Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Hygiene hypothesis wikipedia , lookup
Special needs dentistry wikipedia , lookup
Dental emergency wikipedia , lookup
Transmission (medicine) wikipedia , lookup
Focal infection theory wikipedia , lookup
Henipavirus wikipedia , lookup
Infection control wikipedia , lookup
Herpes simplex research wikipedia , lookup
Marburg virus disease wikipedia , lookup
Unit 3 Autoimmune Diseases That Affect the Oral Cavity 1. Sjogren’s Syndrome (aka Sicca Syndrome, Gougerat-Sjogren Syndrome) Siccus = Dry The specific etiology is unknown. An autoimmune process in which the patient’s own salivary gland and tear-producing (lacrimal) tissue becomes antigenic (capable of causing antibody production). Two types: a. b. Primary: (Sicca Complex) involves eyes and mouth: keratoconjunctivitis sicca (dry eyes-xerophtalmia), and xerostomia (dry mouth). Secondary: Seen with connective tissue disease such as rheumatoid arthritis, lupus or polymyositis. Chief oral complaint is xerostomia. Recurrent and symmetric parotid gland enlargement is seen in about half of patients. No cure; it is a chronic syndrome requiring long-term symptomatic management by dentist, ophthalmologist, and rheumatologist. A significant consequence is the malignant transformation to lymphoma in about 6-7 % of cases. 2. Lupus Erythematosus: (Langlais) An autoimmune process that may be influenced by genetic or viral factors. 20-40% of patients with LE have oral lesions. Discoid (chronic), which involves only the skin; systemic lupus erythematosus (SLE), in which multiple organ systems are involved; and subacute cutaneous with mild systemic symptoms. The cause is unknown. More common in women, with peak age of 30 for SLE, 40 for DLE. Discoid type is least aggressive form and manifests skin lesions only (predilection for the face). Classic feature of discoid type is facial butterfly pattern of erythema over the nasal bridge. Systemic type may have oral lesions that are white and plaque-like, resembling erosive lichen planus but less symmetrically distributed and more subtle striae. Patients often complain of fever, fatigue, and joint pain. Sunburn can trigger acute reactions. Patients may be taking high doses of systemic steroids so be aware of delayed wound healing and risk of infections. Antibiotic prophylaxis required due to risk of subacute bacterial endocardiditis. 3. Pemphigus: (Langlais) Immunopathologic dermatologic disease that is potentially fatal. Histologically, confused antibodies are produced that react with the cementing materials linking adjacent squamous cells of the skin and oral mucosa. These antibodies are readily detected in the blood of patients with pemphigus. They bind to cementing materials (desmosomes) and lead to the destruction of cell-to-cell linkages. With the loss 1 Unit 3 in intercellular linkages the surface epithelium becomes weakened and the cells separate, leading to blister formation and epithelial desquamation. Rapid development of multiple bullae that tend to rupture and leave erosions of the skin and oral mucous membranes. Extremely painful. When there is systemic involvement, severe debilitation may result in death. Disease may be fatal due to septicemia and dehydration. Mortality rate has decreased with introduction of systemic steroids but patient may die from long-term steroid therapy. Four types: vulgaris, vegetans, foliaceous, and erythematosus. 4. Pemphigus Vulgaris: Oral lesions are always present at some time and in about 60% are the first signs of the disease--cutaneous lesions may follow up to 1 year later.Bullae rupture, are painful. Application of mild lateral pressure on clinically normal mucosa in patients with pemphigus often produces blistering and sloughing of the mucosa, leaving a raw, painful surface = Nikolsky Sign. The Tzanck test is the examination microscopically of intact vesicles for the presence of damaged, separated epithelial cells. Direct immunofluorescence is a sophisticated test to detect the presence of abnormal epithelial antibody in the patient’s tissues. Indirect immunofluorescence detects the Ab in the patient’s serum. 5. Cicatricial Pemphigoid (aka Benign Mucous Membrane Pemphigoid-BMMP, ocular pemphigus, mucosal pemphigoid, pemphigus conjunctivae): cicatrix = a scar left by a healed wound. Relatively rare, chronic, self-limiting, mucocutaneous disease. Resembles bullous pemphigoid but bullae are usually on mucous membranes and in the eyes and also conjunctival, pharyngeal, anal, and vaginal. Female 2x. Skin lesions precede oral lesions. Oral lesions are always present, gingiva is most common site. Gingival lesions range from patchy erythema with mild discomfort to intense generalized erythema and ulceration extending beyond attached gingiva. Patients with cicatricial pemphigoid typically demonstrate Nikolsky’s sign. Antibodies are directed against the constituents found in the basement membrane zone between epithelium and connective tissue. These autoantibodies lead to the destruction of the linkage between these tissues. The lesions are from cleavage of the epithelium from the underlying connective tissue. The gingival lesions have been called desquamative gingivitis (a descriptive term...see lichen planus and pemphigus vulgaris). Treated with systemic steroids. 6. Bullous Pemphigoid: Similar to cicatricial pemphigoid but no sex predilection, oral lesions in only about 1/3, otherwise, only the skin is affected. 7. Behcet’s Syndrome (aka oculo-oral-genital syndrome): (Langlais p. 96) Unknown etiology but may be similar to aphthous ulcers. May also be a genetic predisposition. See antibodies to human mucosa = evidence for autoimmune pathogenesis. Lesions affect oral cavity, eye, and genitalia, a triple-symptom complex.. 2 Unit 3 Oral manifestations appear identical to ulcers of aphthous (minor type). Usually treated with systemic steroids. Infectious Diseases Bacterial Infections: 1. Tuberculosis: Infectious granulomatous disease caused by Mycobacterium tuberculosis. TB is found worldwide but is much less prevalent than it was before antibiotics. Case rate varies regionally and depends on factors that favor spread of communicable diseases (poor living conditions, compromised immunity from debilitating or immunosuppressed conditions). Mantoux test and Tine test are skin tests using a tubercular bacillus antigen (PPD = purified protein derivative) to see if person is hypersensitive to antigen challenge. Clinical signs and symptoms of TB are often remarkably inconspicuous. Malaise (discomfort, uneasiness) and fatigue are often chief early features. May be gradual weight loss with persistent cough. TB is highly infectious through transmission of airborne droplets that carry the organism to pulmonary air spaces; the portal of entry is the respiratory tract. Caseous necrosis (looks like cottage cheese) is unique to tuberculosis. Microscopically langerhans giant cells are present. Oral lesions occur, but they are rare. They may be on any mucosal surface…tongue and palate most likely. Lesions occur as superficial or deep, chronic, non-healing ulcers that are usually painful. Infectious hazard to HCW if barriers not used. 2. Miliary tuberculosis: includes widespread involvement of many organs due to blood stream dissemination of microorganisms. 3. Tuberculous Lymphadenitis or Scrofula: Tuberculous infection of the submandibular and cervical lymph nodes that may progress to the formation of an actual abscess, or it may remain as a typical granulomatous lesion. Swelling of the nodes is obvious clinically. They are tender or painful and often show inflammation of the overlying skin. When an actual abscess exists, it typically perforates and discharges pus. There has been a dramatic increase in number of cases, possibly related to HIV. Treatment continues for many months, up to 2 years. Patients become noninfectious after treatment begins. Consult physician to be sure treatment is ongoing and that the patient is no longer infectious. 4. Actinomycosis: Caused by Actinomyces israelii, an anaerobic, gram-positive bacterium found in a majority of healthy individuals. Follows tooth extraction or trauma. Noncontagious. Lumpy jaw from formation of granulation tissue and abscesses in submandibular region. Lesion may become indurated and eventually form one or more 3 Unit 3 draining sinuses, leading from the medullary spaces of the mandible to the skin of the neck. The pus may contain small yellow granules, known as sulfur granules, that are aggregates of A. israelii organisms. Treated with antibiotics. 5. Syphilis: A venereal disease that has been traced as far back as the time of Christopher Columbus. Caused by spirochete, Treponema pallidum. Acquired by: 1) sexual contact with a partner with active lesions, 2) transfusion of infected blood, or 3) transplacental inoculation from an infected mother. Three stages: a. b. c. d. 6. 7. Primary syphilis results in a painless, indurated ulcer (chancre) with rolled margins. It forms at the site of inoculation and heals in 3-12 weeks. The lesion heals spontaneously and enters a latent period. The chancre is highly infectious. Lymphadenopathy also develops. Secondary syphilis (6 weeks after primary) manifests smooth-surfaced mucous patches and possibly split papules at commissure and maculopapular rash…all highly infectious. It develops in most of the untreated cases. (Miller). Fever, flulike symptoms, mucocutaneous lesions. Resolves spontaneously. Tertiary (late-stage) syphilis lesions are seen in about 1/3 of those not treated; appears years after initial infection. CNS and cardiovascular involved with noninfectious gumma commonly on palate and tongue, but can be on any organ. Generalized glossitis (syphilitic glossitis) may develop that may develop squamous cell carcinoma. Congenital syphilis occurs when the T. pallidum organism crosses the placenta from the infected mother. Hutchinson’s triad may be seen as: 1) interstitial keratitis (inflammatory reaction in cornea), 2) eighth nerve deafness, and 3) mulberry molars and notched or screw-driver-shaped incisors. Acute Necrotizing Ulcerative Gingivitis (ANUG): Painful, erythematous gingivitis with necrosis of the interdental papilla. Results in cratering of interdental papilla. Most frequently occurs in young adults. Predisposing factors include poor nutrition to the point of malnutrition, poor oral hygiene and plaque control, psychological stress, and immune suppression. Acute Osteomyelitis: Acute inflammation of bone and bone marrow of mandible and maxilla most often from extension of a periapical abscess. It also can be caused from physical injury (fracture or surgery), or from bacteremia. Infectious. Painful. Not apparent radiographically unless present for more than 1 week. Treated with antibiotics and drainage. 8. Chronic Osteomyelitis: Bone inflammation. May follow acute osteomyelitis or may have never gone through acute phase. Infectious. Irradiated bone is especially susceptible to infection (osteoradionecrosis). Bacteria (staph, strep, actinomyces) are believed to be responsible for the great majority of cases. 4 Unit 3 Mandible more than maxilla. Jaw swelling is seen often, with loose teeth and sinus tracts occurring sometimes. Diffuse radiolucency can become opaque, and then it is called chronic sclerosing osteomyelitis. This condition is treated with debridement and antibiotics. Fungal Infections 1. Candidiasis (aka moniliasis, thrush): The most common oral mycotic infection. Caused by C. albicans, a unicellular yeast organism living in the oral cavity of most healthy persons. This condition is complex and has many clinical presentations along with interrelationships with local and systemic factors. This disease occurs in four groups: 1) the very young; 2) the very old; 3) those with reduced resistance and 4) those on long term antibiotic therapy or immunosuppression. Oral lesions are white, soft plaques that leave an erythematous, tender surface when wiped away. Favored sites include buccal mucosa, oropharynx, and lateral tongue borders. Chronic oral candidiasis is a common finding in AIDS. Pseudomembranous lesions show surface ulceration. In superficial infections, fungi are limited to surface layers of epithelium, in more severe examples hyphae--filaments of mold--will extend deeper into the epithelium. Nystatin (an antifungal mouthwash) or clotrimazole troche to treat. Discontinue oxygenating agents (hydrogen peroxide). Types Of Candidasis (Classification Systems Vary) a. b. c. d. Pseudomembranous Candidiasis (thrush): This is seen in up to 5% of neonates, 5% of cancer patients, and 10% of institutionalized, debilitated elderly patients. Moreover, it is present in 50% of leukemia patients being treated with radiation or chemotherapy and 70% of patients being treated for solid tumors. It presents as a white curd-like material on the mucosal surface. Underlying mucosa is erythematous. Wiping away will leave an erythematous, eroded, or ulcerated surface that is often tender. Chronic Mucocutaneous Candidiasis Localized form is characterized by longstanding, persistent candidiasis of oral mucosa, nails, skin, and vaginal mucosa. Often resistant to treatment. Acute Atrophic Candidiasis (aka erythematous candidiasis): This presents if pseudomembranous persists. Can result from broad-spectrum antibiotics. Chronic Atrophic Candidiasis (aka denture stomatitis): = most common type of Candidiasis. Present in up to 65% of geriatric individuals who wear complete maxillary dentures. Women more than men, palate more than mandibular arch. Poor fitting denture and wearing an appliance at night contribute to development. It is usually asymptomatic. 5 Unit 3 e. f. g. h. Chronic Hyperplastic Candidiasis (aka candida leukoplakia, hypertrophic candidiasis): Some say is premalignant. The white lesion does not wipe off-important diagnostic feature is its response to antifungal medication. Angular Cheilitis: is seen in those with chronic atrophic candidiasis. Often there are deep folds at commissures due to overclosure. Saliva gathers there and is colonized by yeast. Also seen in those who lick their lips habitually. Median Rhomboid Glossitis: (see Ch. 1) Candida organisms identified in some, but not all lesions. Therefore, though often associated with Candida, cause is not yet clear. Chronic Mucocutaneous Candidiasis: Localized form is characterized by longstanding, persistent candidiasis of oral mucosa, nails, skin, and vaginal mucosa. Often resistant to treatment. 2. Deep Fungal Infections (ex. histoplasmosis, coccidiodo-mycosis, blastomycosis, cryptococcosis): Primarily involve the lungs. Infections are distributed regionally. Oral lesions can look like squamous cell carcinoma because they are chronic, non-healing ulcers. Therefore, must biopsy. Treat with antifungal meds such as amphotericin B or ketoconazole. However, lesions may be resistant to treatment and may reappear if the individual’s immune system becomes deficient. 3. Mucormycosis (aka phycomycosis): Rare. Palate perforated from infection by a phycomycete. Seen in a patient with a debilitating illness (diabetic, chemotherapy patient, immunosuppressed transplant patients). Organisms of this family of fungi normally found in bread mold or decaying fruit and vegetable, infect humans when systemic health is compromised. Route of infection is GI tract or respiratory. Lesions in head and neck most likely in nasal cavity, paranasal sinuses, possibly oropharynx. Death is a relatively frequent consequence of this infection, especially if lung is infected. Viral Infections Viruses are composed of an inner nucleic acid core (genome) of either DNA or RNA that represents their genetic code. The genome is surrounded by a protein coat known as a capsid. With some types of viruses, a lipid envelope further encases the capsid. The complete virus particle is known as the virion. Viruses are infective agents that lack the necessary structures for self-replication. They require living cells for maintenance and multiplication. Therefore, viruses are intracellular parasites. The infecting virus attaches to the preferred cell type and penetrates the plasma membrane. Once entry into the cell is accomplished, the capsid (and envelope) are lost, leaving the viral genome to encode the cell for the manufacture of capsid proteins, viral nucleic acid, and enzymes necessary for assembly. The infecting virus also directs intracellular assembly of new particles. Eventually, newly replicated (and enveloped) virus is released, with subsequent infection of other cells. This usually occurs at the expense of the originally infected cell. In certain types of viral infection, cell death may not occur, allowing the virus to infect dividing host cells in a chronic pattern. Viral latency, in which the infectious agent lies dormant within 6 Unit 3 the host cell, is another non-cytocidal infection. This is common to the herpes viruses, papilloma viruses, and retroviruses. In this latter form of viral infection, overt clinical signs and symptoms of viral replication and infection may follow certain triggering events, such as stress or alterations in the immune state. Another non-cytotoxic type of viral infection is related to tumor-associated viruses that have the ability to become incorporated in the host cell DNA. This newly incorporated viral genetic information results in “ transformation” of the host cell into a neoplastic cell. Because viruses are integrally associated with host cell biologic function and metabolic pathways and because they utilize similar enzymatic pathways, development of a chemotherapeutic agent that kills the virus and spares the cell has been especially difficult. Antiviral chemotherapy, therefore, has been directed toward certain enzymes that are virus specific and unique to viral replication. Papillomavirus Infection (Human Papillomavirus--HPV, Papovavirus) 1. Verruca Vulgaris (aka wart): Generally asymptomatic skin neoplasm caused by a papilloma virus. Patients may have verrucae on hands or fingers and oral lesions appear to arise through autoinoculation by finger sucking or fingernail biting. White, papillary, exophytic lesions that look like a papilloma. Treated by excision. 2. Condyloma Acuminatum: Characteristically in anogenital region but may also involve oral mucosa. Caused by HPV. Increasingly seen in AIDS patients. Benign, papillary lesion. Pink, more diffuse than papilloma or verruca vulgaris, and not as well keratinized. 3. Focal Epithelial Hyperplasia (aka Heck’s disease): Definitive etiology unknown but HPV is increasingly suspected. Asymptomatic. Multiple whitish to pale pink nodules distributed throughout the oral mucosa. No treatment indicated--resolve spontaneously in a few weeks. Herpesvirus Two distinct serotypes: herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2) exist. However, these viruses are nearly indistinguishable except for a variable DNA segment. HSV-1 occurs primarily above the waist in the oral-facial area and HSV-2 below the waist in the anal-genital area. Clinically the lesions appear identical, and HSV-1 can occur genitally and HSV-2 orally. Herpes Simplex Infection (HSV-1) Type 1 (Oral Manifestations) 7 Unit 3 1. Primary Herpetic Gingivostomatitis: Usually seen in children between ages of 1 and 10. Typical route of viral exposure is physical contact with an infected individual. With initial inoculation, clinical manifestations may or may not result. Most individuals develop a subclinical infection. Characterized by painful, erythematous, and swollen gingiva and multiple tiny vesicles on the perioral skin, vermilion border of the lips, and the oral mucosa. They progress to form ulcers. Fever, malaise, and cervical lymphadenopathy generally occur first, followed by gingival involvement and mucosal vesicles and ulcers. Intraoral lesions may appear on any mucosal surface (secondary lesions are confined to hard palate and gingiva). Infection lasts 1 week to 10 days and lesions heal without scar. 2. Ocular herpes: is from a primary herpetic eye infection. Usually unilateral. Keratoconjunctivitis and/or follicular conjunctivitis result. Following resolution of primary herpetic gingivostomatitis, the virus migrates along the peri-axon sheath of the trigeminal nerve to the trigeminal ganglion, where it is capable of remaining in a latent state. 3. Recurrent Herpes Simplex Infection: A large majority of the population (up to 90%) have antibodies to HSV, and 1/3 to 1/2 of the U.S. population may develop secondary herpes. Exact triggering mechanism is unknown. Factors associated with reactivation of virus include exposure to sunlight (“fever blisters”), exposure to cold (“cold sores”), trauma, stress, menstruation, and immunosuppression. occur on oral mucosa that is bound to the periosteum. Attached gingiva and hard palate are most common locations. However, lesions may occur anywhere in the oral cavity in patients who are immunocompromised. 4. Herpes labialis (aka cold sore or fever blister): is the most common recurrent oral herpetic infection. Usually prodromal symptoms of tingling, burning, or pain in the site where lesions will appear. Lesions are map-like superficial ulcer(s) that heal without scarring in 1 to 2 weeks. Patients should be advised that if hands come into direct contact with a herpetic lesion, they should be thoroughly washed to prevent cross infections. Some advise against treating patients with active lesions because it is theorized that treatment procedures may prolong the course of the disease and make current lesions more severe. 5. Herpetic Whitlow: Can be primary or recurrent infection. Involves the fingers. Duration may be as long as 4 to 6 weeks. Swelling, itching and redness followed by intense pain. Herpes Simplex Virus (HSV-2) Type 2 (genital infections) 8 Unit 3 1. Primary 2. Secondary Latent virus is maintained in the lumbosacral ganglion. Varicella Zoster Virus (VZV: a herpesvirus) 1. Chickenpox (primary Varicella-zoster): Primary infection for the disease. Oral ulcerations on the palate are common with chickenpox. Oral lesions have no diagnostic significance and present no serious problem. Lesions are on trunk and face primarily and are very pruritic. “Herald spot” is first and largest lesion to appear. 2. Zoster (Secondary Varicella-zoster) (aka Shingles Herpes): Reactivation of latent VZV. Can follow a depressed cellular immune state (hematopoietic or lymphoid malignancy, drug administration, irradiation or surgery on spinal cord, local trauma). Usually in those older than 50. Shingles occurs when VZV is activated from the dorsal ganglion or the trigeminal ganglion where it was sequestered. The previously hidden virus migrates down the peripheral nerve and infects the skin and mucous membranes supplied by the nerve. Lesions begin as prodromal paresthesia or pain, followed shortly by multiple crops of vesicles and subsequent ulcers and crusts. The total lesion duration is usually less than 1 month. Since the virus cannot migrate far beyond the area of skin or mucous membrane supplied by the infected nerve, the lesions usually do not cross the midline but conform to the anatomic pattern of the branches of the affected nerve. Hence, the acutely painful vesicles follow sensory nerves unilaterally (especially thoracic and abdominal nerves). May affect any branch of trigeminal. Oral lesions are rare. Epstein-Barr Virus (EBV: a herpesvirus) 1. Infectious Mononucleosis: Palatal petechiae, lethargy, malaise, bilateral lymphadenopathy, sore throat, fever. Most commonly in adolescents and young adults. Low contagiousness (may be spread by saliva exchange from deep kissing). Oral lesions often are first sign. Multiple red palatal petechiae turn brown and fade after 7 to 10 days. Downey cells (atypical lymphocytes) are diagnostic. Palliative treatment. 1-2 months for recovery. 2. Hairy Leukoplakia: Most commonly on lateral border of tongue in HIV patients. This lesion has been associated with subsequent or concomitant development of the clinical and laboratory features of AIDS in up to 80% of cases. Unilateral or bilateral, irregular surface contour often folded or corrugated. No symptoms. After hairy leukoplakia diagnosed, studies show about 10% have AIDS and 18% developed AIDS within 8 months, 50% at 16 months, 80% at 30 months. Burkitt’s Lymphoma: Considerable but not totally conclusive evidence that the Epstein-Barr virus is causally related to Burkitt’s lymphoma. 3. 9 Unit 3 There is a considerable amount of evidence linking HSV-II to carcinoma of the cervix. Coxsackie virus (a picornavirus) 1. Herpangina: Contagious, painful, light-gray vesicles that rupture to form multiple, discrete, shallow ulcers. Lesions are only found in oropharynx on soft palate and fauces. More often in children than adults and common in the summer months. Symptoms usually last less than a week. Sore throat, fever, malaise, headache, lymphadenitis, abdominal pain, vomiting. 2. Hand, Foot, and Mouth Disease (HFM): Contagious, painful vesicles in oral cavity (tongue, lips and buccal mucosa), on hands and feet (pathognomonic sign). Usually in children under 5 years old. Pain from oral lesions is usually chief complaint. Self limiting, resolves spontaneously in 1 to 2 weeks. Other Viral Infections that May Have Oral Manifestations Paramyxovirus 1. Measles (rubeola): Caused by a paramyxovirus. After 7 to 10 days incubation and prodromal symptoms (fever, malaise, conjunctivitis, photophobia, cough) then will see Koplik’s spots intraorally 1 to 2 days before skin rash. German measles (rubella) is caused by an unrelated virus of the togavirus family. Significant because it can cause congenital defects in developing fetus. 2. Mumps (aka epidemic parotitis): caused by a paramyxovirus. Considered the most common of all salivary gland diseases. 2-3 week incubation then fever, malaise, headache, and chills in addition to preauricular pain. Prevention is now possible using a live attenuated vaccine that induces a non-communicable, subclinical infection. Human Immunodeficiency Virus (see chapter 7) 10 Unit 3 Comparison of oral herpes and aphthous stomatitis Oral herpes (caused by herpes simplex type I) Lesion Location Gingivostomatitis Gingiva, all mucous membranes Herpes labialis Lips—vermilion Intraoral recurrent Gingiva, hard palate, tissue attached to bone Clinical Characteristics Multiple vesicles, multiple ulcers, fever; malaise Prodrome; multiple small vesicles; crust(s) Prodrome; multiple small vesicles; multiple small ulcers Salivary-bearing mucous membrands Singular enlarging ulcers Salivary-bearing mucous membranes Salivary-bearing mucous membranes Singular, very large ulcers; scarring Multiple, small, herpetiform ulcers Apthous Stomatitis Recurrent aphthous ulcers Major apthous ulcers Herpetiform ulcers Course 7-14 days 7-14 days; recurrent; with predisposing factors 7-14 days; recurrent; with predisposing factors 7-14 days; recurrent; with predisposing factors 14-28 days; frequent 7-14 days; frequent 11