Osteomielitis of the jaws: etiology, pathogenesis, classification, clinical course, diagnostics, treatment, complications, prophylaxis. Specific inflammatory processes of MFA (actinomycosis, tuberculosis, syfilis): etiology, classification, clinical course, diagnostics, treatment.
Osteomyelitis Jaw
Osteomyelitis is an infection of the bone. It can be caused by a variety of microbial agents (most common in staphylococcus aureus) and situations, including:
- An open injury to the bone, such as an open fracture with the bone ends piercing the skin.
- An infection from elsewhere in the body, such as pneumonia or a urinary tract infection that has spread to the bone through the blood (bacteremia, sepsis).
- A minor trauma, which can lead to a blood clot around the bone and then a secondary infection from seeding of bacteria.
- Bacteria in the bloodstream bacteremia (poor dentition), which is deposited in a focal (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone often forms around the site.
- A chronic open wound or soft tissue infection can eventually extend down to the bone surface, leading to a secondary bone infection.
Osteomyelitis affects about two out of every 10,000 people. If left untreated, the infection can become chronic and cause a loss of blood supply to the affected bone. When this happens, it can lead to the eventual death of the bone tissue.
Osteomyelitis can affect both adults and children. The bacteria or fungus that can cause osteomyelitis, however, differs among age groups. In adults, osteomyelitis often affects the vertebrae and the pelvis. In children, osteomyelitis usually affects the adjacent ends of long bones. Long bones (bones of the limbs) are large, dense bones that provide strength, structure, and mobility. They include the femur and tibia in the legs and the humerus and radius in the arms.
Osteomyelitis does not occur more commonly in a particular race or gender. However, some people are more at risk for developing the disease, including:
- People with diabetes
- Patients receiving hemodialysis
- People with weakened immune systems
- People with sickle cell disease
- Intravenous drug abusers
- The elderly
Symptoms of osteomyelitis
The symptoms of osteomyelitis can include:
- Pain and/or tenderness in the infected area
- Swelling and warmth in the infected area
- Fever
- Nausea, secondarily from being ill with infection
- General discomfort, uneasiness, or ill feeling
- Drainage of pus through the skin
Additional symptoms that may be associated with this disease include:
- Excessive sweating
- Chills
- Lower back pain (if the spine is involved)
- Swelling of the ankles, feet, and legs
- Changes in gait (walking pattern that is a painful, yielding a limp)
Diagnosing osteomyelitis
To diagnose osteomyelitis, the doctor will first perform a history, review of systems, and a complete physical examination. In doing so, the physician will look for signs or symptoms of soft tissue and bone tenderness and possibly swelling and redness. The doctor will also ask you to describe your symptoms and will evaluate your personal and family medical history. The doctor can then order any of the following tests to assist in confirming the diagnosis:
- Blood tests: When testing the blood, measurements are taken to confirm an infection: a CBC (complete blood count), which will show if there is an increased white blood cell count; an ESR (erythrocyte sedimentation rate); and/or CRP (C-reactive protein) in the bloodstream, which detects and measures inflammation in the body.
- Blood culture: A blood culture is a test used to detect bacteria. A sample of blood is taken and then placed into an environment that will support the growth of bacteria. By allowing the bacteria to grow, the infectious agent can then be identified and tested against different antibiotics in hopes of finding the most effective treatment.
- Needle aspiration: During this test, a needle is used to remove a sample of fluid and cells from the vertebral space, or bony area. It is then sent to the lab to be evaluated by allowing the infectious agent to grow on media.
- Biopsy: A biopsy (tissue sample) of the infected bone may be taken and tested for signs of an invading organism.
- Bone scan: During this test, a small amount of Technetium-99 pyrophosphate, a radioactive material, is injected intravenously into the body. If the bone tissue is healthy, the material will spread in a uniform fashion. However, a tumor or infection in the bone will absorb the material and show an increased concentration of the radioactive material, which can be seen with a special camera that produces the images on a computer screen. The scan can help your doctor detect these abnormalities in their early stages, when X-ray findings may only show normal findings.
Treating and managing osteomyelitis
The objective of treating osteomyelitis is to eliminate the infection and prevent the development of chronic infection. Chronic osteomyelitis can lead to permanent deformity, possible fracture, and chronic problems, so it is important to treat the disease as soon as possible.
Drainage: If there is an open wound or abscess, it may be drained through a procedure called needle aspiration. In this procedure, a needle is inserted into the infected area and the fluid is withdrawn. For culturing to identify the bacteria, deep aspiration is preferred over often-unreliable surface swabs. Most pockets of infected fluid collections (pus pocket or abscess) are drained by open surgical procedures.
Medications: Prescribing antibiotics is the first step in treating osteomyelitis. Antibiotics help the body get rid of bacteria in the bloodstream that may otherwise re-infect the bone. The dosage and type of antibiotic prescribed depends on the type of bacteria present and the extent of infection. While antibiotics are often given intravenously, some are also very effective when given in an oral dosage. It is important to first identify the offending organism through blood cultures, aspiration, and biopsy so that the organism is not masked by an initial inappropriate dose of antibiotics. The preference is to first make attempts to do procedures (aspiration or bone biopsy) to identify the organisms prior to starting antibiotics.
Splinting or cast immobilization: This may be necessary to immobilize the affected bone and nearby joints in order to avoid further trauma and to help the area heal adequately and as quickly as possible. Splinting and cast immobilization are frequently done in children, although motion of joints after initial control is important to prevent stiffness and atrophy.
Surgery: Most well-established bone infections are managed through open surgical procedures during which the destroyed bone is scraped out. In the case of spinal abscesses, surgery is not performed unless there is compression of the spinal cord or nerve roots. Instead, patients with spinal osteomyelitis are given intravenous antibiotics. After surgery, antibiotics against the specific bacteria involved in the infection are then intensively administered during the hospital stay and for many weeks afterward.
With proper treatment, the outcome is usually good for osteomyelitis, although results tend to be worse for chronic osteomyelitis, even with surgery. Some cases of chronic osteomyelitis can be so resistant to treatment that amputation may be required; however, this is rare. Also, over many years, chronic infectious draining sites can evolve into a squamous-cell type of skin cancer; this, too, is rare. Any change in the nature of the chronic drainage, or change of the nature of the chronic drainage site, should be evaluated by a physician experienced in treating chronic bone infections. Because it is important that osteomyelitis receives prompt medical attention, people who are at a higher risk of developing osteomyelitis should call their doctors as soon as possible if any symptoms arise.
Osteomyelitis for Jaw Treatment
Osteomyelitis occurs when a bone becomes infected. Though osteomyelitis most often occurs in the bones of the limbs, spine and pelvis, it can also affect the jaw. Osteomyelitis in the jaw is a rare condition that once had been thought incurable, however advances in medicine make the condition treatable. It can present itself in either acute or chronic forms. Osteomyelitis is a serious condition and if proper treatment is not sought, it can destroy your bones.
Symptoms
The symptoms for people with osteomyelitis in the jaw include pain and tenderness, swelling around the jaw, drainage in the sinus cavity, loss of teeth, discharging of pus and necrotic bones. Factors that can lead to osteomyelitis include tobacco, anaemia, viral infections and malnutrition. Since the condition exhibits symptoms that are common in many other diseases, osteomyelitis can be difficult to diagnose at first. If you have chronic osteomyelitis, debilitating fatigue is also very common symptom.
Diagnosis
If your doctor suspects osteomyelitis, he will order various tests before he can make a firm diagnosis. Though a blood test does not define an osteomyelitis diagnosis, a high level of white blood cells will indicate that body is fighting off an infection. If your osteomyelitis is advanced, an X-ray will show the extent of the damage. If you need a better image, your doctor may recommend a CAT scan or MRI. Your doctor may also remove a piece of your bone for a biopsy. This biopsy will check for the strain of bacteria that has infected your bone.
Treatment
Most often infections of the jaw are polymicrobial oral flora so a regimen of antibiotics are used to treat the infection. You doctor may prescribe penicillin, clindamycin and metronidazole. Depending on the extent of the infection, surgery may be required. Your doctor will decide which procedure is best based on the damage caused by the infection. Some bone and tissue may need to be removed, fractures repaired and rotten teeth extracted. You may also want to consult with an oral-maxillofacial surgeon to see if facial reconstruction is required.
Osteomyelitis
Osteomyelitis is a rare complication of tooth-related infections (incidence of
alveolar (tooth) or periodontal (pyorrhoea / gum disease) abscess or from the para-nasal sinuses, by way of continuity through tissue spaces and planes. It occasionally occurs as a complication of jaw fractures or as a result of manipulations during surgical procedures.
Most patients are adult males with infection of the mandible (lower jaw).
Osteomyelitis of the maxilla (upper jaw) is a rare disease of neonates (newly born) or infants after either birth injuries or uncontrolled middle ear infection.
It is classified as acute or chronic osteomyelitis.
Acute Osteomyelitis
In the acute form (which rarely, may also be of hæmatogenous origin [i.e. seeded from the blood stream]), the infection begins in the medullary cavity (bone marrow) of the bone. The resulting increase of intra-bony pressure leads to a decreased blood supply (and hence diminution of white blood cells and other immune
components) and spread of the infection, by way of the Haversian canals of the bone, to the cortical bone (definition) and periosteum (below the periosteum, a thick
fibrous two-layered membrane covering the surface of bones). This aggravates the ischæmia (decreased blood supply), resulting in necrosis (the death of cells or tissues from severe injury or disease, especially in a localised area of the body. Causes of necrosis include inadequate blood supply [as in infarcted tissue], bacterial infection, traumatic injury and hyperthermia) of the bone.
Acute Osteomyelitis of the Jaws — Potential Sources of
Infection
- Peri-apical infection
- A periodontal pocket involved in a fracture
- Acute gingivitis or pericoronitis (even more rarely)
- Penetrating, contaminated injuries (open fractures or
gunshot wounds)
Important Predisposing Conditions for Osteomyelitis
Local Damage to / Disease of the Jaws
- Fractures, including gunshot wounds
- Radiation damage
- Paget’s disease
- Osteopetrosis
Impaired Immune Defences
- Acute leukaemia
- Poorly-controlled diabetes mellitus
- Sickle cell anaemia
- Chronic alcoholism or malnutrition
- AIDS
- Infection from micro-organisms with great virulence.
In such cases, even a peri-apical abscess may be
implicated in osteomyelitis.
Acute Osteomyelitis of the Jaws — Key Features
- Mandible mainly affected, usually in adult males
- Infection of dental origin – anærobes are important
- Pain and swelling of jaw
- Teeth in the area are tender; gingivæ (gums) are red
and swollen - Sometimes paræsthesia of the lip
- Minimal systemic upset
- After about 10 days, X-rays show ‘moth-eaten’
pattern of bone destruction - Good response to prompt antibiotic treatment and
debridement
The mandible (lower jaw), due to decreased vascularity (blood supply & flow), is
involved 6 times more often than the maxilla (upper jaw).
The mandible has a relatively limited blood supply and dense bone with thick bony
(cortical) plates. Infection causes acute inflammation in the medullary (bone
marrow) soft tissues and inflammatory exudate (a fluid with a high content of
protein and cellular debris which has escaped from blood vessels and has been
deposited in tissues or on tissue surfaces, usually as a result of inflammation. It
may be septic or non-septic) spreads infection through the marrow spaces. It also
compresses blood vessels confined in the rigid boundaries of the vascular canals.
Thrombosis (the formation or presence of a thrombus [a clot of coagulated blood
attached at the site of its formation] in a blood vessel) and obstruction then lead to
further bone necrosis.
Dead bone is recognisable microscopically by lacunae (a cavity, space, or
depression, especially in a bone, containing cartilage or bone cells) empty of
osteocytes (a cell characteristic of mature bone tissue. It is derived from
osteoblasts and embedded in the calcified matrix of bone. Osteocytes are found in
small, round cavities called lacunae and have thin, cytoplasmic branches) but filled
with neutrophils (white blood cells) and colonies of bacteria which proliferate in the
dead tissue.
Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced
along the medulla and eventually reaches the sub-periosteal region by resorption
(an organic process in which the substance of some differentiated structure that
has been produced by the body undergoes lysis and assimilation) of bone.
Distension of the periosteum by pus stimulates sub-periosteal bone formation but
perforation of the periosteum by pus and formation of sinuses on the skin or oral
mucosa are rarely seeow.
At the boundaries between infected and healthy tissue, osteoclasts (a specialised
bone cell that absorbs bone) resorb the periphery of the dead bone, which eventually becomes separated as a sequestrum (a fragment of dead bone separated from healthy bone as a result of injury or disease). Once infection starts to localise, new bone forms around it, particularly sub-periosteally.
Where bone has died and been removed, healing is by granulation with formation of
coarse fibrous bone in the proliferating connective tissue. After resolution, fibrous
bone is gradually replaced by compact bone and remodelled to restore normal
bone tissue and structure (and function).
Piercing, deep and constant pain predominates in the clinical presentation in adults,
while low or moderate fever, cellulitis, lymphadenitis, or even trismus may also be
noted.
In the mandible, changes in sensation affecting the lower lip (paræsthesia or
dysæsthesia of the lower lip) may accompany the disease. When the disease
spreads to the peri-osteum (definition) and the surrounding soft tissues, a firm
painful œdema (definition) of the region is observed, while the tooth becomes loose
and there is discharge of pus from the periodontium. Radiographic examination
reveals osteolytic (definition) or radiolucent (definition) regions.
Therapy entails combined surgical (incision, drainage, extraction of the tooth and
removal of sequestrum) and chemo-therapeutic treatment (with antibiotics).
Summary of Treatment of Osteomyelitis
Essential Measures
- Bacterial sampling and culture
- Vigorous (empirical) antibiotic treatment
- Drainage
- Give specific antibiotics based on culture and sensitivities
- Give analgesics
- Debridement
- Remove source of infection, if possible
Adjunctive Treatment
- Sequestrectomy
- Decortication if necessary
- Hyperbaric oxygen*
- Resection and reconstruction for extensive bone destruction
*Mainly of value for osteo-radionecrosis and possibly, anærobic infections.
Anæsthesia of the lower lip usually recovers with elimination of the infection. Rare
complications include pathological fracture caused by extensive bone destruction,
chronic osteomyelitis after inadequate treatment, cellulitis due to spread of
exceptionally virulent bacteria or septicæmia in an immuno-deficient patient.
Chronic Osteomyelitis
Chronic osteomyelitis is characterised by a clinical course lasting over a month. It
may occur after the acute phase or it may be a complication of tooth-related
infection without a preceding acute phase. The clinical presentation is milder, with
painful exacerbations and discharge of pus or sinus tracts.
Osteomyelitis – Inflammation of the Bone
The terms osteomyelitis, periostitis and ostitis are frequently used as synonyms for inflammation of the bone.
Let’s have a quick look at the definition of the terms. Since the bone itself (the calcium structure) cannot get inflamed osteomyelitis (meaning bone marrow inflammation) and periostitis (meaning bone lining inflammation) would be the correct descriptions for an inflammation of the bone. Nevertheless ostitis is becoming more and more the term used.
The cause of an inflammation of the bone can come from outside – (exogenous factors) or from inside (endogenous factors). When both factors occur at the same time then we speak of combined forms. The so called idiopathic factors may also be regarded as a fourth form, consisting of bone inflammations of unidentifiable origin. Exogenous factors include, for example, numerous bacteria, viruses and fungi. They are potential pathogenic agents. If these pathogens find their way into our body they can cause an inflammation. If the inflammation gets into the bone then it’s a bone inflammation.
In the case of endogenous factors the cause lies in our own bodies. For example, in the case of diabetics the raised level of sugar of a diabetic leads to ever-increasing thickening of the walls of the blood vessels and thus an ever-poorer flow of blood.
The flow of blood can get so bad that certain areas of the body are no longer reached by it any more and the affected tissues die due to lack of oxygen and will be destroyed as a consequence of an inflammatory reaction – this can also occur in the bones, as shown in the animation and that would be an example of an endogenous osteomyelitis.
X-ray of Jaw Structure
Idiopathic osteomyelitis means to the patient that, at the end of the day the doctor cannot find an adequate explanation for it.
In the area of the jaw the most common causes of bone inflammation are exogenous or, more accurately, iatrogenous (caused by the doctor). Thus often extractions and/or badly root-treated teeth lead to bone infections.
In the picture you can see an x-ray of an extraction wound (circled in blue), the bone in this area is inflamed (circled in red) – osteomyelitis. In order to diagnose osteomyelitis an x-ray is usually required. In the same picture you can see a tooth (circled in green), which has an inflammation of the bone going on at the tip of the root (circled in red), as can be seen from the dark spot.
An x-ray can provide a lot of information about the bone but if precision is needed then a CT or MRT scan is very useful. This brings us to the diagnosis of osteomyelitis – CT and MRT scans are very reliable diagnostic aids at a certain stage of the osteomyelitis but at a very early stage of the illness their usefulness is rather limited.
Nuclear medical examinations such as skeletal cintography (Tc-99m) are frequently being made use of in order to detect osteomyelitis. The radioactive element technetium will be seen to be concentrated in the areas with raised bone metabolism after being applied intravenously. This increased concentration can be seen from the outside by means of a special camera (the darker spots in the exposure). Unfortunately it is not possible with this method to distinguish between the different causes of the raised bone metabolism.
Is the cause an inflammation or only an innocent build-up of bone after all?
With the addition of special factors (marked anti-granulocyte antibodies for additional investigation) the examination can however be made more specific. Blood tests are likewise not specific and unfortunately the blood values of the inflammation do not always correlate with the values of the osteomyelitis – especially in the jaw area. A bone biopsy is usually the most reliable means of diagnosis, as this way the bone can be viewed very precisely under the microscope (histological examination), and it may be possible to isolate the offending pathogen on the culture glass (bacteriology). If this succeeds then an antibiogram can be carried out in order to find the antibiotic with which to destroy the pathogen.
Bone Scan Scintigraphy
However, biopsy has a couple of disadvantages. The examination is invasive (therefore a wound is unavoidable) and not all areas of bone can be biopsied easily. Sometimes the bacteriological investigations are not successful or it may happen that during the taking of the sample there is contamination of the sample, for example by non-specific bacteria from the mouth.
Finally, let us take a look at the treatment options for osteomyelitis. There are various treatment options available – in the worst case the affected bone must be removed but this is very seldom necessary. The most frequent and simplest treatment option is the prescription of antibiotics, which can be swallowed or applied intravenously. The latter gives a higher concentration of the active ingredient in the blood.
By means of oxygen therapy we enrich the concentration of oxygen in the blood, since within the inflamed bone there is frequently insufficient blood supply and consequently, too little oxygen, ideal conditions for the multiplication of bacteria which do not tolerate oxygen – anaerobic bacteria as they are known. Oxygen-rich blood should have an effect on them, as per the motto: a little blood but very rich.
Another very much talked about treatment is the removal of the sick bone and the filling of the resultant gap with replacement donor bone which has been enriched with an antibiotic. In the animation you can see how the donor bone with the antibiotic (shown in green here) is put in place. The inflamed bone (shown in red here) will be removed and the donor bone will be inserted in the resulting cavity. The antibiotic will then pass continually into the body over months and simultaneously the replacement bone can regenerate.
The advantage of this treatment is that far higher concentrations of medication can be placed specifically in the affected area unlike with the usual means of application (orally or intravenously). Examination over a long period of time is still needed in order to evaluate this treatment over several years.
Ideally you want to avoid it getting to that stage. At least the iatrogenic forms of osteomyelitis can be avoided through sterilisation and cleanliness in the dental clinic.
Osteomyelitis
Odontogenic infection via a root canal, a periodontal pocket or an extraction wound is the most common local cause of osteomyelitis of the jaws. Rarely, a fracture serves as in infection route. Haematogenous spread of an infective agent from another part of the body also occurs. A distinct type of osteomyelitis, osteoradionecrosis, occurs after therapeutic irradiation of oral and neck malignancies.
Figure 20.
An ill-defined periapical and interdental osteolytic lesion in the mandibular anterior region three weeks after onset of clinical symptoms of osteomyelitis.
Figure 21.
Chronic suppurative osteomyelitis with three sequestra (arrows). Osteolytic as well as sclerotic areas are present.
Osteomyelitis is more common in the mandible than in the maxilla. In the mandible, it occurs predominantly in the posterior parts, the ramus included, whereas in the maxilla, it is more frequent in the anterior than in the posterior parts. In the acute phase, osteolysis is not visible radiographically until one or two weeks after the onset of clinical symptoms which are: pain, fever, local lymphadenopathy, increased white blood cell count, and teeth sensitive to percussion. Numbness of the lower lip is another common sign of mandibular osteomyelitis.
The initial radiographic changes are blurring and thinning of the trabeculae and subsequent enlargement of the bone marrow spaces. Without treatment, large volumes of the bone tissue can rapidly become involved, causing loosening of the teeth (Fig. 20).
If acute osteomyelitis becomes chronic, it is frequently possible to distinguish between chronic suppurative osteomyelitis (Fig. 21) and chronic sclerosing osteomyelitis (Fig. 22), both of which have ill-defined borders. In the suppurative form, radiolucent areas alternate with sclerotic, giving the bone a “moth-eaten” appearance. This is further enhanced when sequestra develop. In chronic sclerosing osteomyelitis, radiolucent areas occur, but there is a predominance of radiopaque changes due to the formation of sclerotic bone. The bone is often enlarged through periosteal bone formation (Figs. 22, 23). Over time, the distribution of sclerotic and radiolucent areas varies, indicating disease activity.
Cropped panoramic radiograph of suppurative osteomyelitis at the right mandible. Osteolytic change is observed from around the molar tooth roots to the body of the mandible (arrows).
How to Diagnose Osteomyelitis
Osteomyelitis is an infection of the bone, generally caused by the Staphylococcus Aureus bacteria. This bacteria infects the bones because it travels through the blood from other infected areas. It can also come directly from a wound and travel straight to the bone. A common cause of Osteomyelitis is an open fracture, where not only the bone breaks, but the skin breaks too.
Instructions
1. Perform a physical examination of the patient. Be sure to take a complete medical history and list any medications the patient is already taking. Also ask about any recent problems with the area the patient says is painful.
2. Take a blood sample to perform a blood test to pinpoint if the patient’s white blood cell count is high, which is often a sign of infection. Look for signs of infection in the body, such as areas that are inflamed, red and warm.
3. Send the patient for a bone x-ray. A bone x-ray can show if there is an infection in the bone, but might not be as accurate for someone who has just started complaining of pain. If the bone x-ray does not come back positive, but the patient exhibits signs of Osteomyelitis, send them for a bone scan, which gives you a more detailed view of the bone.
4. Follow up with an MRI, if the bone scan indicates osteomyelitis. MRIs are a valuable test to run. In addition to diagnosing osteomyelitis, the MRI can also help determine how long the infection has been in the bone.
Osteomyelitis may manifest itself in acute, subacute, or chronic forms. Chronic osteomyelitis will result in variable sclerosis and deformity of the affected bone. After the age of 50, the majority of the blood supply to the mandible comes from the overlying periosteum and attached musculature, due to age and atherosclerosis-related involution of the inferior alveolar artery. With an infection of the bone, the subsequent inflammatory response will elevate this overlying periosteum, leading to a loss of the nourishing vasculature, vascular thrombosis, and bone necrosis, resulting occasionally in formation of sequestra. These become areas that are more resistant to systemic antibiotic therapy due to lack of the normal Haversian canals that are blocked by scar tissue, inflammatory exudate, and necrotic bone. At this point, not only systemic antibiotic therapy, but also surgical debridement maybe required to remove the affected bone and prevent disease propagation to adjacent areas. The relative hypoxia seen in infected bone will impair leukocyte bacterial killing, and impede fibroblastic collagen production that is required to support angiogenesis. Thus, it is not surprising that the concomitant use of hyperbaric oxygen therapy maybe beneficial in cases refractory to medical management alone or in patients with a severely compromised immune response. Generally, 20 dives (2.8-3.0 at 100% oxygen for 90 minutes) are administered preoperatively, followed by 20 dives after the debridement of necrotic tissue.
Radiographic imaging may be deceptively unremarkable in acute osteomyelitis, particularly with plain x-rays. Computed tomography (CT) scanning is the standard for evaluating the bone for sequestrum formation. Generally, one sees areas of lytic destruction and overlying periosteal reaction. It is much more common to find cortical plate disruption in the buccal plate than in the lingual plate. Technetium99 bone scanning is often positive within 24 hours of an acute infection. Unfortunately, persistent uptake maybe present for 2 years after eradication of osteomyelitis. Gallium-67 scanning normalizes after successful treatment of mandibular osteomyelitis.
In acute osteomyelitis, or in chronic forms without evidence of formation of sequestra, culture-driven antibiotic therapy is important to allow for disease eradication and decrease the likelihood of formation of antibiotic resistant strains resulting from inadequate subtherapeutic antibiotic therapy. Occasionally, repeated cultures may be required to allow for pathogen isolation, especially in cases of chronic osteomyelitis. Open biopsy of the bone allows for the most accurate culture results. Alpha hemolytic streptococcus, often in conjunction with oral anaerobes, is the most commonly isolated organism noted today. Although acute osteomyelitis is often adequately treated with a culture-driven 6- to 8-week course of antibiotic therapy, chronic osteomyelitis generally requires surgical debridement as well. Antibiotic therapy should be continued for 4 to 6 weeks from the date of last debridement, from resolution of the patient’s symptom complex and/or normalization of the gallium scan (if performed). Refractory osteomyelitis may benefit from the addition of hyperbaric oxygen therapy. Vancomycin or clindamycin are generally effective in the treatment of group A or B streptococci. However, as stated, culture-driven antibiotic therapy is required. With the propagation of multidrug-resistant varieties, treatment with nontraditional antibiotic regimens, such as fluroquinolones, may be required. Attention to optimal management of any underlying systemic immunocompromising conditions, such as diabetes mellitus, steroid usage, and HIV infection is important in all cases.
Clinical features, Radiographic features and treatment of Chronic Osteomyelitis of mandible
Clinical feature:
1. Site: Mandible
2. At early stage:
a. General constitutional symptoms:
• Intermittent fever
• Malaise
• Nausea, vomiting
• Anorexia
b. Pain:
• Deep seated
• Paresthesia of the lower lip
Radiology of Chronic OML• Facial cellulitis
• Trismus
• Swelling
3. Established case of OML:
a. Deep pain
b. Loosening of involved teeth
c. Pain on percussion
d. Sensitivity
e. Purulent discharge of pus
f. Regional lymphadenopathy
g. Trismus
Radiological feature:
1. In early stage, there are no findings
2. The changing begins 4-6 weeks after infection
3. In ate stage of Osteomyelitis, we find sequesterum, involucrum, scattered area, moth eaten appearance in conventional radiograph.
4. For specialized image, we do: CT scan, Radionucleido bone scan, Positron emission tomography.
Treatment:
1. Conventional treatment:
a. Complete bed rest
b. Supportive therapy:
• Nutritional support
• High protein diet
• High calorie and multivitamin diet
c. Rehydration by IV fluid
d. Blood transfusion
e. IV antimicrobial agent
2. Surgical treatment:
a. Incision and drainage b. Extraction of the offending tooth c. Debridement of the affected area by irrigating with H2O2 and normal saline d. Sequestrectomy e. Decortication f. Saucerisation g. Resection
Post operative care:
1. Continuous use of antibiotics
2. Analgesics
3. Adequate hydration
4. Complete bed rest
5. Follow up
Suppurative mandibular osteomyelitis
Suppurative mandibular osteomyelitis refers to agents that invasion of the mandible, the bone tissue as a whole, including the periosteum, cortical bone, bone marrow and the blood vessels, nerves, inflammation, alveolar abscess, periodontitis, and the third molar crown weeks go far odontogenic infection from which the highest incidence of mandibular osteomyelitis.
Disease Overview
When agents that invaded the jaw, will cause the entire jaw organizations, including the periosteum, cortical bone, bone marrow, and one of the blood vessels, nerve inflammation range of leisure, known as purulent maxillary osteomyelitis. Classification of Diseases 1 performance classification, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesions originating in the maxillary central cancellous bone and bone marrow, known as the Central osteomyelitis, lesions originating in the periosteum and cortical bone of the jaw around the , called the edge of osteomyelitis, according to the nature of the lesions can be divided into acute and chronic phase, the scope of the validation can be divided into localized or diffuse suppurative disease cause of mandibular osteomyelitis of up to alveolar abscess, periodontitis, third molar pericoronitis go far odontogenic infection from, followed by invasive infection due to a comminuted fracture or gunshot wound in open injury to bone by the blood circulation of sepsis or sepsis infection. this situation occurred in the maxilla of the infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. put the treatment of oral cancer or nasopharyngeal carcinoma, osteomyelitis common major pathogens Staphylococcus aureus bacteria, followed by Streptococcus, a few other pyogenic bacteria, stereotypes of mixed infections. pathophysiology of mandibular osteomyelitis compared with the previous mandibular osteomyelitis is more common condition than maxillary bone marrow serious, this is because the upper jaw bone dense fascia and strong muscles, present jaw infection, pus is not left around the puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, it is easy to form a large sequestrum. diagnostic tests 1, details incidence and its treatment, consultation, attention to the relationship with the teeth, identify pathogen teeth. 2, with or without empyema sense of volatility, can be used to puncture confirmed suspicious when pus for bacterial culture and antibiotic sensitivity determination. fistula, exploration probes and other instruments with or without sequestrum sequestrum separation, X-ray, chronic identifying bone destruction, with or without sequestrum formation or infection of the low toxicity to the bone cortical hyperplasia. .
Clinical symptoms
Symptoms characteristic of central mandibular osteomyelitis, acute early inflammation is often restricted to the alveolar bone or bone marrow of the mandibular body, and then invasion of mandible, from the center to the edges of cortical bone and periosteum. 2. stage, patients may feel a severe toothache, pain along the trigeminal nerve distribution area for radiation lesions of the gingival mucosa hyperemia and edema, teeth percussion pain and loose, and may have gingival sulcus overflow pus or the formation of alveolar abscess , this stage of the lesion has not been timely drainage, the infection will continue to spread to the medullary cavity, can cause diffuse osteomyelitis or perforation of cortical bone formation in subperiosteal abscess, then patients with systemic poisoning symptoms became worse, and this when patients with serious manifestations of anemia, dehydration, exhaustion, body temperature increased to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling in the affected region of the majority of teeth to loosen, some patients would be a serious concurrent disease, such as sepsis, intracranial infections, such as inflammation has not yet been brought under control, the maxilla infection can cause suppurative maxillary sinusitis and infraorbital cheek, or zygomatic, or pterygopalatine concave, temporal, concave and other regional proliferation. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw weeks, stimulate the open jaw muscles, causing limited mouth opening, can be complicated by the jaw weeks more space infection, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting in jaw nutritional disorders and necrosis, and thus transferred to the chronic phase. 6, transferred from the acute to the chronic phase of about 2 to 3 weeks later, the pain and other systemic symptoms have begun reduced, but the mouth gums can form multiple fistula and pus. sequestrum with healthy bone will be in about a month later, new bone layer, caused by the separation of the sequestrum with healthy bone. this stage without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula osteomyelitis of the mandible can cause large sequestrum formation of pathogenic pathologic fracture, marginal mandibular osteomyelitis clinical features , limitations with young people, the lesions occurred, with chronic symptoms, does not appear large sequestrum. 2, occurred in young people under the jaw, the lesion is more limited spread of the infection pathway is not the first damage to bone marrow, but in the periosteum inflammation or subperiosteal abscess on the basis of the first involving the cortical bone, but also to the deep development involving the bone marrow, but rarely large sequestrum formation of the infections originated in the mandibular third molar crown Zhou Yan, can cause masseter muscle space infection subperiosteal abscess, resulting in the mandible of the ascending branch and corner Nutrition disorders of the cortical bone necrosis, showing chronic symptoms, local mild chronic inflammatory swelling and pitting edema due to masseter muscle and pterygoid muscle involvement, and limited mouth opening. pericoronitis infection if not controlled, often repeatedly made. 5, the edge of mandibular osteomyelitis after repeated anti-inflammatory medication, could easily lead to pathogen resistance, the formation of low toxicity and infection jaw inflammation.
Signs and symptoms
In particular, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesionsoriginating in the maxillary centralBone trabecular and bone marrow, known as the Central osteomyelitis lesions originating in the periosteum and cortical bone of the jaw around, known as the edge of osteomyelitis according to the nature of the lesions can be divided into acute and chronic phase, according to The scope of the validation can be divided into localized or diffuse. central mandibular osteomyelitis: the maxilla than the mandible more common in teeth with severe pain, persistent, and radiating pain along the trigeminal nerve distribution. teeth and adjacent teeth loose, percussion pain, vestibular groove fullness, cheek swelling. mandibular alveolar abscess, the pus is not easy worn develop into acute diffuse osteomyelitis and lack of drainage, the patients with systemic symptoms get worse, fever, chills, leukocyte, dehydration and other toxic manifestations. mandibular osteomyelitis refers to agents that invaded the jaw, causing the entire bone tissue, including periosteum, cortical bone, bone marrow and the blood vessels, nerve inflammation, Chinese medicine called ‘bone slot wind ‘or’ wear gills were sharply acute onset of high fever, increased white blood cells, can shift to the left. body poisoning, and with general malaise, headache, loss of appetite and other symptoms can occur in patients toothache, and the pain along the trigeminal nerve distribution area of radiation, and can quickly spread to the adjacent teeth. the short term, there may be multiple tooth mobility, periodontal pocket pus, inferior alveolar nerve by inflammatory damage to the lower lip numbness due to the spread of inflammation to the surrounding maxillofacial swelling which can occur, such as infection spread to the masticatory muscles can be trismus such as infection control in a timely and quickly to the infraorbital, inferior temporal, the pterygopalatine concave and by the mandibular foramen caused the wing jaw space infection. systemic complications such as sepsis, and intracranial infection may also occur.
Disease etiology
Suppurative osteomyelitis of jaw up to the alveolar abscess, periodontitis, the third molar pericoronitis go far odontogenic infection from, followed by open injury due to comminuted or anger injury caused by bone invasive infection, sepsis or infections, sepsis and blood circulation more than occurred in the maxilla of infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. major pathogens Staphylococcus aureus, followed by Streptococcus few other pyogenic bacteria stereotypes mixed infection.
Pathophysiological
Mandibular osteomyelitis compared with maxillary osteomyelitis more common condition than the maxilla bone marrow serious, this is because the upper jaw bone is dense, and some surrounding fascia and strong muscles, present jaw infection, pus left After puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, easy to form a large sequestrum.
Diagnostic tests
A detailed consultation incidence after treatment, and attention teeth identify pathogen teeth.
2, with or without empyema sense of volatility suspicious can be used for puncture confirmed. 3, pus for bacterial culture and antibiotic sensitivity determination, with or without fistula, probes and other instruments to probe whether the sequestrum sequestrum separation. 5, X-ray, the chronic phase to identify bone destruction, with or without sequestrum formation or infection of the low toxicity of the bone cortex hyperplasia type.
Disease Prevention
No special
Safety Tips
1, the disease mostly occurs in the infant’s maxillary marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase 2, the timely treatment of the crown Zhou Yan, the periapical Yandeng odontogenic infection to prevent occurrence of mandibular osteomyelitis. has formed should be a thorough treatment to avoid to chronic osteomyelitis, in the acute phase.
Treatment programs
Acute systemic antibiotics, local incision and drainage or removal of loose teeth, diffuse patient performance Decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions and enhance systemic resistance to the chronic phase sequestrum curettage and extraction of teeth lesions mainly purulent maxillary bone marrow after a course of inflammation, and generally can be divided into two phases of acute and chronic phase. to The sequestrum began to take shape used to be collectively referred to as the acute phase by the onset, generally about 3 to 4 weeks if the infection fails to be completely controlled in the acute phase, into the chronic phase. must be used in sufficient quantities and effective antimicrobial treatment. use drugs in order to control the infection in the acute phase, use of antibiotics against Staphylococcus aureus and mixed infections, the other based on bacterial culture and susceptibility to choose effective antibiotics. In the initial stages of infection, but also with the physical therapy. When the infection into the suppuration of Early incision and drainage. wait for his condition slightly eased, the mouth opening slightly improved, should try to extraction, so that the pus from the socket to get the drainage, to prevent the spread of infection in the bone of acute suppurative osteomyelitis oncoming acute, severe illness, can cause blood and brain complications, and therefore close observation, as early as the appropriate emergency treatment of acute systemic application of antibiotics, local incision and drainage removal of loose teeth mainly diffuse patient performance decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions, enhanced systemic resistance to the chronic phase to sequester scrape and lesions in tooth extraction based. 1, the disease occurred in the maxilla of infants and young children. marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase. and timely treatment of pericoronitis, periapical go far odontogenic infection, on the prevention of mandibular osteomyelitis. such as formation of osteomyelitis in the acute phase should be a thorough treatment so as not to become chronic. acute phase of infection control, enhance the body resistance-based, anti- infection drugs should be selected according to the sensitivity of pathogenic bacteria. mandibular osteomyelitis more mixed bacterial infection, it is appropriate in order to use broad-spectrum antibiotics. In addition, as has been clear for odontogenic infection, early removal of the lesions teeth in order to facilitate drainage, to avoid more extensive bone destruction. case of subperiosteal abscess or infection jaw week gap, it is timely incision in chronic phase, the lesion has been limited or has been sequestrum formation, while the surgical treatment of the main supplemented by drug treatment. marginal mandibular osteomyelitis are generally large sequestrum formation, mostly for the proliferation of subperiosteal cortical bone, the texture is more loose, and should be completely clear, pus foci of cortical bone surface where infection and the granulation organizers should be scraping, postoperative use of antibiotics to control infection in 7 to 14 days to avoid relapse.
Clinical manifestations
Clinical presentation of osteonecrosis of the jaw. (A) Typical lesion of osteonecrosis of the jaw showing exposed infected bone involving the mylohyoid ridge. (B) Osteonecrotic bone below a dental implant. (C) Spontaneous exfoliated teeth with underlying exposed dead bone. (D) Operative picture showing well-demarcated dead bone involving the whole alveolus. (From Badros A, Weikel D, Salama A, et al. Osteonecrosis of the jaw in multiple myelomoa patients: clinical features and risk factors. J Clin Oncol 2006;24:948; with permission. Copyright © 2006 by American Society of Clinical Oncology.)
Suppurative mandibular osteomyelitis from the clinical course of disease, pathogens, routes of infection and lesions involving the siteCan be manifested as acute and chronic stages, and often divided into two types of central and edge (a central mandibular osteomyelitis is usually odontogenic inflammation spread to the bone marrow, spread to the bone from the jaw center around cortex and periosteum in the bone marrow of early acute inflammation is often restricted to the alveolar bone or the mandibular body, patients feel severe toothache, pain along the trigeminal nerve distribution of radiation lesions of the gingival mucosa hyperemia and edema, teeth that is, obvious pain and loose, and can gingival sulcus septic overflow or the formation of alveolar abscess. acute phase has not been timely drainage, infections continue to spread to the medullary cavity can cause disseminated osteomyelitis or perforation of cortical bone formation in subperiosteal abscess. exacerbate symptoms of systemic poisoning at this time, the body temperature to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling the affected regions the majority of loose teeth. If the inflammation is not brought under control, the maxillary infection can cause purulent maxillary sinusitis and infraorbital, buccal, zygomatic or pterygopalatine concave, temporal concave and other areas to spread. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw week to stimulate the open jaw muscles, causing limitation of mouth opening can be complicated by the infection of the jaw week more than the gap, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting iutritional disorders of the jaw and necrosis, and thus transferred to the chronic phase. turn by the acute phase into the chronic phase of about two to three weeks later, pain and other systemic symptoms began to ease, but the mouth gums can form more than one fistula and pus out about a month later, the sequestrum with healthy bone between the new bone layer, causing the separation of the sequestrum with healthy bone without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula. osteomyelitis of the mandible can cause large piece of dead bone formation, can be pathogenic pathological fractures appear bite (occlusal disorders. Suppurative mandibular osteomyelitis (two marginal mandibular osteomyelitis spread of the infection pathway is not the first damage to bone marrow, but the basis of periostitis or subperiosteal abscess the first involving the cortical bone occurred in adolescents mandible, more limited lesions, infections originated in the mandibular third molar pericoronitis inflammation, caused by the masseter muscle space infection and subperiosteal abscess, resulting in lower jaw of the ascending branch and the corner of cortical bone nutritional barriers necrosis. clinical manifestations of chronic symptoms, the symptoms of the acute phase of infection and jaw week gap coexist but often overlooked in local mild chronic inflammatory swelling and pitting edema due to the chewing muscles and wing muscle involvement and limited mouth opening. lesions confined to the cortical bone, or to the deep development involving the bone marrow, but rarely large sequestrum formation. pericoronitis infections if not controlled, often repeatedly made by anti-inflammatory drugs after treatment, could easily lead to pathogen resistance, the formation of low toxicity and infection, no obvious purulent and sequestrum formation process and significant cortical hyperostosis, sclerosis and periosteal thickening of cortical bone lysis little part the formation of small abscess and granulation tissue. cortical hyperplasia of the mandibular ascending branch of the Ministry of mandibular angle can cause facial asymmetry, X-ray showed obvious subperiosteal hyperostosis.
Specific inflammatory processes of MFA (actinomycosis, tuberculosis, syfilis): etiology, classification, clinical course, diagnostics, treatment.
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: Causes, Symptoms and Treatment
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
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.
Clinical synopsis
A 58-year-old previously healthy man presented to the emergency center with a 12-month history of progressive right-sided facial swelling. The patient reported only mild pain exacerbated by eating and difficulty opening his mouth. He denied fever, chills, or weight loss. He had a 40-pack per year history of smoking tobacco and consumed
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 2) were the most frequent sites of oral involvement.
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.
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.46 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.1 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 theecessary 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 (Figure 3A). The murein layer in Gram-negative bacteria is thinner but it is surrounded by a second, outer lipid bilayer membrane (Figure 3B). The cell wall of mycobacteria, which include the causative agent of tuberculosis, is similar to that of Gram-negative bacteria (Figure
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 [
2. Polymerization of the monomers into linear peptidoglycans.
3. Crosslinking of the polymers into a three-dimensional meshwork.
In mycobacteria the
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.
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.
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
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
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.27-
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
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.31 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.32 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.33 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,
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.
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.
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
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 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 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.
This image is what the initial infection may look like when a child, or young adult is first infected with the Herpes Simplex virus. This is called “Primary Herpes stomatitis“, and as you can see, it can look quite severe with blisters both inside and outside the mouth. (“Stomatitis” means inflammation of the entire mouth.) The patient is quite sick, but this primary infection will disappear after 10-14 days with rest and lots of fluids. In healthy people, this infection happens only once in a lifetime. The presence of the virus only becomes apparent in adulthood whenever a cold sore appears.
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.
For more basic information on the various forms herpes simplex takes, visit HerpesEductaion.Org.
A Note on Genital Herpes
Herpes Simplex type I (HSV-1) tends to infect the face and oral cavity. This virus is the one responsible for traditional cold sores, as well as primary herpes stomatitis. However, there is a second variety of Herpes that prefers to infect the genital areas. Herpes Simplex Type II (HSV-2) is called “genital Herpes” because of its tendency to be transmitted sexually. Both HSV-1 and HSV-2 produce similar lesions. The difference between them is their site specific preferences. Both varieties establish latency (in other words, they take up permanent residence) ierve roots and once established, tend to cause occasional recurrent outbreaks with active lesions (sores) in areas of the body serviced by that particular somatic nerve root. Herpes Simplex type 1 prefers to live in the trigeminal nerve root where it causes lesions in the mouth and on the face. HSV-2 takes up residence in the sacral ganglion, located at the base of the spine, where it may cause genital lesions (see the dermatome chart on the Herpes zoster page).
Even though each type of Herpes virus has site specific preferences, they are genetically similar, and can take up residence ierve roots in other parts of the body, including in each other’s territory. However, outside of their own home territories neither virus is especially virulent, and rarely cause recurrent outbreaks.
HSV-2 (genital herpes) causes approximately 90% of all cases of genital herpes outbreaks. The other 10% is caused buy HSV-1. Genital herpes caused by HSV-1 is generally much milder than that caused by HSV-2. HSV-1, the “cold sore virus”, is usually transferred to the genital area by direct oral/genital contact, but upon occasion can be transferred from a patient’s mouth to their own genitals (or someone else’s) by simple manual transfer. Thus the use of saliva as a lubricant can transfer HSV-1 to the genital area. Most people infected with HSV-
On the other hand, HSV-1 causes almost all cases of oral and facial herpes. Oral herpes caused by HSV-2 is not likely to cause recurrent infections, except in immunocompromised patients.
Human Papillomavirus lesions (warts)
Warts are caused by a virus. In the oral cavity, they tend to be somewhat flatter than the type occurring on hands, but if they are dried with air, the tiny projections characteristic of regular warts become evident. The causative agent is the Human Papillomavirus (HPV). These growths generally are not painful and can be ignored unless they interfere with appearance or function. Persons infected with HIV may develop very large, multiple warts. They may be removed using lasers, cautery or cold steel blades. The presence of oral warts is not in itself an indication of AIDS, although some strains of the virus are associated with squamous cell carcinoma (oral cancer). HPV is contagious. Click on the image for more information on HPV and its association with oral and cervical cancer
Neoplasms (tumors, or “growths“ )
Kaposi’s Sarcoma (KS) (pronounced “cap-o-zeez”)
Kaposi’s Sarcoma is a form of cancer consisting of an overgrowth of tiny blood vessels. It is generally dark red or deep purple. It may be flat, but sometimes presents as a swollen mass. The lesions are rarely painful, unless they become secondarily infected. Thus good oral hygiene is important in the management of these tumors when they occur in the mouth.
Kaposi’s Sarcoma is most frequently seen on the skin. However tumors can occur in the gastrointestinal tract and the oral cavity as well. Lesions in the oral cavity occur mostly on the palate (the roof of the mouth). Kaposi’s is technically a form of cancer, however there is evidence that it is actually the result of a secondary infection with Herpes virus type VIII. An abundance of this virus is found in the saliva of infected individuals. However, the virus causes Kaposi’s Sarcoma only in patients with very compromised immune systems. It is believed that in most
modern cases, Herpes virus type VIII is transferred through deep kissing.
Kaposi’s tumors were once seen exclusively in elderly men with compromised immune systems. Today, however, they are seen more frequently in young men with AIDS. The occurrence of one of these lesions anywhere on the body of a young man is indicative of the presence of HIV. Kaposi’s is rarely seen in women, even women infected with HIV. It is also rarely found in men who have contracted AIDS by way of intravenous drug use. It is not known why women and heterosexual males with AIDS do not generally get Kaposi’s sarcoma, although there is probably an association between the gay lifestyle and the transfer of the herpes type VIII virus. Kaposi’s occurs as the initial manifestation of AIDS in approximately 11% of patients.
Non Hodgkin’s Lymphoma (NHL) is a form of cancer. It starts in a lymph node and then spreads to other areas of the body through the blood vessels and the lymphatic system. Before the era of AIDS, Non Hodgkin’s lymphoma usually affected older individuals (median age 67). Unfortunately, since the beginning of the AIDS epidemic the incidence of NHL has increased substantially in younger persons. Lesions like those in the image to the right, especially when present in a younger person, may be the first indication that a patient has an HIV infection. NHL is usually accompanied by a generalized lymphadenopathy (generalized swelling of the lymph nodes). However, persons with no history of immunosuppression (or HIV) may contract the disease. Click the image for more information on this condition and its relation to HIV.
Bacterial diseases associated with AIDS
Periodontal Disease
In order to understand how periodontal disease (gum disease) affects persons with AIDS, it will be helpful to read my explanation of regular periodontal disease, since the process in HIV infected people is the same (albeit more severe and much more rapidly progressing) as in otherwise healthy people. The treatment for HIV infected persons is also the same as the treatment for otherwise healthy persons with
Periodontal disease, except that irrigation with Betadine (an Iodine solution) and more aggressive antibiotics are used.
In light of the fact that Gum Disease in HIV infected patients is so similar to the variety seen in the normal population, it is unlikely that a dentist would draw a parallel between the presence of this process and the presence of HIV until the condition presented itself like the picture below and to the right.
The image to the right shows a case of necrotizing ulcerative periodontitis. The difference between periodontitis and gingivitis is the degree of bony involvement and the depth of the pocketing. The white, red and bleedy area under the necks of the lower teeth is indicative of necrotizing (in the process of dying) tissue. While the process can be halted by aggressive intervention from a dentist and periodontal health maintained by good oral hygiene, the damage to the gums and bone is permanent. Periodontal disease is caused by poor oral hygiene and is not contagious.
Acute Necrotizing Ulcerative gingivitis (trench Mouth)
A less severe form of this condition found in the non HIV infected population (also seen in early stages of AIDS) is called Acute Necrotizing Ulcerative Gingivitis (ANUG), formerly called “Trench mouth“. In ANUG, only the gingiva immediately surrounding the teeth becomes necrotic. ANUG is often found in people with poor oral hygiene who are either ill or under extreme physical or emotional stress. (It was named “trench mouth” because it was common in soldiers who fought in the trenches during world war I. These men were certainly under extreme physical and emotional stress, and had little opportunity to brush their teeth.)
ANUG, being a bacterial infection, is very easily treated by gentle cleaning of the teeth and irrigation of the affected gums with 3% hydrogen peroxide. The bacteria that take advantage of a patient’s run-down condition tend to be anaerobic which means that they die in the presence of oxygen. Hydrogen peroxide liberates oxygen (hence the bubbles) when it is exposed to blood, and the oxygen acts as an antiseptic and speeds healing of the damaged gum tissue. The patient is sent home with a prescription for Penicillin and instructions on cleaning the teeth to prevent further problems. ANUG is not contagious.
Dentists today rarely see cases of ANUG, however the disease is making a comeback in communities in which there is a lot of drug addiction. It is especially prevalent in populations of methamphetamine addicts and is a part of the syndrome now known as Meth Mouth.
Acute Necrotizing Oral Stomatitis
This condition is never seen except in a hospital setting. If the immune system is severely compromised, the body is unable to fight off bacterial infections that a normal immune system is able to combat easily. Without a functioning immune system, normal environmental bacteria can attack a living body in the same way they would attack a dead body. HIV attacks the immune system, immobilizing it. Without a properly functioning immune system, there is no defense against parasitic bacteria and viruses, and a living body can start to decay.
Other indications of immune deficiency
Geographic tongue–This condition is thought to be an oral form of psoriasis (a common skin condition), and is characterized by the disappearance of the filiform papillae from irregular patches on the top surface of the tongue. These patches then “heal” up and reoccur on another part of the tongue at a later date. One can see lesions in varying stages of healing over large expanses of the tongue. The cause of this condition is unknown. These patients often complain of pain when eating sharp foods. The condition can be treated with topical application of steroid gels or mouth rinses. In general, however, it is not treated. Geographic tongue is not a contagious condition. This condition might be seen more frequently in AIDS patients, however the presence of geographic tongue does NOT mean that the patient has AIDS. It may be more prevalent in persons with HIV because the virus attacks the immune system, and psoriasis is caused by a mal fun ti on of the immune system. Click the image on the right for a larger view.
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