an organism and be on mucosas as a saprophyte. Transition of Actinomyces from saprophytical in a parasitic state is promoted by inflammatory diseases of mucosas of an oral cavity, a respiratory and gastrointestinal tract. On a place of introduction of Actinomyces the infectious granuloma which sprouts in surrounding tissues is formed. In granulations there are abscesses which, breaking, form fistulas. The skin lesion has secondary character. In formation of pyeses the role and secondary, mainly staphylococcal infection contamination plays. Antigens of radiant mushrooms lead to a specific sensibilization and allergic rearrangement of an organism (a hypersensibilization of the slowed down phylum), and also to antibody formation (complement-linked, agglutinins, precipitin, etc.). Symptoms and actinomycosis flow Duration of an incubation interval is not known. He can fluctuate over a wide range and reach till several years (from time of a becoming infected development of demonstrative forms of an actinomycosis). The basic clinical forms of an actinomycosis: 1.     An actinomycosis of a head, tongue and a neck 2.     A thoracal actinomycosis 3.     The abdominal 4.     An actinomycosis of genitourinary organs 5.     A skin actinomycosis 6.     A mycetoma 7.     An actinomycosis of the central excitatory system The actinomycosis concerns to initially-persistent infections with long progressing flow. At infiltrate growth the skin is involved in process. In the beginning very dense and almost painless infiltrate is defined, the skin becomes tsianotichno-crimson, there is a fluctuation, and then educe is long not healing fistulas. In pus find belovato-yellowish fine lumps (druses). Cervicofacial actinomycosis meets most often. On expression of process it is possible to secure the deep (muscular) form when process is localised in an intermuscular fat, hypodermic and dermal forms of an actinomycosis. At the muscular form process is localised mainly in masseters, under a fascia covering them, forming dense, cartilaginous consistences an infiltrate in the field of a mandible angle. The person becomes azygomorphous, the masticatory spasm of various intensity educes. Then in an infiltrate there are locuses of a ramollissement which are spontaneously dissected, forming the fistulas abjointing purulent or krovjanisto-purulent fluid, sometimes with an admixing of yellow grains (druses). A cyanotic coloration of a skin round fistulas it is long remains and is characteristic implication of an actinomycosis. On a neck original changes of a skin in the form of cross-section located platens are formed. At the dermal form of an actinomycosis infiltrates ball-shaped or semiball-shaped, localised in a hypodermic fat. A masticatory spasm and disturbances of processes of chewing it is not observed. The dermal form meets seldom. Actinomycotic process can grasp cheeks, labiums, tongue, tonsils, a trachea, orbits, a larynx. Flow rather congenial (in comparison with other forms). Thoracal actinomycosis (an actinomycosis of organs of a thoracal lumen and a thoracal side), or an actinomycosis of lungs. The beginning gradual. There is a delicacy, subfebrile temperature, tussis, in the beginning dry, then with a mucopurulent sputum, is frequent with a blood admixing (the sputum has an odour of the earth and taste of copper). Then the peribronchitis picture educes. The infiltrate extends from the centre to periphery, grasps a pleura, a thoracal side, a skin. There is a tumescence with extremely expressed stinging morbidity at a palpation, the skin becomes bagrovo-cyanotic. Fistulas educe, in pus druses of Actinomyces are found. Fistulas intercommunicate with bronchuses. They settle dowot only on a thorax, but can appear on a loin and even on a hip. Flow serious. Without treatment patients die. On frequency the thoracal actinomycosis takes the second place. Abdominal actinomycosis also meets often enough (takes the third place). The primary locuses are more often localised in ileocecal range and in the field of an appendix (over 60 %), then there are other departments of a colon and the stomach or a thin intestine, an esophagus is very seldom amazed initially. The abdominal wall is amazed again. The primary infiltrate is localised in ileocecal range more often, quite often imitates surgical diseases (an appendicitis, impassability of an intestine, etc.). Extending, the infiltrate grasps also other organs: the liver, nephroses, a column, can reach an abdominal wall. In the latter case there are characteristic changes of a skin, the fistulas intercommunicating with an intestine. Are located usually in inguinal range. At an actinomycosis of a rectum infiltrates cause occurrence of specific paraproctites, fistulas are dissected in perianal range. Without etiotropic treatment the lethality reaches 50 %. Genital actinomycosis and Pelvic actinomycosis meets rare. As a rule, it is secondary lesions at infiltrate diffusion at an abdominal actinomycosis. Primary actinomycotic lesions of generative organs meet very seldom. Actinomycosis of bones and joints meets rare. This form arises or as a result of transition of an actinomycotic infiltrate from the next organs, or is a consequence of hematogenous drift of a mushroom. Osteomyelites of bones of an anticnemion, a basin, a column, and also a lesion patellar and other joints are described. Quite often process is preceded by a trauma. Osteomyelites proceed with a destruction of bones, formation of sequesters. Attracts attention, that despite the expressed osteal changes, sick keep ability to move, at lesions of joints function seriously is not broken. At formation of fistulas there are characteristic changes of a skin. Skin actinomycosis arises, as a rule, again at primary localisation in other organs. Skin changes become appreciable when actinomycotic infiltrates reach a hypodermic fat and are especially characteristic at formation of fistulas. Mycetoma – an original variant of an actinomycosis. This form was known for a long time, often enough met in the tropical countries. Disease begins with appearance on stop, mainly on a sole, one or several dense circumscribed knots in size from a pea and more, covered at first not variated skin, further over inspissations the skin becomes red-violet or brownish. In the neighbourhood with pristine knots appear new, the skin swells, autopodium is enlarged in volume, changes the form. Then knots are softened and dissected with formation of deeply going fistulas excreting purulent or is serous-purulent, sometimes bloody fluid, is frequent with a fetor. In abjointed fine grains of usually yellowish colour (druse) are appreciable. Knots are almost painless. Process slowly progresses, all sole is penetrated by knots, toes turn up. Then knots and fistulous courses appear and on autopodium back. All autopodium turns to the deformed and pigmented mass penetrated by fistulas and lumens. Process can pass to muscles, tendons and bones. The atrophy of muscles of an anticnemion is sometimes observed. Usually process grasps only one autopodium. Disease proceeds very longly (10-20 years). Complications. Stratification of a secondary bacteriemic infection contamination. The diagnosis and the differential diagnosis. In far come cases with formation of fistulas and characteristic changes of a skin the diagnosis of difficulties does not represent. It is more difficult to diagnose initial forms of an actinomycosis. For diagnostics the intracutaneous test with actinolysathos has some value. However in attention it is necessary to accept only positive and sharply positive assays as weakly positive intracutaneous tests often happen at patients to diseases of dens (for example at an alveolar pyorrhea). Assay Negative takes not always allow to exclude an actinomycosis as at patients with serious forms they can be negative owing to sharp oppression of cellular immunodefence, they are always negative at a HIV-infected. Abjection of culture of Actinomyces from a sputum, a mucosa of a fauces, a nose has no diagnostic value as Actinomyces are quite often found and in healthy faces. The reaction of binding complement with actinolysathos which happens positive at 80 % of patients has diagnostic value. The greatest diagnostic value has abjection (detection) of Actinomyces in pus from fistulas, in biopsy samples of the amazed tissues, in druses, in the last is sometimes microscopically mycelium strands are found only. In these cases it is possible to try to secure culture of Actinomyces by stuff sowing on medium of the Aloe. Actinomycosis of lungs is necessary for differentiating from neoplasms of lungs, abscesses, other deep mycoses (an aspergillosis, a nocardiosis, a histoplasmosis), and also from a pulmonary tuberculosis. The abdominal actinomycosis should be differentiated from various surgical diseases (an appendicitis, a peritonitis and so forth). A lesion of bones and joints-from of purulent diseases. Actinomycosis treatment The best results are given by a combination of a causal treatment (antibiotics) and immunotherapies. At the is cervical-maxillofacial form prescribe inside a phenoxymethylpenicillin for 2 grammes/days and at duration of a course not less than 6 weeks. It is possible to prescribe also Tetracyclinum in the big doses (on 0,75 gramme 4 times a day within 4 weeks or on 3 gramme a day only in the first 10 days, and then on 0,5 gramme 4 times a day within last 18 days). Erythromycin is prescribed on 0,3 gramme by 4 times a day within 6 weeks. At abdominal forms and at an actinomycosis of lungs prescribe the big doses of a benzylpenicillin (10000000 Unit/day and more) intravenously within 1-1,5 months with the subsequent transition to a phenoxymethylpenicillin in a daily dose of 2-5 gramme within 2-5 months. At consecutive infection stratification (staphilococcuses, an anaerobic microflora) prescribe long courses of a dicloxacillin or antibiotics of tetracycline bunch, at a mephitic gangrene – metronidazole. For an immunotherapy actinolysathos it is possible to introduce subcutaneously or intradermally, and also it is intramuscular. Under a skin and intramusculary introduce on 3 ml actinolysathos 2 times a week. On a course of 20-30 injections, duration of a course 3 months At an abscess, an empyema spend surgical treatment (dissecting and a drainage). At extensive damages of a pulmonary tissue sometimes resort to a lobectomy. From antibiotics the most effective are Tetracyclinums, then go a phenoxymethylpenicillin and erythromycin is less effective. Refractory to these antibiotics of strains of Actinomyces did not meet. Actinomycosis forecast Without etiotropic treatment the forecast serious. At an abdominal actinomycosis 50 % of patients died, at the thoracal all patients perished. Rather the is cervical-maxillofacial actinomycosis is easier proceeded. All it causes necessity of early diagnostics and the beginning of therapy before development of serious anatomical damages. Considering possibility of relapses, convalescents should be under long observation (6-12 months). Actinomycosis preventive maintenance and actions in the locus Hygiene of an oral cavity, timely treatment of dens, inflammatory changes of tonsils and an oral cavity mucosa. Specific preventive maintenance is not developed. Actions in the locus do not spend.

 

Actinomycosis

Actinomycosis is a long-term (chronic) bacterial infection that commonly affects the face and neck.

Causes

Actinomycosis is usually caused by an anaerobic bacteria called Actinomyces israelii, which is a common and normally not disease-causing (nonpathogenic) organism found in the nose and throat.

Because of the bacteria’s normal location in the nose and throat, actinomycosis most commonly appears in the face and neck. However, the infection can sometimes occur in the chest (pulmonary actinomycosis), abdomen, pelvis, or other areas of the body. The infection is not contagious.

Symptoms occur when the bacteria enters the facial tissues after trauma, surgery, or infection. Common triggers include dental abscess or oral surgery. The infection has also been seen in certain women who have had an intrauterine device (IUD) to prevent pregnancy.

Once in the tissue, it forms an abscess, producing a hard, red to reddish-purple lump, often on the jaw, from which comes the condition’s commoame, “lumpy jaw.”

Eventually, the abscess breaks through the skin surface to produce a draining sinus tract.

Symptoms

Actinomycosis of Maxilla. The disease spread to opposite side; finally implicated base of skull, and proved fatal. Treated by radium.

• Draining sores in the skin, especially on the chest wall from lung infection with Actinomyces

• Fever

• Minimal or no pain

• Swelling or a hard, red to reddish-purple lump on the face or upper neck

• Weight loss

Exams and Tests

• Culture of the tissue or fluid shows Actinomyces species.

• Examination of drained fluid under a microscope shows “sulfur granules” in the fluid. They are yellowish granules made of clumped organisms.

• Examination under a microscope shows the Actinomyces species of bacteria.

Treatment

Treatment of actinomycosis usually requires antibiotics for several months to a year. Surgical drainage or removal of the lesion may be needed. If the condition is related to an IUD, the device must be removed.

Outlook (Prognosis)

With treatment, you should recover fully.

Possible Complications

Meningitis can rarely develop from this infection.

When to Contact a Medical Professional

Call your health care provider if you develop any of the symptoms of this disorder. Beginning treatment promptly helps quicken the recovery.

Prevention

Good oral hygiene and regular dentist visits may help prevent some forms of actinomycosis.

Alternative Names

Lumpy jaw

Actinomycosis is an infection caused by a bacterium called Actinomyces israelii (A. israelii).

Actinomycosis (also known as Rivalta disease, big jaw, clams, lumpy jaw or wooden tongue) is an infection, commonly of the face and neck, that produces abscesses (collections of pus) and open-draining sinuses (tracts in the skin).

 

Actinomycosis is caused by a bacterium called Actinomyces israelii (A. israelii). It occurs normally in the mouth and tonsils. This bacterium may cause infection when it is introduced into the soft tissues by trauma, surgery or another infection. Once in the tissues, it may form an abscess that develops into a hard red to reddish purple lump. When the abscess breaks through the skin, it forms pus-discharging lesions.

Causes of Actinomycosis

Actinomycosis is caused by a strain of bacteria called actinomycetales. Actinomycetales are found in many of the body’s cavities, such as inside the mouth and less commonly the bowel.

In women, they can also be found in the womb and the fallopian tubes (through which eggs are released into the womb).

How actinomycosis spreads

Actinomycetales are anaerobic bacteria, which means they cannot survive in oxygen-rich environments. Therefore, they do not present a problem when they are in one of the body’s cavities, such as the mouth or the intestinal tract.

However, if actinomycetales break through the protective lining (mucus membrane) that surrounds the cavities, they can penetrate deep into your body’s tissue. As the deep layers of human tissue are low in oxygen, the bacteria are able to reproduce quickly and infect healthy tissue.

Abscesses

In an attempt to combat the infection, your immune system (the body’s natural defence against infection and illness) will send infection-fighting cells to the source of the infection. However, these cells do not have the ability to kill the bacteria and will quickly die.

As the infection-fighting cells die, they accumulate into a yellowish-coloured liquid called pus. Having failed to kill the infection, your immune system will attempt to limit its spread by using healthy tissue to form a protective barrier around the pus. This is how a pus-filled swelling, known as an abscess, is formed.

Unfortunately, the actinomycetales strain of bacteria has the ability to penetrate the protective barrier of an abscess and move into more healthy tissue. Your immune system will attempt to counter the infection by producing more abscesses.

Sinus tracts

Your body will eventually need to get rid of the accumulation of pus. To do this, small channels called sinus tracts will develop that lead from the abscesses to the surface of your skin.

The sinus tracts will leak pus, as well as ‘sulphur granules’, which are a yellow, powdery substance. The sulphur granules are actually made up of lumps of bacteria, but they are known as sulphur granules as they are the same colour as the chemical sulphur.

Opportunistic infection

Actinomycosis is an opportunistic infection that does not cause any symptoms unless an opportunity arises for it to penetrate into the body‘s tissue.

Oral cervicofacial actinomycosis

Opportunities for oral cervicofacial actinomycosis include:

• tooth decay – particularly if the decay is left untreated for many years

• gum disease

• dental abscess

• tonsillitis

• inner ear infection

• dental surgery, such as a tooth extraction, or root canal treatment

• jaw surgery

Thoracic actinomycosis

Most cases of thoracic actinomycosis are thought to be caused by small particles of food or other ingested material that get mixed up with the actinomycosis bacteria. Rather than passing harmlessly down into the stomach, the particles are mistakenly passed down into the windpipe and the airways of the lungs.

People with long-term drug or alcohol problems are particularly at risk of developing thoracic actinomycosis for two reasons:

• being drunk or intoxicated increases your risk of accidentally ingesting material into your lungs

• long-term drug and alcohol misuse weakens the immune system, which makes a person more vulnerable to developing an infection

Abdominal actinomycosis

Abdominal actinomycosis occurs when something tears the wall of the intestine (bowel), allowing the bacteria to penetrate into deep tissue.

The intestine can tear as a result of an infection, such as a burst appendix that damages the wall of the intestine. Or it can be damaged through injury – for example, when someone mistakenly swallows a fish bone.

There have also been some reported cases of abdominal actinomycosis occurring as a complication of bowel or abdominal surgery.

Pelvic actinomycosis

Most cases of pelvic actinomycosis have been recorded in women who were using the intrauterine device (IUD) form of contraception. The IUD is a small, T-shaped contraceptive device made from plastic and copper that fits inside the womb. The women affected tend to be long-term users of the IUD (eight years or more).

One explanation for the high number of cases of pelvic actinomycosis in women who are using the IUD is that over time the IUD may damage the womb lining, allowing bacteria to penetrate into deep tissue. However, no research has yet been done to find out whether or not this is the case.

It should be stressed that developing pelvic actinomycosis as a result of using an IUD is very unlikely. In England, millions of women use the IUD device and there have only been a handful of reported cases of pelvic actinomycosis.

Actinomycosis Symptoms

The list of signs and symptoms mentioned in various sources for Actinomycosis includes the 17 symptoms listed below:

* Symptoms of facial actinomycosis:
o Swollen jaw
o Jaw pain
o Tooth pain
o Pus in the mouth
* Symptoms of other abscesses:
o Pain
o Fever
o Weight loss
* Varies depending on site
* Commonly includes the mouth
* Rectum and vagina
* Fever
* Pain
* Abscess formation
* Weight loss
* Abnormal vaginal bleeding and vaginal discharge

Actinomycosis Treatment

Medical Care

In most cases of actinomycosis, antimicrobial therapy is the only treatment required, although surgery can be adjunctive in selected cases. Penicillin G is the drug of choice for treating infections caused by actinomycetes.

Surgical Care

Attempt to cure actinomycosis, including extensive disease, with aggressive antimicrobial therapy alone initially. Surgical therapy may include incision and drainage of abscesses, excision of sinus tracts and recalcitrant fibrotic lesions, decompression of closed-space infections, and interventions aimed at relieving obstruction (eg, when actinomycotic lesions compress the ureter).

Consultations

1)    Interventional radiologist

2)    Surgeon

3)    Infectious diseases specialist

 

Diet

No specific dietary precautions are indicated in patients with actinomycosis.

Activity

Patients with actinomycosis may be active to the degree tolerated.

 

ORAL MANIFESTATIONS OF TB DISEASE

The estimated prevalence of oral tuberculous lesions ranges from 0.05 to 5%.  Oral lesions are usually secondary, reflecting oral inoculation with infected sputum or as a result of hematogenous spread.  Rare cases of primary tuberculous involvement of oral structures have been reported.  In one study evaluating patients with TB disease and co-infection with HIV, the prevalence of oral tuberculous lesions was found to be 1.33%. Oral tuberculous lesions are nonspecific in their clinical presentation, and their consideration in the differential diagnosis requires a high degree of awareness. While all oral tissues may be affected, in the cohort of patients with both TB disease and HIV-infection, the palate and dorsum of the tongue (Figure) were the most frequent sites of oral involvement.

 

Oral tuberculous lesion of the dorsum of the tongue in a patient with both TB disease and HIV infection. 

These data are in agreement with those reported by other investigators in patients with TB disease without HIV-infection. Pain and cervical lymphadenopathy are common but not universal findings. A rare case of tuberculous osteomyelitis of the mandible and several cases of tuberculous parotitis have been documented.

Diagnosis

Early diagnosis of infection with MBT is important because of the nature of the disease. The tuberculin skin test (TST) or a blood assay for Mycobacterium tuberculosis (BAMT) are useful for screening groups of people for LTBI with exposure rates that substantially exceed those of the general population (Table 1).

 

The TST, which is the Mantoux intradermal test, using 5 tuberculin units of Tween-stabilized purified protein derivative (PPD)-tuberculin is the traditional method of diagnosing LTBI.  The antigen is injected intracutaneously into either the volar or dorsal surface of the forearm.  In patients with LTBI, the TST evokes a delayed hypersensitivity reaction to the tuberculin mediated by T-lymphocytes producing an area of redness and swelling.  The test is read at 48 to 72 hours.  Erythema is disregarded, and the diameter of the induration is measured (Table 1).

While the relative specificity of the TST skin test is high, both false positive and false negative reactions have been reported. False-positive reactions may be due to previous sensitization with mycobacterial antigens, as may be seen following vaccination with Bacille Calmette-Guerin (BCG). False-negative reactions to the TST have been reported in immunocompromised patients, in patients with recent exposure to MBT, and in very young children. 

The CDC recommends persons with a positive TST undergo further evaluation.In recent years a number of in vitro diagnostic tests in the form of BAMT have been developed. However, the QuantiFERON®-TB Gold (QFT-G) test is the only such test approved by the Food and Drug Administration (FDA) for the detection of latent TB infection. This test detects the release of interferon-gamma in fresh heparinized blood from sensitized persons when it is incubated with mixtures of synthetic peptides representing two proteins present in MBT. The sensitivity of QFT-G is statistically similar to that of TST for detecting TB infection. However, the QFT-G measures cell-mediated response to peptides from two MBT proteins that are not present in any BCG vaccine strains and are absent from the majority of mycobacteria other than MBT. Hence, the QFT-G has greater selectivity.

Although the history, physical examination, TST and/or QFT-G data, and other studies such as chest radiographs are helpful and at times may strongly suggest TB disease, definitive diagnosis usually requires the demonstration of MBT in the patient’s tissues or secretions. Bacteriologic examination, which includes obtaining a specimen of sputum, detection of acid-fast bacilli (AFB) in stained (Ziehl-Neelsen method) smears examined microscopically, may provide the first bacteriologic clue to TB disease. However, not all AFB are tubercle bacilli, therefore, a positive bacteriologic culture for MBT is essential to confirm the diagnosis. DNA probes specific for the genus Mycobacterium now are used routinely to identify specific mycobacterium. When the presence of MBT has been confirmed, it is then necessary to perform drug susceptibility testing on positive cultures.

Immunization with viable Mycobacterium bovis BCG is the most widely used preventive measure to control tuberculosis worldwide. Administered to newborns in a single dose, it prevents severe disease and reduces mortality among children from miliary and meningeal disease. However, BCG does not protect against pulmonary tuberculosis in children or adults. As mentioned earlier, optimal immune response to MBT infection appears to involve both CD4+ and CD8+ T-cells. BCG activates CD4+ T-cells by being taken up by macrophages and residing within phagosomes which are membrane-enclosed vacuoles. These antigens, once processed in the phagosomes, then readily interact with MHC class II molecules. However, the ability of the bacillus to block acidification of the phagosomes precludes its release into the cytoplasm and for an antigen to bind to MHC class I molecules it must be processed in the cytoplasm of the infected cells. Consequently, BCG fails to elicit a CD8+ T-cell response. A recently developed recombinant bacillus with an impaired ability to counter the acidification of phagosomes will soon enter phase 1 clinical trials. This new vaccine is likely to be more effective because it targets both CD4+ and CD8+ T-cells.

The goal of antibacterial chemotherapy is to induce selective toxicity. Selectivity can be realized by attacking targets that are:

• unique to the pathogen,

• similar to but not identical to those of the host,

• shared by the host but that vary in importance between pathogen and host.

One target is the bacterial cell wall, a structure that is both unique and essential for the survival of most pathogenic bacteria. The bacterial cell wall is a three-dimensional meshwork of peptide-crosslinked sugar polymer (peptidoglycan or murein) surrounding the cell just outside its cytoplasmic membrane.

Bacteria may be conveniently divided into two groups, Gram-positive and Gram-negative, based on the relative abilities of bacteria to retain purple Gram-stain after being washed with an organic solvent such as acetone. Gram-positive bacteria retain the stain and appear purple, whereas Gram-negative bacteria lose the stain and appear pink. The ability to retain stain results from two distinguishing characteristics of cell wall architecture. In Gram-positive bacteria, the cell wall is composed of a thick layer of murein. The murein layer in Gram-negative bacteria is thinner but it is surrounded by a second, outer lipid bilayer membrane. The cell wall of mycobacteria, which include the causative agent of tuberculosis, is similar to that of Gram-negative bacteria.

Both Gram-negative bacteria and mycobacteria are enclosed by an inner cytoplasmic membrane, a thin murein layer, and an outer membrane. The main difference is that, in mycobacteria, the outer membrane is thick, composed of two leaflets that are asymmetrical in size and composition. The inner leaflet is composed of arabinogalactan and mycolic acid, and the outer leaflet is composed of extractable phospholipids. Cell wall biosynthesis takes place in the following three major steps:

1.     Synthesis of murein monomers from amino acids and sugar building blocks (N-acetylglucosamine [NAG] and N-acetylmuramic acid [NAM]).

2.     Polymerization of the monomers into linear peptidoglycans.

3.     Crosslinking of the polymers into a three-dimensional meshwork.

In mycobacteria the NAM residues of the cell wall are modified by the addition of a long chain consisting of a NAG-arabinogalactan linker topped with mycolic acid. The addition of arabinose units is catalyzed by the enzyme arabinosyl transferase. The synthesis of mycolic acid includes the formation of saturated hydrocarbon chains catalyzed by the enzyme fatty acid synthetase 1 (FAS1), which are then linked by the enzyme fatty acid synthetase 2 (FAS2). The linked products undergo further enzymatic transformations to become mycolic acid.

Standard antimycobacterial treatment regimens include antibiotics that target unique targets such as the synthesis of NAG-arabinogalactan and the early steps in mycolic acid synthesis (Table 4).

The treatment of infections with MBT can be divided into treatment of LTBI and treatment of TB disease. Guidelines with detailed management recommendations are published and updated regularly.

The risk for progression from LTBI to TB disease is highest during the first two years after infection and is often predicated on concomitant medical conditions that alter the ability of the immune system to maintain the isolation of MBT (Table 2).  HIV infection is the most important risk factor.  It has been estimated persons infected with MBT and co-infected with HIV have a 6-10% risk per year of developing TB disease, while an immunocompetent person infected with MBT has a 10% life-time risk for TB disease.  Isoniazid, given for nine months in a single daily dose, is the drug of choice for the treatment of LTBI.  Persons exposed to patients with known isoniazid resistant TB disease and those with intolerance to isoniazid may be treated with rifampin for four months.  For patients with known exposure to multi-drug resistant TB disease, a regimen with two drugs to which MBT is susceptible is recommended for nine to 12 months.

Tuberculosis (TB) – Prevention

Active tuberculosis (TB) is very contagious. The World Health Organization (WHO) estimates that one-third of the world’s population is infected with the bacteria that cause TB.

To avoid getting an active TB infection:

• Do not spend long periods of time in stuffy, enclosed rooms with anyone who has active TB until that person has been treated for at least 2 weeks.

• Use protective measures, such as face masks, if you work in a facility that cares for people who have untreated TB.

• If you live with someone who has active TB, help and encourage the person to follow treatment instructions.

Can the TB vaccine help?

A TB vaccine (bacille Calmette-Guerin

, or BCG) is used in many countries to prevent TB. But this vaccination is almost never used in the United States because:

• The risk of getting TB is low in the U.S.

• The vaccine is not effective in adults who receive it.

• The BCG vaccine may cause a tuberculin skin test to indicate a TB infection even if a person is not infected with TB. This complicates the use of the tuberculin skin test to check people for TB.

Oral manifestations of syphilis

The past decade has shown a significant rise in the prevalence of infective syphilis in the developed world, and striking increases in its frequency have occurred in Eastern Europe, particularly the UK, and in the US. Although oral manifestations of syphilis are most likely to be observed during secondary disease, all stages of the disease can give rise to oral lesions. Significant oral lesions such as gumma-associated bony destruction and a possible predisposition to oral squamous cell carcinoma are associated with tertiary disease. Since the prevalence of infective syphilis in heterosexuals has been increasing, there has now been a gradual rise in the number of children born with congenital syphilis. Consequently, the congenital disease gives rise to dental anomalies as well as bone, skin, and neurological anomalies of the face. The aim of this report is to review syphilis-related oral lesions, as well as to summarize the relations between human immunodeficiency virus (HIV) and syphilis.

CHANGING EPIDEMIOLOGY OF INFECTIVE SYPHILIS

Infective syphilis is caused by the anaerobic filamentous spirochete, Treponema pallidum. In the past decade there has been a significant rise in the prevalence of infective syphilis in the developed world. Striking increases in the frequency of syphilis have occurred in Eastern Europe, and smaller rises have been reported in Western Europe and the US. The changing epidemiology of syphilis reflects the falling use of barrier methods of contraception, high numbers of sexual partners,⁷ sexual promiscuity, lack of relevant knowledge, the sex industry, the health care breakdown in former Communist communities, and the deterioration of public health responses to sexually transmitted infection (STI) control (e.g. faster notification). In Eastern Europe, the increased frequency of syphilis has been predominantly in heterosexuals, while in the UK and US, the outbreaks have occurred in heterosexuals and in men having sex with men. Outbreaks in the US have sometimes been associated with the use of crack cocaine, and rapid spread of syphilis has occurred in prisons where recent arrestees may already be infected.

PRIMARY SYPHILIS

The mouth, perhaps surprisingly, is rarely the site of primary syphilis, and because of its transient nature, the oral ulceration of primary syphilis often goes unnoticed by the patient or by any unsuspicious clinician. In addition, albeit rarely, the lesions of primary disease may be confused with other pre-existing mucocutaneous disease. A chancre develops within 1 to 3 weeks of acquisition. Primary syphilis is usually the consequence of orogenital or oroanal contact with an infectious lesion. Kissing may, very rarely, cause transmission; indeed, it has been suggested that intrafamilial oral acquisition of syphilis in a child may have occurred via this route, although more usually oral syphilis in a child is indicative of sexual abuse.

Primary syphilis of the mouth manifests as a solitary ulcer usually of the lip or, more rarely, the tongue. The upper lip is more commonly affected than the lower in males, while the opposite occurs in females—probably reflecting the anatomy involved with fellatio and cunninlingus. The pharynx or tonsils may rarely be affected. The ulceration is usually deep, with a red, purple, or brown base and an irregular raised border. There is usually an accompanying cervical lymphadenopathy. The ulceration of primary syphilis may be confused with other solitary ulcerative disorders, most notably traumatic ulceration, squamous cell carcinoma, and non-Hodgkin’s lymphoma.

The diagnosis of primary syphilis may be aided by detailed analysis of the sexual and/or social lifestyles of the patient and of any of the available sexual partner; however, often the diagnosis of early disease can be difficult. Affected patients often do not have a positive nonspecific reaginic test, eg, Rapid Plasma Reagin (RPR) or Venereal Disease Reference Laboratory (VDRL) tests. The specific tests for IgG antibodies to T. pallidum become positive before the reaginic tests, and thus should be carried out when the nonspecific tests prove negative but a diagnosis of primary disease is still likely.

Treponemes are present in primary lesions and can be detected by dark field microscopy; however, this test is fraught with the risk of nosocomial transmission and is thus no longer considered suitable. In addition, there can be confusion between the spirochetes of T. pallidum with the normal commensals of the mouth.

Histopathology is not always helpful, as there are no specific histopathological features, and the detection of T. pallidum with Warthin-Starry stain or silver nitrate stain may not be possible. Monoclonal anthodyl immunoperoxidase staining techniques can detect T. pallidum and is a relatively routine clinical investigation of biopsy material. However, molecular methods such as in situ and tissue PCR still remaionroutine investigations for all types of syphilis. The tests used to detect IgM antibodies to T. pallidum may detect early infection.

OUTCOMES OF THERAPY

The primary chancres spontaneously heal within 7 to 10 days, although they can persist much longer, only resolving with appropriate antimicrobial therapy.

SECONDARY SYPHILIS

The features of secondary syphilis reflect the hematogenous spread of T. pallidum, and similarly to its other mucocutaneous features, the oral manifestations of secondary syphilis can be more extensive and/or variable than those of the primary disease. Oral lesions arise in at least 30% of patients with secondary syphilis, although very rarely oral ulceration may be the only manifestation of infection. The 2 principal oral features of secondary syphilis are mucous patches and maculopapular lesions, although nodular lesions may rarely arise.

MACULOPAPULAR LESIONS

• Macular syphilides: Macular lesions tend to arise on the hard palate and manifest as flat-to-slightly raised, firm, red lesions.

• Papular syphilides: These are rare. They manifest as red, raised, firm round nodules with a grey center that may ulcerate. The papules usually arise on the buccal mucosa or commissures.

•  Mucous patches: A variety of descriptions of mucous patches have been reported, but in general these manifest as oval-to-crescenteric erosions or shallow ulcers of about 1 cm diameter, covered by a grey mucoid exudate and with an erythematous border. The patches usually arise bilaterally on the mobile surfaces of the mouth although the pharynx, gingivae, tonsils, and very rarely the hard palate can be affected. At the commissures, the mucous patches may appear as split papules, while on the distal and lateral aspects of the tongue, they tend to ulcerate or manifest as irregular fissures. The mucous patches may coalesce to give rise to, or arise de novo as, serpiginous lesions, sometimes termed snail track ulcers.

ULCERONODULAR DISEASE (LUES MALIGNA)

Ulceronodular disease is an explosive generalized form of secondary syphilis characterized by fever, headache, and myalgia, followed by a papulopustular eruption that rapidly transforms into necrotic, sharply demarcated ulcers with hemorrhagic brown crusts, organized in rupioid layers commonly on the face and scalp. The mucosa is involved in about one third of affected patients. Lues maligna gives rise to crateriform or shallow ulcers on the gingivae, palate or buccal mucosa, with multiple erosions on the hard and soft palates, tongue and lower lip.

NODULAR DISEASE

Rarely, secondary syphilis can manifest as nodules alone. This nodular eruption of syphilis has a predilection for the face, mucous membranes, palms of the hands and soles of the feet.²⁶ Lesions may occur on the vermillion, mimicking squamous cell carcinoma or keratoacanthoma.

DETECTION OF INFECTION IN SECONDARY DISEASE

Treponema pallidum can usually be detected on the surface of erosions or ulcers by darkfield microscopy, although as noted above, this test should be avoided. The patient will have positive serological tests.

The histopathological features of secondary syphilis are variable. Often the changes are nonspecific, although they may include perivascular infiltrates with a preponderance of plasma cells and epidermal psoriasiform hyperplasia. Warthin-Starry strains will only detect spirochetes in about a third of instances, although newer methods may increase the in situ detection of the causative agent.

OUTCOMES OF THERAPY

The lesions of secondary syphilis will resolve spontaneously within 3 to 12 weeks, regardless of therapy, and about 25% of untreated patients will have recurrence of secondary disease.

LATENT SYPHILIS

In early latent syphilis, usually the first 12 months after secondary disease, affected patients are infectious. In late latent syphilis the infectivity falls.

TERTIARY SYPHILIS

Clinical disease arises in about one third of patients with untreated secondary syphilis. The oral complications of tertiary syphilis center upon gumma formation, and much more rarely, syphilitic leukoplakia (and risk of oral squamous cell carcinoma) and neurosyphilis.

GUMMA FORMATION

Gummas tend to arise on the hard palate and tongue, although very rarely they may occur on the soft palate, lower alveolus, and parotid gland.A gumma manifests initially as 1 or more painless swelling.When multiple, they tend to coalesce, giving rise to serpigninous lesions. The swellings eventually develop into areas of ulceration, with areas of breakdown and healing. There may be eventual bone destruction, palatal perforation, and oro-nasal fistula formation. Rarely, a gumma may erode into blood vessels—eg, the inferior alveolar artery. Gumma manifests radiologically as ill-defined radiolucencies that may resemble malignancy. The areas of ulceration eventually heal, although the resultant scarring can, at least on the tongue, cause fissuring.

SYPHILITIC LEUKOPLAKIA AND RISK OF SQUAMOUS CELL CARCINOMA

Syphilitic leukoplakia would appear to be a homogenous white patch affecting large areas of the dorsum of the tongue. There are few good descriptions of syphilitic leukoplakia, and it is unclear whether this lesion truly reflects syphilis, or more likely a tobacco smoking habit—indeed this was observed by Hutchinson in the 19th century.

An association between tertiary syphilis and oral squamous cell carcinoma—particularly of the tongue—has been suggested for many years. Both clinically- and serologically-based studies have suggested an increased prevalence of syphilis in patient groups with squamous cell carcinoma of the tongue (up to 60% in one study), the association being stronger in males than females. A relatively recent study of 16,420 people with syphilis resident in the US found a significantly raised frequency of cancer of the tongue (and Kaposi’s sarcoma) in males. A noncontrolled study found that 5 of 63 UK patients with squamous cell carcinoma of the tongue had serological evidence of past syphilis as detected by both specific and nonspecific tests. However, it remains unclear whether any risk of oral squamous cell carcinoma in syphilis is a direct consequence of infection (which seems unlikely) or is the effect of recognized causative factors for oral malignancy, ie, tobacco, alcohol, and malnourishment.

NEUROSYPHILIS

Aside from the well-recognized Argyll Robertson pupil, tertiary syphilis can give rise to both unilateral and bilateral trigeminal neuropathy and facial nerve palsy. Potentially, syphilitic osteomyelitis may give rise to trigeminal neuropathy.

DETECTION OF INFECTION IN TERTIARY DISEASE

Gummas are characterized histopathologically by endarteritis obliterans, necrosis with epithelioid and giant cells and a plasma cell infiltrate. Spirochetes are difficult to detect. In tertiary disease, the nonspecific tests may not be positive; the most reliable test is FTA, although this may remain positive even after successful therapy.

CONGENITAL SYPHILIS

As discussed previously, in some communities there is a rising prevalence of congenital syphilis. Treponema pallidum crosses the placenta only after the 16th week of intrauterine life; hence, depending upon the time of infection, it may variably affect the facial structures. Resembling its systemic features, the orofacial manifestations of congenital syphilis can be split into early and late. Early features include diffuse maculopapular rash, periostitis (frontal bossing of Parrot), and rhinitis. Late features, manifesting at least 24 months after birth, comprise the Hutchinsonian triad of interstitial keratitis of the cornea, sensorineural hearing loss, and dental anomalies.

The dental anomalies of congenital syphilis only arise in teeth in which calcification occurs during the first year of life, hence typically the permanent incisors and first molars. Of note, the maxillary incisors are more commonly affected than the mandibular ones. The incisors have a screwdriver shape, there being a convergence of the lateral margins towards the incisal edge. In some, there may be notching of the incisal edge, while in others, there may be a depression on the labial surface. The first molar may be bud-shaped and reduced to the size of the adjacent second molar. The normal mesiodistal convexity of the crown may be reduced. Enamel hypoplasia may occur. Yellow discoloration of the skin about the lips can arise soon after birth; the area then becomes increasingly rigid with crack formation and eventual (Parrot’s) radial scars—rhagades—of the lips. There may be a loss of the well-circumscribed border of the vermillion.

Other, less common orofacial features include atrophic glossitis and a high, narrow palatal vault. Facial neuropathies may rarely occur as can palatal gumma in adulthood.

INTERACTIONS BETWEEN HIV AND SYPHILIS

According to WHO, Brazil had about 660,000 people living with human immunodeficiency virus (HIV) at the end of 2003, and 15,000 people had died of AIDS during that year. Heterosexual transmission, sex between men, and injecting drug users (IDU) continue to be almost equally responsible for the burden of HIV infection. However, the HIV epidemic in Brazil has changed over the last decade, with IDU being responsible for almost 30% of all HIV cases.

Strong evidence supports several biologic mechanisms through which sexually transmitted diseases (STDs) facilitate HIV transmission by increasing both HIV infectiousness and HIV susceptibility. Thus, the detection of STDs and the establishment of effective treatment is an important strategy of HIV control.

INFLUENCE OF HIV DISEASE UPON SYPHILIS

It was initially suggested that concurrent HIV infection and syphilis is not uncommon, particularly in young adults, men having sex with men, and traders of commercial sex. HIV disease might significantly influence the clinical source of syphilis, as it does for some STDs and other conditions related to HIV-associated immune deficiency, and the associated infection is often more aggressive than the mono-infection. A Nigerian study of 31 people with concurrent HIV infection and syphilis found that 64.2% of the patients had developed unusual lesions affecting more than 50% of the body. Also, the chancres seen at the sites of inoculation had an atypical appearance.

However, a recent detailed study suggests that other than an increased number and frequency of genital ulcers in secondary disease, HIV disease does not greatly impact the clinical care of syphilis. Nevertheless, there have been reports of prolonged primary disease and secondary disease; additionally, neurosyphilis may present more quickly and ulceronodular disease is more likely in patients infected with HIV than in those not infected.

INFLUENCE OF ORAL SYPHILIS UPON HIV DISEASE

Patients with concurrent HIV infection and syphilis usually have a history of sexually transmitted infection, and it is common that these patients have more than 1 condition (eg, genital ulcers, injected drug addition, etc) that are potential sources of exposure. The genital ulceration of syphilis increases the risk of HIV transmission. Nonulcerative STD, however, also have the capacity of increasing the likelihood of HIV transmission, and the detection and treatment of syphilis can probably help to reduce HIV transmission. While there are no data to support the notion, it is likely that oral syphilis principally influences HIV disease by increasing the likelihood of HIV transmission (and other related viruses) by oral sexual routes. A recent study found no association between early syphilis and changes in blood or semen viral load or CD4 count in HIV-positive individuals. According to the study, increased HIV-1 infectivity associated with early syphilis is unlikely to be associated with increased levels of HIV-1 RNA in blood or semen. There is now compelling evidence, based upon case and epidemiological studies, that HIV can be transmitted via orogenital contact. In addition, as persons in high-risk groups for HIV move away from high-risk sexual activities, there is likely to be an increased frequency of orogenital contact, and hence oral sex will contribute to a greater frequency of new infections than previously. Oral ulcerative disease, such as that of all the stages of syphilis, will increase the HIV load in the mouth, and hence the potential for HIV transmission via oral sex.⁴⁴ In addition, this increased risk of HIV transmission will be further worsened by ulcerative disease secondary to the use of the recreational drugs, crack cocaine⁴⁵ and cocaine powder. Finally the oral ulcerative disease of syphilis is likely to increase the nonsexual spread of human herpes virus 8 (HHV-8).

HOW DOES HIV AFFECT THE MOUTH?

In the early years of the HIV epidemic, dentists were often the first health professionals to notice signs of a weak immune system. These signs were infections that are normally controlled by a healthy person. When people get tested for HIV infection and get treatment, most of these infections never show up. However, many people do not get tested for HIV. They may be infected and now know it. Regular dental care is an important way they may learn they have a weak immune system.

According to the US Health Resources and Services Administration, over one third of people with HIV will have at least one major oral health problem, and almost two thirds do not receive regular dental care.

DON’T IGNORE MOUTH PROBLEMS!

Pain or bleeding in your mouth can be a sign of infection. It can keep you from eating normally. Severe pain makes some people skip taking their medications. Serious infections in your mouth can cause other health problems. Be sure to see a dentist or let your health care provider know if you have trouble swallowing, changes in how food tastes, or pain or other problems with your mouth or teeth.

Some dentists or their office staffers do not want to treat patients with HIV. This goes against community standards and violates the Americans with Disabilities Act. Dental health care workers know how to protect themselves from diseases carried in the blood of their patients, including HIV.

WHAT ARE THE SIGNS OF HIV IN THE MOUTH?

Several problems with the teeth, mouth and gums can show up in people with HIV. These are discussed below.

• Dry Mouth and Tooth Decay

• Candidiasis (thrush)

• Canker sores (apthous ulcers)

• Cold sores (herpes simplex)

• Gum disease (periodontitis)

• Hairy leukoplakia

• Kaposi’s Sarcoma

• Enlarged saliva glands

• Shingles (herpes zoster)

• Oral warts (human papillomavirus):

Dry Mouth and Tooth Decay
Many people with HIV have dry mouth. They don’t make enough saliva to chew and swallow comfortably. Saliva protects teeth and gums from infection and decay.

HIV infection can cause dry mouth. So can some medications, as well as coffee, carbonated beverages, alcohol, and smoking. If you have dry mouth, take frequent drinks of water. You can talk to your health care provider about using sugar-free gum or candy, or a saliva substitute.

Candidiasis (thrush) This infection is caused by a fungus (yeast) called Candida. It shows up as red patches on the tongue or roof of the mouth or white lumps that look like cottage cheese that can form anywhere in the mouth. Candidiasis infection can move into the throat. It can also cause painful cracks at the corners of the mouth called angular chelitis. Many anti-fungal treatments can treat thrush. However, some cases of thrush are resistant to the usual medications.

Canker sores (apthous ulcers) are small, round sores on the inside the cheek, under the tongue, or in the back of the throat. They usually have a red edge and a gray center. The sores can be quite painful. They can be caused by stress or by certain foods such as eating too many tomatoes. Hot and spicy or acidic foods or juices make them hurt more. Some ointments, creams or rinses can help.

Cold sores are caused by herpes simplex a common infection. In people with HIV, cold sores can be more severe and can keep coming back. The most common treatment is the antiviral drug acyclovir.

Gum Disease (periodontitis or gingivitis) is swelling of the gums. Sometimes painful and bloody, it can progress from gum loss to loosening and even loss of teeth. This can happen as quickly as 18 months. Dry mouth and smoking can make gum disease worse. Brush your teeth, floss, and see a dentist regularly.

Recently, gum disease has been linked to higher levels of inflammation, throughout the body. This can increase the risk of heart disease and stroke.

Hairy Leukoplakia is an irritation that usually shows up as painless, fuzzy white patches on the side of the tongue. It can be an early sign of HIV infection.

Kaposi’s Sarcoma (KS), usually shows up as dark purple or red spots on the gums, the roof of the mouth, and the back of the tongue. It is rarely seen when people are tested early and start using antiretroviral therapy for HIV infection. It can be the first sign of HIV infection in people who have not been tested for HIV. The best treatment for oral KS in someone with HIV is effective antiretroviral therapy.

Oral Warts – Human Papillomavirus, HPV is a sexually transmitted disease. Some strains of HPV cause warts or cancer. HPV warts can show up in the mouth. The warts can be frozen or cut out.

THE BOTTOM LINE

Signs of HIV infection often show up in the mouth. You might know people who haven’t been tested for HIV. Encourage them to pay attention to any mouth problems.

Keep your mouth healthy by brushing your teeth and flossing. Get your teeth cleaned regularly by a dental health professional. See a health or dental care provider about any serious issues.

The following may be warning signs of infection with HIV:

• Rapid weight loss

• Dry cough

• Recurring fever or profuse night sweats

• Profound and unexplained fatigue

• Swollen lymph glands in the armpits, groin or neck

• Diarrhea that lasts for more than a week

• White spots or unusual blemishes on the tongue, in the mouth or in the throat

• Pneumonia

• Red, brown, pink or purplish blotches on or under the skin or inside the mouth, nose or eyelids

• Memory loss, depression and other neurological disorders

 

Fungal Infections

Candidiasis(Thrush)

 

 

Thrush is a common problem for infants since their immune systems are not yet fully developed. In healthy adults, however, thrush infections happen only rarely, and usually are an indication of a lowered immune response.  Often it is due to illnesses other than AIDS such as general viral infections or stress related fatigue.  It is characterized by creamy white, soft plaques that are easily scraped off the mucosa (the lining of the mouth) revealing a red, inflamed patch underneath.  This type is seen in the picture to the right.  It is easily treated with topical antibiotics like Nystatin.

The image above, top left shows pharyngeal candidiasis.  The pharynx is the throat, and pharyngeal candidiasis is an indication of the severe immune system depression characteristic of AIDS.  This form of yeast infection was considered pathognomonic of AIDS until it was realized that persons who use inhaled steroid medications for the treatment of asthma are also prone to this sort of infection.  (Once again, the presence of pathognomonic signs of a disease, –which means observable things that are frequently associated with a particular disease– do not necessarily mean that the patient has that disease, but a blood test is strongly recommended in such cases.)   Oral and pharyngeal candidiasis are not contagious.

Angular Cheilitis

Angular cheilitis is a very common condition.  It is a fungal infection of the corners of the lips.  It can plague healthy people who tend to have moist lips, especially in the cold winter months.  This condition is caused by a persistent fungal infection, and left untreated, tends to remain active for many months.  It generally looks like a reddened,  dry area at the corners of the l ips.  The severe, white, ulcerated variety shown to the left is more indicative of the type seen in AIDS.  Even a severe case like this, by itself, does not indicate that the patient has AIDS.  It is easily treated with Nystatin cream which is simply an antibiotic that kills the fungus.  Angular cheilitis is not contagious.  click the image on the left to see more images of angular cheilitis.

Viral associated signs of HIV

Hairy Leukoplakia

Hairy leukoplakia is one of the most common HIV associated oral signs.  It is a white, corrugated or “hairy” “coating” on the lateral borders of the tongue.  Unlike thrush, it is not easily scraped off.  It is painless, but patients occasionally complain of its appearance and texture.  It is caused by the body’s reaction to the Epstein-Barr virus (responsible for Mononucleosis), and can be eliminated with a viral antibiotic like acyclovir (Zovirax®), famciclovir (Famvir®) or valacyclovir (Valtrex®).  This condition is rarely seen in patients not infected with  HIV.  However, some healthy patients may develop a “callous”  on the lateral borders of the tongue due to the nervous habit of continually scraping the tongue over the teeth.  This can lead to embarrassment if the dentist suggests an AIDS test to a person who believes such a suggestion is an insult!  It is never meant as a value judgment.  Hairy Leukoplakia is not contagious.  click the image to see a larger version of this image and more information on hairy leukoplakia.   

Herpes Zoster (Shingles)

Herpes Zoster (better known as shingles) is caused by the same virus that causes Chicken Pox.    Herpes zoster “hides out” in a somatic nerve branch after the initial Chicken Pox infection (which usually happens in childhood), and flares up again later in life when the immune system begins to fail.  Shingles is common in otherwise healthy elderly persons.  It generally does not occur in younger people unless they are concurrently infected with the AIDS virus.  The distribution of the rash on the body is the key to the diagnosis of shingles, and distinguishes the herpes zoster virus from other forms of herpes viruses.  The distribution of the rash caused by herpes zoster in shingles is almost always on one side of the body, and is confined to the distribution of a single nerve root.  The skin surface distribution of each spinal or cranial nerve is called a dermatome.  The image on the left shows a rash which is confined to the dermatome defined by the third branch of the trigeminal nerve.  It is outlined in blue to make it easier to see.  Click the image to see larger images, as well as a great deal more on the concept of somatic dermatomes.  Shingles infections are quite painful, and they generally go away after four or five weeks, but shingles may reoccur again at a later date.  It frequently leaves those so afflicted with “postherpetic neuralgia” (PHN),  which is severely sensitive skin, well after the infection.  

Persons infected with HIV are prone to this disease if they have previously been infected with Chicken Pox.  For people with AIDS, this condition can be severe and even life threatening.  In the mouth, it is identified by its distribution. It is limited to one side of the affected organ.  The image to the right shows the Herpes zoster virus infecting half of the upper posterior palate.  It is easy to confuse Herpes zoster with Herpes simplex which may occur in the same distribution purely by chance.  While the Herpes simplex virus is contagious, Shingles, surprisingly is not.  Since a large percentage of the population already has been exposed to Chicken pox, most people harbor an immunity to Herpes zoster, and the probability that anyone will develop this disease depends more on the state of their immune system than on recent exposure to the virus.

Herpes Simplex (the “cold sore” or “fever blister” virus)

 

Herpes Simplex (type I) is the virus that causes  cold sores iormal, healthy adults.  The image at the right shows a typical cold sore, sometimes called a fever blister due to its propensity to appear when the patient has a cold or other febrile (fever causing) illness.  This is another bug that, like Shingles, tends to “hang out” in a nerve root for  the life of the patient after the initial infection, which often occurs in childhood.  Once infected, the patient remains infected for life.  However the  virus remains dormant inside the nerve root most of the time until the patient suffers an illness or other problem which lowers his immune response.  The virus takes advantage of the drop in immune response to flare up in the typical cold sore seen in this image.  Click the image above for more on Herpes simplex.

Whenever an adult appears in a clinic with a case of Primary Herpes Stomatitis, this infers a severely depressed immune response, and the dentist might consider referring the patient to a physician for diagnosis of an underlying disorder.  Adults presenting with severe herpes stomatitis should consider being tested for HIV.  It must be remembered, however, that a primary herpes stomatitis can happen at any time of life if the patient has never before had a cold sore.  Click on the image to see larger views of this condition.

Patients with AIDS have immune systems much more depressed thaormal people with a cold or the flu.  AIDS victims may get not only recurrent cold sores, but recurrent (repeating) cases of full blown Herpes Stomatitis as well.  Whenever an adult appears in a clinic with a case of Primary Herpes Stomatitis, this infers a severely depressed immune response, and the treating physician or dentist may suspect an undiagnosed HIV infection underlying the Herpes infection. New antibiotics like acyclovir (Zovirax®), famciclovir (Famvir®) or valacyclovir (Valtrex®) are effective in suppressing the Herpes. 

Herpes simplex blisters can sometimes occur in the oral cavity on tissues not generally associated with cold sores.  They always happen on tissue that is firmly bound down to underlying bone, such as the gums immediately around the teeth or on the roof of the mouth.  As you can see, the appearance of this infection in the mouth can easily be confused with Herpes Zoster (shingles), especially if it occurs on only one side of the mouth.  The viruses are closely related, and the blisters in the oral cavity can look identical.

The presence of this type of infection in the mouth does not indicate the presence of HIV, although this infection is more common in AIDS patients than in the non-HIV population.  This can happen to anyone who harbors the Herpes Simplex virus.  Left alone, provided the patient is not immunologically compromised, it disappears in 10 to 14 days and may be treated with acyclovir (Zovirax®), famciclovir (Famvir®) or valacyclovir (Valtrex®) for quicker recovery.  The herpes simplex virus is very contagious and if one person in a family develops a cold sore, then others in the family may develop one as well. 

 

Periodontitis: classification, clinic, prophylaxis, surgical methods of treatment. Odontogenic granuloma of the face: clinic, treatment. Odontogenic periostitis o jaw (acute, chronic): clinic, diagnostics, treatment, complications, physiotherapy.

Introduction

 In the past decade the field of endodontics has seeumerous advances, the scope of which have reached all facets of endodontic treatment in both conventional and surgical aspects. These technological advances have introduced new instruments and materials that did not exist before and revolutionized the way endodontic treatment is performed. This change could not be more evident than in the field of surgical endodontics, where both theoretical and practical aspects have completely transformed. The purpose of this chapter is to present to the surgical-minded general dentist the current standards and techniques in performing apical surgery with evidence-based rationales.

Problems with Traditional Endodontic Surgery

Traditional apical surgery is viewed as an invasive, difficult, and less successful procedure than conventional endodontic treatment. Many reasons contribute to this, examples of which include working on a conscious patient in an area with restricted access, limitations in visibility, and operating on minuscule microstructures that are often obscured by bleeding. To manage these challenges, operators had to prepare large osteotomies to gain sufficient access that would accommodate the large surgical instruments that were traditionally utilized. This unnecessary removal of healthy buccal bone structure sometimes resulted in incomplete healing. The root apex was routinely resected with a 45-degree bevel angle with no biological or clinical imperative. Such a practice was performed merely to allow visualization of root canal anatomy and to facilitate retropreparation and retrofilling. This steep-bevel angle root resection created more problems than solutions. It exposed more dentinal tubules, which translated into an increase in apical leakage. In addition, this method sacrificed more periodontal support of the buccal root surface, shortening the distance between the base of the gingival sulcus and the osteotomy site. This further predisposed the tooth for an endodontic-periodontal communication. This resection technique also frequently resulted in an incomplete root resection in which the root apex was merely beveled rather than excised and in which the lingual aspect of the root was never resected. Surgeons thus neglected to eliminate apical ramifications and lateral canals and failed to identify more lingually situated additional canals. Finally, it produced a distorted and elongated view of the internal root canal anatomy that makes it harder to clearly and accurately identify and treat the apical anatomy. Figure 6.1 illustrates most of the common problems associated with conventional apical surgery and how microsurgical techniques can address and correct these deficiencies.

Comparison of Traditional Surgery to Microsurgery

Introduction of the surgical operating microscope and ultrasonics paved the way in changing how endodontic surgery is performed. The microscope provides illumination and magnification of the surgical site where it is most needed. The ultrasonic tips allow a coaxial preparation of the root canal system to a depth of 3 mm that provides an optimum apical seal. These two advances led to the miniaturization of surgical instruments. The net result of all the previously mentioned developments revolutionalized the traditional technique into a more precise method—an apical surgery with minimal healthy bone removal and a conservative shallow-bevel angle root resection. This transformation allows periradicular surgery to be performed on a solid biological and clinical basis.

The Need for Endodontic Surgery

The success rate of endodontic treatment varies and has been reported to be as high as 94.8 percent or as low as 53 percent. This variability stems from many factors, such as the type of study, sample size, pulpal and periapical status, followup period, and number of treatment visits. Conventional retreatment has a lower success rate that ranges between 48 percent and 84 percent. One important fact remains—a certain percentage of failures will be encountered even when the root canal treatment has been carried out to the highest quality. The following etiological factors explain why some conventional endodontic treatments fail and eventually necessitate surgical intervention.

ANATOMICAL FACTORS Careful examination of the root canal system reveals enormous complexities such as accessory canals, C-shaped canals, fins, and isthmuses. These microstructures are more abundant in the apical onethird of the root 5, 6 and are farthest away from the operator’s control. By providing a safe haven for bacteria from biomechanical instrumentation, these anatomical complexities can impair the treatment outcome in cases in which the pulp space is infected. This contributes to the lower success rate of endodontic treatment in infected cases.       

Surgical Technique

ANESTHESIA AND HEMOSTASIS The ability to achieve profound anesthesia and hemostasis in the surgical site is crucial in microsurgery. Profound anesthesia will eliminate patient discomfort and anxiety during, and for a significant time following, the procedure. Excellent hemostasis will improve visibility of the surgical site, allow microscopic inspection of the resected root surface, and minimize the surgery time. Hemostatic control can be divided into preoperative, intraoperative, and postoperative phases. These phases are interrelated and dependent on each other.

Preoperative Phase

An anesthetic solution containing a vasoconstrictor is indicated to achieve anesthesia and hemostasis. While 2 percent lidocaine with 1:100,000 concentrations of epinephrine is recognized as an excellent anesthetic agent, clinical evidence suggests that 1:50,000 concentration offers better hemostasis. The amount of the anesthetic solution containing 1:50,000 epinephrine that is necessary to achieve anesthesia and hemostasis is dependent on the size of the surgical site; however, 2.0 to 4.0 ml is usually sufficient. This amount of local anesthetic should be slowly infiltrated using multiple injections. Solution should be deposited throughout the entire submucosa superficial to the periosteum at the level of the root apices in the surgical site. It is worth mentioning that there is a narrow margin of error in delivering local infiltration. Skeletal muscles respond to epinephrine with vasodilation instead of vasoconstriction as they contain blood vessels that are mostly innervated with _-2 adrenergic receptors. Thus, great care should be taken to avoid infiltrating into deeper skeletal tissue beyond the root apices and over basal bone instead of alveolar bone. In the maxilla, anesthesia and hemostasis are usually accomplished simultaneously by local infiltration in the mucobuccal fold over the apices of the tooth in question and two adjacent teeth both mesial and distal to that tooth (5 teeth total). This should be supplemented with a nerve block near the incisive foramen to block the nasopalatine nerve for surgery on maxillary anterior teeth, or near the greater palatine foramen to block the greater palatine nerve for surgery on the maxillary posterior teeth (see Figure).  

  

In the mandible, anesthesia and hemostasis are usually achieved separately. Anesthesia is established by a regional nerve block of the inferior alveolar nerve, using 1.5 cartridges of 2 percent lidocaine with 1:100,000 epinephrine. Hemostasis is established with two cartridges of 2 percent lidocaine with 1:50,000 epinephrine at the surgical site via multiple supraperiosteal injections into the mucobuccal fold. An additional supplement of 0.5 cartridge is also injected into the lingual aspect of the tooth. The rate of injection will relate to the degree of hemostasis and anesthesia obtained. A rate of 1–2 ml/min is recommended. Injecting at a faster rate results in localized pooling of the solution, delayed and limited diffusion, and less than optimal anesthesia and hemostasis. It is essential to allow the deposited solution sufficient time to diffuse and reach the targeted area to produce the desired effects before any incision is made. The recommended wait time is usually 10–15 minutes, until the soft tissue throughout the surgical site has blanched.

 Intraoperative Phase

 The most important measure in achieving hemostasis is effective local vasoconstriction. Following osteotomy, curettage, and root resection, hemostasis needs to be established again as newly ruptured blood vessels emerse the bone crypt and the buccal plate with blood. The use of a topical hemostatic agent is frequently needed at this point of surgery to control bleeding. Such an agent maintains a dry surgical field that will allow microscopic inspection of the resected root surface, adequate visibility during ultrasonic retropreparation, and good isolation during retrofilling material placement. Many topical hemostatic agents are available. The two most widely used by endodontists are epinephrine cotton pellets and ferric sulfate solution. The following is a presentation of the properties of these two chemical agents and their mechanisms of action.

Epinephrine pellets.

Racellets are cotton pellets containing racemic epinephrine HCl (Pascal Company, Inc., Bellvue, WA). The amount of epinephrine in each varies depending on the number on the label. Racellet #3 pellet contains an average of 0.55 mg of racemic epinephrine and is usually recommended for apical surgery. The racellet pellets are inexpensive and highly effective in achieving hemostasis in the bone crypt via the vasoconstriction effects of epinephrine coupled with the pressure applied on these pellets. It has been shown that one to seven pellets of Racellets #3 can be applied directly to the bone crypt and left for two to four minutes with no evident cardiovascular changes.

Ferric sulfate.

This is another chemical hemostatic agent that has been used for a long time in restorative dentistry. Its mechanism of action is not completely clear, but it is believed to be due to agglutination of blood proteins when in contact with this very acidic solution (pH 0.21). The agglutinated proteins form plugs that occlude the capillary orifices to achieve hemostasis. Ferric sulfate is commercially available in different solutions with different concentrations. The recommended solution for endodontic surgery is Cutrol, which contains 50 percent ferric sulfate. Cutrol is an excellent surface hemostatic agent on the buccal plate of bone and inside the bone crypt. It should be applied directly to the bleeding point with a microapplicator tip or a cotton pellet. Upon contact with blood, this yellowish solution immediately turns dark brown. This color change is helpful in identifying any remaining bleeders that need to be addressed in the same manner. Ferric sulfate is a very effective hemostatic agent that works instantly, but it is also cytotoxic and causes tissue necrosis. For this reason, it should not come in contact with the flap tissue. The use of this agent should be limited as an adjunct to other hemostatic measures. For example, if bleeding persists after using the epinephrine cotton pellet technique. When used correctly as described in the previous paragraph, systemic absorption is unlikely since the coagulum stops the solution from reaching the blood stream. Ferric sulfate also has been proved to damage bone and delay healing when used in large amounts and left in situ after surgery (Lemon 1993). It should therefore only be used in small amounts and should be immediately and gently irrigated with saline after application. If the coagulum is thoroughly removed and irrigated before closure, there is no adverse reaction. The following steps outline the most effective method to achieve local hemostasis quickly during apical surgery: 1. Complete all the cutting necessary (osteotomy and root resection) and then thoroughly remove all granulation tissue from the bone crypt. 2. Place a small Racellet #3 cotton pellet in the bone crypt and firmly pack it against the lingual wall. 3. In quick succession, additional Racellet pellets are packed in against the first pellet, until the entire crypt is filled with pellets. Depending on the size of the crypt, this can take a variable number of pellets. A study by Vickers26 has shown that up to seven Racellets #3 pellets can be safely used to fill the crypt. If more are needed due to the large size of the crypt, then some sterile cotton pellets should be added until the crypt is completely filled. 4. Pressure is applied on these pellets with a blunt instrument (for example, back of a micromirror handle) for 2–4 minutes until no further bleeding is observed (see Fig 6.39C). 5. All pellets are removed one by one, except the last epinephrine pellet, which is left inside the crypt to avoid reopening of the ruptured vessels. This pellet should only be removed at the end of the surgical procedure before final irrigation and flap closure. 6. If small bleeders are still present on the buccal plate or inside the crypt, then Cutrol should be applied directly to the bleeding areas. Without disrupting the coagulum, the solution is quickly rinsed with saline to remove any excess. The coagulum formed should be left intact during the surgical procedure but must be thoroughly curetted and the corresponding area rinsed before closure.

Postoperative Phase

Periradicular surgery should be performed within a reasonable amount of time so that complicated and hemostasis-dependent steps are completed before reactive hyperemia occurs. As restricted blood flow returns to normal, it rapidly increases to a rate well beyond normal to compensate for localized tissue hypoxia and acidosis. Reactive hyperemia is clinically variable and unpredictable. It can be prevented or reduced by compressing the flap tissue for three minutes and applying firm finger pressure with saline-soaked gauze pads placed over the surgical site. This is done to induce hemostasis, prevent hematoma formation, and enhance good tissue reapproximation.28 Flap compressions should be followed immediately with postsurgical cold compressions to the cheek.

FLAP DESIGNS

 The semilunar flap used to be the flap of choice for apical surgery (see Figure).   

It is not advocated today for a number of reasons. The semilunar flap provides a restricted surgical access and has limited potential for further extension if deemed necessary. It also carries the danger of postsurgical defects by incising through tissues that are not supported by underlying bone.29 Furthermore, this type of incision results in maximum severage of periosteal blood vessels. This compromises the blood supply, which could lead to shrinkage, gapping, and secondary healing. Another disadvantage to the semilunar flap is the close proximity of the incision to the osteotomy site, which makes hemostatic control more challenging. The following are flap designs recommended for periradicular surgery.

Full Mucoperiosteal Tissue Flap

There are strong biological reasons to use this kind of flap whenever possible.18, 30 It maintains intact vertical blood supply and minimizes hemorrhage while providing adequate access. It allows a survey of bone and root structures, which facilitates excellent surgical orientation. However, since this flap involves the gingival papilla and exposes the crestal bone, it can carry a few potential risks including loss of tissue attachment, loss of crestal bone height, and possible loss of interdental papilla integrity. The two recommended designs of full mucoperiosteal tissue flaps for periradicular surgery are the triangular and rectangular (trapezoidal) designs. The triangular flap design is the most widely used flap design in periradicular surgery, and it is indicated in the anterior and posterior regions of both the mandible and the maxilla. It requires a horizontal intrasulcular incision and a single vertical releasing incision (see Figure).  

The horizontal incision is made with the scalpel held near a vertical position, extending through the gingival sulcus and the gingival fibers down to the level of the crestal bone. When passing through the interdental region, care should be taken to ensure that the incision is separating the buccal and lingual papillae in the midcol area. A microblade will ease this separation if the embra sure space is narrow (for example, mandibular anterior area). A clean incision located exactly midcol is vital to prevent sloughing of the papillae due to a compromised blood supply and to prevent the unaesthetic look of double papillae. The vertical releasing incision is prepared between the root eminences parallel to the long access of the roots. In anterior surgery, the vertical incision is prepared in the flap perimeter closest to the surgeon. In posterior surgery, it always constitutes the mesial perimeter of the flap. It is important to keep the base of the flap as wide as the top so that the vertical incision is kept parallel to the vertically positioned supraperiosteal microvasculature and tissue-supportive collagen fibers. In this manner, the least number of vessels and fibers are severed, which will translate into faster healing without scarring (see Figure).  

Vertical incisions should terminate at the mesial or distal line angles of teeth and never in the papillae or the midroot area. It also should meet the tooth at the free gingival margin with a 90-degree angle (see Figures).  

The advantages of the triangular flap design are simplicity, rapid wound healing, ease of flap reapproximation, and ease of suturing. A disadvantage, on the other hand, is the limited surgical access. In situations where more access is warranted, either the horizontal or the vertical incisions can be extended to allow some additional mobilization of the flap. Alternatively, a rectangular flap design should be considered if maximum access is required. The rectangular flap design is very similar to the triangular design except for the addition of a second vertical releasing incision (see Figure).    

The rectangular flap design is indicated for anterior surgery when more access is needed. It is also used when multiple teeth will be operated on or when the roots are long (for example, cuspid). Potential disadvantages associated with this flap design include technique sensitive wound closure and a higher chance for flap dislodgment.   

Limited Mucoperiosteal Tissue Flap (Scalloped Flap)

This limited tissue flap does not include the marginal and interdental gingival within its perimeter. It is indicated in teeth with existing fixed restorations and in cases where aesthetics are a major concern. The limited tissue flap can be used in both the maxillary anterior or posterior regions but only when sufficient width of attached gingiva is available. It is usually contraindicated in the mandible since the attached gingiva is narrow in that region and aesthetics are not a major concern. An absolute minimum of 2 mm of attached gingiva from the depth of the gingival sulcus must be present before this flap design is selected32. This submarginal flap design is formed by a scalloped horizontal incision and one or two vertical releasing incisions depending on the surgical access needed. The scalloped incision reflects the contours of the marginal gingiva and provides an adequate distance from the depth of the gingival sulci.18 It also serves as a guide for correctly repositioning the elevated flap for suturing. All the flap corners, either at the scalloping or at the junction of horizontal and vertical incisions, should be rounded to promote smoother healing and minimize scar formation. The angle of the incision in relation to the cortical plate is 45 degrees to allow the widest cut surface as well as better adaptation when the flap is repositioned. This 45-degree bevel at the scalloped horizontal incision is made with the tip of the scalpel pointing away from the gingival sulcus. This adds an additional safety measure to protect the minimum 2 mm of attached gingiva. The submarginal flap has the advantage of leaving the marginal and interdental gingiva intact in addition to leaving the crestal bone unexposed. The major disadvantage is the severance of supraperiosteal vessels, which could leave the unreflected tissue without blood supply. This can be prevented by preserving an adequate width of unreflected gingival tissue, which will derive secondary blood supplies from the PDL and intraosseous blood vessels. The healing of this flap seems to be quite similar to the full mucoperiosteal flap.

ELEVATION AND RETRACTION

 Tissue elevation always starts in the attached gingiva of the vertical incision. This allows the periosteal elevator to apply reflective forces against the cortical bone and not the root surface while elevating the tougher fibrous tissue of the gingiva. Special attention should be directed to ensure that the periosteum is entirely lifted from the cortical plate with the elevated flap. The elevator should then be moved more coronally to elevate the marginal and interdental papilla atraumatically using the undermining elevation technique.18 In this technique, all reflective forces should be applied to the bone and periosteum, with minimal forces on the gingival tissue. Subsequently, the elevation continues in a more apical direction into the submucosa to expose the root tip area and to render the flap more flexible and movable.    

At this point a retractor should be used to provide access to the periradicular tissue. The retractor tip should rest on bone with light but firm pressure and without any trauma to the flap soft tissue. The surgeon must ensure that minimal tension exists at all perimeters of the flap before the osteotomy. If tension exists, then one or both of the releasing incisions should be extended or the reflected tissue should be elevated further. It is important to evaluate the cortical plate bone topography (flat, convex, or concave) to choose the right retractor tip—a shape that will fit the anatomy to maximize stable anchorage. For example, if the cortical bone anatomy is convex such as the area of the canine eminence or the zygoma, then a retractor with a concave or V-shaped tip will best fit this anatomy. An appropriate retractor tip will allow maximum surface contact between the retractor and bone to prevent unintentional retractor slippage and possible flap impingement. For posterior mandibular surgery, the groove technique should be used to provide a stable anchor for the retractor. In this technique, a 15 mm shallow horizontal groove is prepared using the Lindemann bur. This groove is prepared beyond the apex for molar surgery and above the mental foramen for premolar surgery. The use of a plastic cheek retractor underneath the surgical retractor provides better access and visibility to the surgical site while protecting the patient’s lips at the same time. The amount of time that the tissue is retracted is an essential factor in the speed of healing. Although related literature does not give a specific answer, it seems logical to keep this time to a minimum. On the other hand, operators should take sufficient time to solve the clinical goals of the surgical procedure.  By keeping the surgical site well hydrated with sterile saline, there seems to be no specific time limit to the procedure.

OSTEOTOMY

The purpose of the osteotomy in endodontic surgery is to deliberately and precisely prepare a small window through the cortical plate of bone to gain direct visual and instrumental access to the periapical area. The osteotomy should allow identification of the root apex and thorough enucleation of the periapical lesion. The osteotomy size should be as small as possible but as large as necessary. However, a minimum diameter of 4 mm is absolutely essential. This is very important in order to allow a 3-mm root resection and to accommodate free manipulation of microsurgical instruments inside the bone crypt. An ultrasonic tip can be used to verify if the osteotomy is adequate. Ideally, the ultrasonic tip (which is 3 mm long) should fit freely inside the crypt without any contact on bone. When a larger lesion is encountered, the osteotomy might have to be further extended to ensure complete curettage of the lesion. The osteotomy should be accurately prepared over the root apex to prevent any unnecessary overextension. This is an easy task when fenestration through the cortical plate is present. On the other hand, when the buccal cortical plate is intact and the lesion is   limited to the medullary bone space, a careful assessment should precede any osteotomy preparation. An important clinical clue in finding the apex is the estimated root length, which can be measured from a preoperative radiograph or simply be obtained from working length recorded in the patient’s chart. The length measurement is then transformed to the buccal plate using a file or periodontal probe.

 In addition to the length, the radiograph should be carefully examined for root curvature, position of the apex in relation to the cusp tip, and proximity of the apex to the adjacent apices or anatomical structures (mental foramen, mandibular nerve, and maxillary sinus). In most cases, a visual inspection of the buccal bone topography will reveal the root location and direct the surgeon to the root apex. In other cases, osseous palpation using an endodontic explorer is recommended in an attempt to penetrate through the thinned cortical plate into the lesion to confirm the exact location of the apex. If the operator is still unsure about the exact location of the apex, the following procedure can provide better orientation. Using   a surgical #1 round bur, an indentation is prepared on the cortical plate over the estimated location of the apex. The indentation is then filled with a radio-opaque material such as gutta-percha or tin foil. A radiograph is taken with the marker in place to ascertain the location of the apex in relation to the marker. The osteotomy is usually accomplished with a Lindemann bone cutter bur mounted on a surgical high-speed handpiece such as the Impact Air 45. It is used in a brushstroke fashion coupled with copious saline irrigation. The Lindemann bur has fewer flutes than conventional burs, which results in less clogging and more efficient cutting with minimal frictional heat  produced. The Lindemann bur also produces a smoother bone surface with divergent walls and fewer undercuts in comparison to a round bur. The advantage of the Impact Air 45 handpiece is that water is directed along the bur shaft while air is ejected out of the back of the handpiece, thus minimizing the chance of emphysema. During the osteotomy preparation, it is essential to use the microscope at a lower magnification (4_ to 8_) in order to make the distinction between bone and root tip. The root structure can be identified apart from bone by texture (smooth and hard), color (darker yellowish), lack of bleeding upon probing, and the presence of an outline (PDL). When the root tip cannot be distinguished, the osteotomy site is stained with methylene blue dye, which preferentially stains the periodontal ligament (see Figure 6.59) and identifies the root apex.

PERIRADICULAR CURETTAGE

 It is important to emphasize that periradicular curettage alone does not eliminate the origin of the lesion but, rather, temporarily relieves the symptoms. The purpose of the curettage is only to remove the reactive tissue, whether it is a periapical granuloma or cyst. It is usually performed prior to or in conjunction with root-end resection. Curettage is accomplished with bone curettes (#2/4 Molt), with the concave surface of the instrument facing the bony wall first18 (see Figure 6.59). Pressure is applied only against the bony crypt until the tissue is freed along the lateral margins (see Figure 6.60A–E). Then, the bone curette can be rotated around and used in a scraping motion. Once loosened, tissue forceps are used to grasp the tissue and transfer it directly to the biopsy bottle. Periodontal curettes (Columbia 13/14, Jaquette 34/35, and mini- Jaquette) can be used to remove any remaining lesion tissue or tags, especially in the region lingual to the apex.   

APICAL ROOT RESECTION

This is also referred to as apicoectomy. Apical root resection is performed to ensure the removal of aberrant root entities and to allow microscopic inspection of the resected root surface. Similar to the osteotomy, it is usually accomplished with the Lindemann bur in an Impact Air 45 handpiece using copious saline spray and under low range of magnification (4_ to 8_) (see Figure 6.61). The smooth resected root surface produced by the Lindemann bur facilitates and eases microinspection (see Figure 6.62). There are two important factors to con    sider with this procedure: the extent of apical resection and the bevel angle.

Extent of Apical Resection

The amount of root resection depends on the incidence of lateral canals and apical ramifications. Apical resection of 3 mm at a 0-degree bevel has been shown to reduce lateral canals by 93 percent and apical ramifications of lateral canals, deltas, and isthmi by 98 percent. Additional resection does not reduce this percentage significantly. The level of root resection may need to be modified due to the presence of the following factors: • Presence and position of additional roots (for example, a mesiopalatal root of a maxillary molar that is shorter than the mesiobuccal root). • Presence of a lateral canal at the root resection level (see Figure).   

• Presence of a long post and the need to place a root-end filling. • Presence and location of a perforation. • Presence of an apical root fracture. • Amount of remaining buccal crestal bone (a minimum of 2 mm should remain to prevent periodontic-endodontic communication). • Presence of an apical root curvature.

Bevel Angle Apical root resection should be performed perpendicular to the long axis of the root (see Figure 6.66). This 0-degree bevel will ensure equal resection of the root apex on both buccal and lingual aspects.35 In some situations, a 0-degree bevel might not be possible (for example, severe lingual inclination of an anterior tooth, wide roots in a buccolingual dimension). In these cases, the operator should use a small bevel angle (up to 10 degrees). This bevel should be kept to the smallest angle possible, since the real bevel angle is almost always greater than   what it appears to be depending on the angle at which the tooth is proclined in the alveolus. For example, mandibular and maxillary anterior teeth have lingual inclinations. Surgeons might resect the root at what seems to be a 10-degree bevel, but in reality the root is being resected with a bevel of 20 degrees or more. The surgeon should compensate for this distortion of perspective by minimizing the angle of the bevel, keeping it as close to 0 degrees as possible.3, 35 An important advantage of the perpendicular root resection is the minimal exposure of dentinal tubules, which results in a reduction in apical leakage1. In addition, the root canal anatomy is no longer elongated in a buccolingual direction as it is by traditional wide-angled methods, thus facilitating retropreparation and retrofilling procedures.

 Stabilization with Sutures and Suture Removal

 A variety of suture materials are available, each demonstrating advantages and disadvantages. Suture materials are divided into absorbable and nonabsorbable. They can also be monofilament or multifilament. Silk sutures have been used for years. They are easy to handle and inexpensive. Unfortunately, since silk sutures are braided, they exhibit a wicking effect in which they attract fluid and bacteria in as early as 24 hours postoperatively, making them highly inflammatory to the wound. However, with smaller suture sizes (5-0 or 6-0), proper suture placement, use of chlorhexidine rinse, and timely suture removal in 48–72 hours, this problem can be minimized.18 Chromic gut sutures are resorbable. The treatment of this type of suture with chromic acid prolongs its retention in tissues. Nevertheless, they are difficult to handle. The use of synthetic monofilament sutures such as nylon is desirable. They are nonresorbable and available in small sizes and cause minimal tissue reaction. They are the sutures of choice in areas with higher esthetic demand. The only disadvantage is their high cost. Of the many suturing techniques available, the interrupted and sling suturing techniques seem to be the ones most commonly used because they are simple and effective. The interrupted suturing can be used for the vertical releasing incision, while the sling suture technique can be used for the sulcular incision. Suture knots should always be placed away from the incision line to minimize microbial colonization in that area. The minimal number of sutures that provide adequate flap reapproximation should be used. All sutures should be removed in 48–72 hours.

  POSTSURGICAL CARE

Postoperative patient instructions should include the following: 1. Intermittent application of ice pack to the surgical site (30 minutes on, 30 minutes off ) starting immediately after the surgery and continuing for six to eight hours. 2. Strenuous activity, smoking, and alcohol should be avoided. 3. Normal food is permitted with emphasis on the avoidance of hard, sticky, and chewy food. 4. Do not pull the lip or facial tissues. 5. Continue the use of analgesics given presurgically (600 mg ibuprofen every 6 hours as needed). Slight to moderate discomfort is expected for the first 24–48 hours. Narcotic analgesics are provided and used only as an adjunct to ibuprofen if needed. 6. Oozing of blood from the surgical site is normal for the first 24 hours. It can be managed with application of a wet gauze pack to the site, pressed in place with an ice pack. 7. The day following the surgery, chlorhexidine rinses should be used twice a day, continuing for three to four days. Warm salt water rinses can be used every two hours. 8. Brushing of the surgical site is not recommended until the sutures are removed. Cotton swabs can be used to clean the surgical site.

SURGICAL SEQUELAE AND COMPLICATIONS

Oral and written postoperative instructions will minimize the occurrence and severity of surgical sequelae and will reduce patients’ anxiety when and if problems develop. Pain, swelling, and hemorrhage are the most common postsurgical complications. They can be easily managed with NSAIDs, pressure, and ice application. After two to three days, if signs of infection are present (for example, fever, pain, and progressive swelling with pus drainage), antibiotics should be considered. If patients develop a serious facial space infection, they should be immediately referred for emergency medical care and intravenous antibiotics. Rarely, ecchymosis can develop. It is characterized by a discoloration of the facial and oral soft tissue due to the extravasation and subsequent breakdown of blood in the interstitial subcutaneous tissue. Usually it occurs below the surgical site due to gravity. It can also develop in a higher site like the infraorbital area. Paresthesia can develop when surgery is performed near the mental foramen even when the surgical site is far from the nerve. It is usually transient iature and is mainly caused by the inflammatory swelling of the surgical site that impinges on the mandibular nerve. If the nerve has not been severed, normal sensations usually return in few weeks, but it can take up to a few months. On rare occasions paresthesia can be permanent.

 

 

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3.  Roderick Nairn, Matthew Helbert.  Immunology for medical students / / Hardboun. – 2012. –326 p.

4.  Linda Cox.  Allergen Immunotherapy, An Issue of Immunology and Allergy Clinics // Published: May 2011.-  Hardbound, – 312p.

5. Dédée Murrell. Autoimmune Diseases of the Skin, An Issue of Immunology and Allergy Clinics.-  Imprint: Saunders.- Published: May 2012