MindMap Gallery General review of oral mucosal diseases
A general review mind map about oral mucosal diseases, lip and tongue diseases, infectious diseases, ulcerative diseases, etc. Hope this helps!
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
General review of oral mucosal diseases
introduction
Oral mucosa and oral mucosal diseases
1. Content
(1) Diseases that mainly occur on the oral mucosa, such as traumatic ulcers of the oral mucosa
(2) Skin-mucosal diseases that occur simultaneously on the skin or alone on the oral mucosa, such as lichen planus
(3) Certain diseases that combine origins of ectoderm and mesoderm, such as erythema multiforme that combines the vulva, anus, conjunctiva, and iris, Behcet's disease, etc.
(4) Oral symptoms of sexually transmitted diseases or systemic diseases, such as AIDS, blood diseases, etc.
2. Basic features
(1)Gender
(2)Age
: For example, recurrent aphthous ulcers are more common in young adults and peptic sores are more common in middle-aged and elderly people.
(3) Parts
The floor of the mouth - the U-shaped area on the belly of the tongue, the triangular area inside the corner of the mouth, and the soft and soft complex are known as the three major danger areas of the oral mucosa.
(4)Damage
(5)Diagnostic methods
Cross-sectional comparison of clinical lesions for diagnosis and differential diagnosis
Pathological examination
In addition to tissue sections, immunohistochemistry and molecular pathology may also be involved.
Clinically necessary therapeutic diagnosis
(6)Treatment
l) Treat the same disease with different treatments
2) Treat different diseases with the same treatment
3) Systemic treatment of local diseases
4) Integrated Traditional Chinese and Western Medicine Treatment
(7)Projection
Most oral mucosal diseases have a good prognosis
Risk of developing cancer
Signs of serious systemic disease
Structure and function of oral mucosa
The structure of the oral mucosa
Epithelial layer
basal layer
stratum spinosum
granular layer
corneum
non-keratinocytes
melanocytes
Basal layer, dendritic, derived from neural crest
Its function is to form melanin, which can be transmitted to keratinocytes through cell processes.
Langerhans cells
The basal layer, or the upper part of the basal layer, is a type of cell with dendritic processes and special Langerhans granules in the cytoplasm.
Regulates the division and differentiation of epithelial cells, immune presentation function and epithelial keratinization
Merkel cells
Neuroectodermal cells, closely related to nerve endings within the epithelium
probably a sensory receptor
basement membrane
The basement membrane is not a membrane in the ultrastructure, but a fibrous complex composed of collagen fibers of connective tissue connected with the dense layer and the transparent layer, which is called the basement membrane complex (object).
The basement membrane mainly has the following functions
1. Bioactive soluble substances from connective tissue must pass through the basement membrane to enter the epithelial layer, thereby affecting epithelial cells. For example, lgG can be found in the epithelial layer, but lgM cannot pass through the basement membrane and reach the epithelial layer.
2. Cells interact with the matrix, and the basement membrane can induce epithelial cells to produce hemidesmosomes. When epithelial cells come into contact with basement membrane (type IV) collagen, the former's need for epithelial growth factors is significantly reduced.
lamina propria
The lamina propria plays a role in supporting and nourishing the epithelial layer.
submucosa
The submucosa is loose connective tissue that contains glands, blood vessels, lymphatic vessels, nerves, and fatty tissue. It is mainly distributed in the covering mucosa. However, there is no submucosal layer in the heels of teeth, most areas of the hard cheeks, and the back of the tongue.
The submucosa provides nutrition and support to the lamina propria
Function of oral mucosa
barrier function
Physical and chemical barriers
The physical and chemical barrier of the mucosa itself
saliva
immune barrier
Lymphocytes
Secretory immunoglobulin (SlgA)
mucin in saliva
Lysozyme in saliva
sensory function
pain
touch
temperature
Taste
Other functions
Temperature adjustment
secretion
Renewal of oral mucosal tissue
Maturation of epithelial keratinocytes
Basal layer cells are moving to the upper layer
The organelles responsible for cell metabolism (nucleus, mitochondria, ribosomes, endoplasmic reticulum) will gradually decrease
The products of keratin formation (tension filaments, keratin bodies, and transparent keratin granules) will gradually increase
After reaching the stratum corneum, the transparent horny granules are closely connected with the tension filaments to form the stratum corneum, at which time almost all other cell structures disappear.
Keratin mortar silk
In basal cells, keratin filaments are loosely arranged in bundles, mostly distributed around the nucleus and parallel to the long axis of the cell.
In spiny cells, tension filaments gradually increase and become denser, interwoven into a network structure surrounding the nuclear membrane, running through the entire cytoplasm, and inserting desmosomes to form a scaffolding structure
In granulocytes, keratin filaments are associated with hyaline granules and interact with phosphorylated histone-rich proteins
After reaching the cornified layer cells, the histone-rich proteins are dephosphorylated and become basic proteins in the cornified layer. The keratin filaments gather into bundles, are embedded in the basic proteins, and are surrounded by thickened cell membranes, thus forming a complete keratin. stromal epithelium
Oral mucosal epithelial cell cycle
The cell cycle can be divided into: division phase (M phase) - post-division growth phase (Gl phase) - DNA synthesis phase (S phase) - pre-division growth phase (G2 phase)
The duration of period M is 40~75 minutes
The variation in Gl phase is obvious, ranging from 14 hours to 140 hours
The S period is between 7 and 12 hours, with an average of 8 hours
G2 period 1 ranges from 0 to 90 minutes
Regulation of oral mucosal epithelial cell cycle
Regulated by the neuroendocrine system
The epithelium itself also produces substances that inhibit and stimulate cell division
Oral mucosal epithelial renewal time
It is shorter than the epidermis of the skin but longer than the cells of the gastrointestinal tract. It is estimated to be about 4 to 14 days.
epidermis
28~75 days
gingival epithelium
28~40 days
buccal mucosa
5~16 days
small intestinal epithelium
2~14 days
Age-related changes in oral mucosa
Exterior
Atrophy, thinning, paleness, dryness and reduced elasticity
Histological structure
Epithelial layer
thickness becomes thinner
Decreased cell density
Reduced cellular level
thickening of corneum
Cell volume becomes smaller
Decreased number of Langerhans cells
connective tissue
Decreased cellular content in the lamina propria and submucosa,
Fibroblasts shrink in size and number
Increased insoluble collagen fibers
Collagen degeneration and rupture
Minor salivary glands appear significantly atrophied, secretion decreases, and are replaced by fibrous tissue
Function
barrier function
Saliva secretion gradually decreases
The mechanical flushing effect is weakened
The lubrication and antioxidant capabilities of saliva also gradually weaken
The body's immune function, especially cellular immune function, is significantly reduced
The proliferative response of peripheral blood T lymphocytes to various antigen stimuli gradually weakens
The concentration of defense protein components such as mucin and lgA decreases to varying degrees with age.
sensory function
Reduced taste sensitivity
Decreased spatial perception and two-point discrimination ability
Basic clinical lesions of oral mucosal diseases
Spots and patches
Macules and patches both refer to color changes on the skin and mucous membranes.
Not higher than the mucosal surface
Not thick
No induration changes
erythema
Dilation, proliferation and congestion of blood vessels in the lamina propria of the mucosa
dark spots
Caused by melanocyte deposition in the basal layer of the epithelium
Addison's disease
Or there is hemosiderin from old bleeding in the lamina propria of the mucosa, making the surface black.
Some metal particles are deposited in the mucosa
Papules and plaques
Papules
A papule is a small solid protrusion on the mucous membrane, about the size of a pinhead, usually less than 1cm in diameter - Lichen plana
Base shape is round or oval
Surface shape can be pointed, round or flat
Under the microscope, epithelial thickening, serous exudation, and inflammatory cell infiltration can be seen
Color is off-white or red
Leaves no trace after fading
plaque
Plaque is also translated as papule. Most of them are formed by the dense fusion of multiple papules, with a diameter greater than 1cm. Their boundaries are clear and vary in size.
Oral leukoplakia and cancer
chronic discoid lupus erythematosus
Slightly raised and firm lesions
white or off-white
The surface is relatively smooth or rough
Fissures can be seen dividing the lesions.
Scar and the big shop
Storage of fluid in the mucous membrane causing ulcerative lesions
If the diameter of the damage is less than 1cm, it is called a damage.
If the diameter of the damage is more than 1cm, it is called a large one.
Commonly seen in cerebrospinal sores or cerebrospinal sores
Allergic diseases, such as erythema multiforme
Contents are different
abscess
blood scar
restaurant
epithelial or spinous epithelium
The location of the cook is within the epithelium
Only part of the epithelium forms the wall, and the wall is thin and soft
If the running site is under the epithelium
basal subepithelial tract or subepithelial tract
The scar wall is composed of a full layer of epithelium, so the scar wall is thicker
Once the cook wall ruptures, erosion or ulcers will form.
ulcer
An ulcer is a continuous defect or destruction of the integrity of the mucosal epithelium, resulting in a depression formed by necrosis and detachment of the surface layer.
Superficial ulcers only destroy the epithelial layer and heal without scars, such as mild aphthous ulcers.
In deep ulcers, the lesions spread to the submucosal layer, leaving scars after healing, such as recurrent necrotizing perimucosal adenitis
There may be erythema of varying sizes around the ulcer
cause pain
erosion
A superficial defect in the mucosa, which is partial damage to the epithelium and does not damage the basal cell layer.
Indeterminate size and shape, unclear boundaries, smooth surface
After epithelial endothelial ulcer
simple rash
childhood scars
mechanical trauma
Line with blurred edges
There may be pain
Nodules
Solid lesions protruding from the oral mucosa
The surface epithelium protrudes outward, forming superficial lesions
They vary in size, generally 5cm in diameter, and vary in shape.
pink to deep purple
Fibroids or grief
tumor
A solid growth that projects outward from the mucous membrane
Various sizes, shapes and colors
shrink
The size of tissue cells decreases, but the number does not decrease
Redness may occur
The epithelium covering the surface becomes thinner, and the rich blood vessel distribution in the connective tissue is clearly visible
The lesion is slightly depressed
Some of the characteristic epithelial structures disappear and are replaced by a thin layer of epithelium. For example, atrophy of the tongue papilla can make the tongue surface smooth and red.
chapped
Linear tears on the mucosal surface, caused by inflammatory infiltration that causes the tissue to lose its elasticity and become brittle.
Such as riboflavin deficiency caused by cleft corner of the mouth
Only within the epithelium, leaving no scar after recovery
If it reaches the submucosal layer, it can cause bleeding, burning, and scarring after healing.
pseudomembrane
Off-white or yellow-white film
Inflammatory exuded cellulose, necrotic and exfoliated epithelial cells and inflammatory cells
Can be wiped off or peeled off
Pseudomembrane often forms on the ulcer surface
scab
Usually occurs on the skin, but can also appear on the lipstick area
Mostly yellowish white
Bleeding turns dark brown
It is formed by adhesion and coagulation of fibrinous and inflammatory exudates to the epithelial surface.
scales
Epidermal keratinocytes that have fallen off or are about to fall off, often resulting from hyperkeratosis and parakeratosis
Necrosis and gangrene
Necrosis
Pathological death of local cells in the body
gangrene
Large-scale necrosis and decay due to the action of rotten parasites are called gangrene
Examination and diagnosis of oral mucosal diseases
Medical history
The history of oral mucosal disease is more detailed than that required by other clinical disciplines involved in the field of oral medicine.
First of all, attention should be paid to the characteristics, extent, and nature of the main complaint (such as paroxysmal severe pain, persistent burning pain, or itching pain, etc.), duration, pattern of onset time, aggravating or alleviating factors, and location.
In the treatment history, special attention should be paid to drug allergies and their efficacy, whether antibiotics, immune preparations, etc. have been used
Pay attention to the relationship between pregnancy and disease in the past history
Pay attention to genetic factors and family diseases in family history
Personal smoking and drinking habits as well as professional and personality characteristics cannot be ignored.
examine
Basic oral examination
Oral hygiene, periodontal health, dental health, and possible restorations, etc.
Oral mucosal examination
In order, they are lipstick, labial mucosa, buccal mucosa, floor of the mouth and tongue abdominal mucosa, tongue mucosa, cervical mucosa, pharyngeal mucosa and dental limit.
Auxiliary inspection
Hematology tests
In addition to routine blood tests, tests such as blood glucose, serum biochemical indicators, C-reactive protein, erythrocyte sedimentation rate, coagulation function, serum iron, folic acid, vitamin B12, and tumor markers are all commonly used auxiliary examination methods for the clinical diagnosis of oral mucosal diseases.
Human immunodeficiency virus antibody detection, syphilis serology detection, large scar disease specific antibody detection, fungal antigen detection, Mycobacterium tuberculosis related gamma-interferon in vitro release quantitative test, parasitic disease serological diagnostic test in some special oral diseases It has important reference value in the diagnosis of mucosal diseases
Immunological examination
Systemic immune examination has become a routine auxiliary examination item for oral mucosal diseases
Severe oral mucosal candida infection
Routine cellular immunity and humoral immunity examination
severe recurrent aphthous ulcer
Systemic immunological examination
scar patients
Detection of autoantibodies against epithelial junction substances
Patients with oral mucosal amyloidosis
Serum eggshell electrophoresis, blood and urine immunofixation electrophoresis, urine protein and other related immunological tests
microbiological examination
Oral mucosal bacterial culture examination, oral mucosal fungal smear examination and oral mucosal fungal culture examination
exfoliative cytology
Viral diseases and acne
biopsy
The purpose of oral mucosal disease biopsy is: first, to confirm the diagnosis and assist in differential diagnosis; second, to rule out malignant transformation
It is not a routine procedure that must be done in every case. Excisional biopsy is generally used for smaller lesions.
The depth reaches at least the submucosa.
Immunohistochemical examination
Commonly used in the diagnosis and identification of general diseases
molecular biology
Urine routine
Stool routine
Film degree exam
Infectious diseases
Viral infection
oral herpes simplex
Herpes simplex virusHSV
Classification
Type I
Skin and mucous membrane infections
Type II
genital anus
symptom
Clusters of small blisters are self-limiting and prone to recurrence
Clinical symptoms
1. Primary herpetic stomatitis
Features
Type I
Under six years old, especially 6 months to 2 years old
Immunity comes from mother before 6 months
installment
prodromal stage
Have a history of exposure to herpes lesions
Children salivate, refuse to eat, and are irritable. After 1-2 days, the oral mucosa becomes widely congested and edematous, and acute inflammation often occurs in the attached gingiva and gingival margin.
blister stage
Clusters of small, pinhead-sized blisters on any part of the body
erosion stage
Small blisters gather into clusters, and after rupture, they can form large-scale erosion, covered with white pseudomembrane
healing period
The course of the disease is 7-10 days. If there are antibodies, it is easy to relapse.
2 Recurrent herpetic stomatitis
Recurrent damage may occur in about 30% to 50% of cases
parts
on or around lips
feature
clusters of blisters, recurring
clinical manifestations
Prodromal stage: slight fatigue and discomfort, secondary and burning pain in the lesion area…………
heal
Course of disease 10 days
healing performance
No scarring, may have pigmentation
pathology
Epithelial cells undergo ballooning degeneration and reticular liquefaction, forming a cyst within the epithelium.
There are eosinophilic virus bodies, also called viral inclusion bodies, in the nuclei of balloon-shaped cells. They are mostly located at the bottom of restaurants.
Three changes can be seen: ground glass nuclei, multinucleated syncytia, and intranuclear inclusions.
diagnosis
Clinical symptoms
Differential diagnosis
Herpetic gingivostomatitis and stomatitis
trigeminal herpes zoster
Hand, foot and mouth disease
herpangina
erythema multiforme
treat
systemic treatment
Nucleoside antiviral
Acyclovir (acyclovir), valacyclovir,...Lowei
Broad spectrum antiviral
Ribavirin
topical treatment
Chlorhexidine, ethacridine
supportive care
Traditional Chinese Medicine
Banned hormones
prevention
Oral respiratory tract transmission, mainly avoid contact with patients
Shingles
Varicella Zoster Virus VZV
Unilateral
along the nerve
clusters of small blisters
neuralgia
Chickenpox in children, herpes zoster in adults
The incidence of shingles gradually increases with age
Thoracic and abdominal>lumbar>trigeminal nerve
treat
antiviral drugs
Acyclovir
Pain relief
Non-systemic analgesics: Acetaminophen
Tramadol can be used if it is invalid
Severe: carbamazepine
hormone
Glucocorticoids
prednisone
neurotrophic drugs
Vitamin Bl
immunomodulatory drugs
Thymus enteric coated tablets
cimetidine
topical treatment
Intraoral mucosal lesions
Chlorhexidine
Povidone dish solution
Perioral and maxillofacial skin lesions
Acyclovir ointment
physical therapy
laser irradiation
branch
The first one
forehead
Canthus mucous membrane, even blindness
second branch
Lip, palate, infratemporal, zygomatic, and infraorbital skin
The third branch
Tongue, lower lip, cheek and buccal skin
geniculate ganglion
Ramsay-hunt syndrome
Facial paralysis, earache, external auditory canal herpes
Bacterial infections
coccal stomatitis
Main pathogenic bacteria
Staphylococcus aureus
viridans streptococci
Hemolytic Streptococcus
pneumococci
Pseudomembranous lesions (membranous stomatitis)
Gray-white-yellow-brown pseudomembrane
Wipe away bloody erosion and inflammatory bad breath
Oral mucococcal infection (mixed infection)
Diagnosis: smear, bacterial culture
treat
antibacterial drugs
vitamins
Traditional Chinese medicine mouthwash
Oral tuberculosis
Mycobacterium tuberculosis human or bovine
clinical manifestations
Tuberculous sores (primary syndrome)
Rare clinically, mostly seen in children, but also seen in adults
tuberculous ulcer
A common secondary tuberculosis lesion in the oral cavity is tuberculous ulcers
The ulcer has clear or linear borders and appears as a superficial, slightly concave and flat ulcer.
There is a little purulent exudate at the base. After the exudate is removed, dark red mulberry-like granulomas can be seen.
The edge of the ulcer is slightly raised, in the shape of a rat's gnaw, and curls toward the center to form a submerged edge.
The texture of the ulcer base may be similar to the surrounding normal mucosal tissue
Small yellow-brown miliary nodules can be seen at the edge
Lupus vulgaris
It is clinically rare and is cutaneous tuberculosis caused by reinfection in patients with a positive tuberculin test.
Histopathology
Tuberculous nodules may be seen in connective tissue
The center is a structureless cheese-like substance
Surrounded by many epithelioid cells and Langerhans cells
The outermost layer contains a large number of lymphocytes
Proliferated fibroblasts can be seen between tuberculosis nodules
The diagnosis of oral tuberculosis lesions mainly depends on histopathological examination
disease management
Early, regular, full course, appropriate amount and combined use of anti-tuberculosis drugs
Commonly used anti-tuberculosis drugs
Smoke trap (Remi seal)
(2) Ethambutol
(3) Streptomycin
(4)Rifampicin
Oral tuberculosis treatment
Tuberculosis limited to oral mucosa or skin
Oral isotope
Can be combined with intramuscular injection of streptomycin
or oral administration of para-aminosalicylic acid
Treating Oral Tuberculous Lesions
Streptomycin can be used for local sealing
Symptomatic treatment
Eliminate infection, remove local irritants, use supportive care, and eat nutritious foods
Necrotizing and stomatitis
Acute necrotizing ulcerative oral lesions with Clostridium and Treponema infection as the main causes
Complicated mixed infections are common
Clostridium and spirochetes
Incorporate other bacteria
Streptococci, filamentous bacteria, melanobacteria, etc.
Histopathology
Mainly tissue necrosis (necrosis)
Nucleus and cytoplasm lysis
Beginning of nuclear pyknosis
nuclear fragmentation
dissolution finally occurs
HE staining showed that the necrotic tissue appeared as a homogeneous and structureless light red or granular area.
disease management
Acute phase treatment
First, gently remove the necrotic tissue on the heel papilla and margin, remove large pieces of calculus, and rinse or rinse with 1. 5% to 3% hydrogen peroxide solution locally. Povidone Carbon or 0.2% Chlorhexidine Rinse
Systemic anti-infection
Beta-lactam antimicrobials
Penicillins and cephalosporins
Nitroimidole antimicrobials
Metronidazole, Tinidazole
Can be used jointly
systemic supportive care
High-vitamin, high-protein diet to enhance nutrition. Provide infusion if necessary to replenish fluids and electrolytes
Chinese medicine treatment
Prognosis and outcome
Early detection and timely treatment lead to a good prognosis
If treatment is not timely, the condition will progress rapidly, and serious conditions may lead to death of the patient.
After treatment and healing, the cheek is defective and deformed, with scars remaining, affecting the appearance and physiological functions.
prevention
Pay attention to oral hygiene and treat periodontal disease promptly
Eat a reasonable diet and strengthen nutrition
Actively exercise and enhance the body’s resistance
fungal infection
Oral candidiasis
Candida albicans
Opportunistic pathogens
unicellular yeast-like fungi
Bacteria are round or oval in shape
Gram stain positive
Intolerant to heat, loves acid and alkali
The appropriate pH is 4~6
Complete cell wall, cell membrane, cytoplasm and nucleus
There is a close relationship between its cell wall and its pathogenicity
Mainly composed of polysaccharides
a-mannan
B-Glucan
The outer layer of proteins and mannan form a complex to form a network structure on the surface, which contributes to the expression of surface antigens and is related to adhesion.
biphasic fungi
buds give birth to spores
pseudohyphae
Pathogenic forms of spore blooms
Cause
Toxicity of pathogenic bacteria
Host defense capabilities and susceptibility factors
Decreased skin and mucosal barrier function
Primary and secondary immune function decline
Long-term and misuse of broad-spectrum antibiotics
hormone imbalance
after major surgery
After head and neck radiotherapy
Sjogren's syndrome
HIV infection
diabetes
The relationship between candida infection and oral leukoplakia
Most scholars believe that Candida albicans infection plays a role in promoting epithelial abnormal proliferation and canceration in oral leukoplakia.
clinical manifestations
pseudomembranous type
acute pseudomembranous type
Oral Thrush (Snowy Mouth Disease)
Infants and young children, white as snow, 4%
Mucosal bleeding, small spots as white as snow, the child is restless and crying
Subjective symptoms include dry mouth, burning discomfort, and mild pain.
atrophic
Acute atrophic (erythema) type
Long-term use of broad-spectrum antibiotics
The tongue coating is thickened and the papillary mass on the dorsum of the tongue atrophies
More common after long-term use of antibiotics, hormones and HIV infection
Subjective symptoms include dry mouth, abnormal taste, pain and burning sensation
Chronic atrophic (erythema) type
Wearing dentures
Bright red spots are scattered in the denture area. There may be granular hyperplasia on the surface of the erythema, and the papilla on the back of the tongue may atrophy.
The damage site is often on the palate and gingival mucosa that are in contact with the palatal side of the maxillary denture.
Denture stomatitis is mostly asymptomatic, and a few patients have symptoms such as mucosal burning and dry mouth.
Proliferative type
Chronic hypertrophic (proliferative) type
Medial triangle of the corner of the mouth, symmetrical, nodular
nodular granular hyperplasia
Candida vitiligo
Buccal mucosal lesions
Malignant transformation rate higher than 4%
Seek early biopsy
Thousands of hyphae penetrate deeply into the mucosa, causing parakeratosis, thickening of the spinous layer, epithelial hyperplasia, formation of micro-abscesses, and inflammatory cell infiltration of the papillae of the lamina propria.
Related diseases
Median rhombus tongue
Candida cheilitis
Dry mouth burning pain irritation pain
Common on lower lip
Candida angular cheilitis
Wet white erosion
bilateral
Children, the elderly, the infirm
Fungal angular cheilitis characterized by wet white erosions
Affected on both sides
Cracks in the skin and mucous membranes at the corners of the mouth
There are often erosions and exudates at the cracks, or there may be thin knots
Pain or bleeding when opening mouth
Congestion of adjacent skin and mucous membranes
Histopathology
thickened parakeratotic epithelium
Candida albicans hyphae invade and cause epithelial surface edema
There is neutrophil infiltration in the cornified layer, often forming micro-abscesses.
Hyphae can be seen in the outer 1/3 of the cornified layer or epithelium
epithelial acanthosis
Epithelial spikes are round
The basement membrane is partially destroyed by inflammation
HE staining is not very clear
Strongly positive PAS
Because Candida hyphae and spores contain polysaccharides
There are congested capillaries and a large number of lymphocytes, plasma cells and neutrophils infiltrating in the connective tissue.
laboratory tests
smear method
direct microscopic examination
a
Positive
PAS staining
Spores are red and pseudohyphae are blue.
isolation culture method
Saber weak medium
cotton swab method
saliva culture
Gargle concentrate method
paper chip method
Blot culture and membrane culture
Biopsy
Biopsy
Immunization method
Determination of anti-Candida fluorescent antibodies in serum and non-irritating mixed saliva by indirect immunofluorescence
False positive rate (false detection rate) is high
molecular biology methods
Classification and identification of yeasts based on gene sequence analysis
Pathogen identification
Germ tube test, thick-walled spores test, biochemical testing
diagnosis
Microscopic hyphae, spores, microabscesses
direct microscopic examination
First choice of auxiliary diagnostic technology
treat
Mainly local treatment
2~4% sodium bicarbonate (acid-loving and alkali-loving)
A purple water
Chlorhexidine
antifungal drugs
Nystatin
Amphotericin B
The antibacterial effect of this drug may be due to the release of potassium by damaging the cell membrane, thereby causing the cell to cease glycogen decomposition and lose vitality.
Miconazole
It can directly damage the fungal cell membrane and impede the synthesis of ergosterol to achieve antifungal purposes.
fluconazole
Can inhibit the synthesis of ergosterol, the main component of fungal cell membranes
The most widely used antifungal drug in clinical practice
If resistant, choose itraconazole
Comprehensive Treatment
Surgical treatment
No hormones, broad-spectrum antibiotics and hydrogen peroxide are ineffective
Deep mycosis
mainly include
candidiasis
Cryptococcosis
Aspergillosis
mucormycosis
sporotrichosis
Penicillium maneffei
Histoplasmosis
Paracoccidioidomycosis
blastomycosis dermatitis
Cause
Candida accounts for more than 80%
Except Candida spp.
yeast
Aspergillus
Cryptococcus neoformans
Mainly invades the central nervous system
Main susceptibility factors
Large-scale, long-term or combined use of multiple broad-spectrum and highly effective antibiotics
use of hormones or immunosuppressants
Elderly patients
Serious basic diseases, such as hematoma, malignant tumors such as lung cancer and liver cancer, chronic nephritis, uremia, kidney transplantation, chronic obstructive pulmonary disease, pimples, cerebral hemorrhage, diabetes and AIDS, etc.
organ transplant
Various catheter interventional treatments such as organ cannulation and urinary catheterization
radiotherapy, chemotherapy
The route of infection is usually hematogenous dissemination and ascending infection
disease management
(1) Preventive treatment
Drugs commonly used for preventive use include Dican, itracan, amphotericin B, and posaconazole.
(2) Empirical treatment
Empiric treatment options include amphotericin B, liposomal amphotericin B, azacan, itracon, voriconazole, and caspofungin.
(3) Preemptive treatment
Antifungal therapy in high-risk patients with evidence of fungal infection but no clinical manifestations
(4) Targeted treatment
Patients with deep fungal infections whose pathogenic fungi have been identified are treated with antifungal drugs targeting the pathogenic fungi.
Class 3 drugs can be used to treat deep fungal infections
polyenes
Traditional amphotericin B, liposomal amphotericin B (L-AmB)
Class
Nitracan, Itracan, Vorican, Posacon, Nitracan, etc.
Echinocandins
Caspofungin, anidulafungin, micafungin
In addition to Zhaconazole and Itraconazole, commonly used clinical drugs against deep fungal infections include
(1) Amphotericin B
(2) 5 - cell cry
(3) Vulikangli
(4) Caspofungin
allergic disease
allergy
Also called allergic reaction or hypersensitivity reaction
Cause tissue damage and dysfunction
complete antigen
macromolecular substances
Microorganisms, parasites, pollen, fur, fish and shrimp, allogeneic tissue cells, allogeneic serum egg mortar
Complete antigens have the characteristics of immunogens and reactogens and can cause allergic reactions when entering the body.
hapten
Mostly synthetic drugs
The molecule is the smallest and cannot cause an immune response, but after entering the body and combining with human tissue proteins, it becomes a macromolecular substance, which has antigenicity and has the conditions to induce allergic reactions.
Classification
immediate allergic reaction
Type 1 allergy (reagin type)
immediate allergic reaction
Type 1I allergic reaction (cytolytic or cytotoxic)
Antibodies are mainly lgG, with a few lgM and lgA
Sichuan type allergy (immune complex type)
immune complex mediated
The free antigen combines with the corresponding antibody to form an immune complex
Type IV allergy (delayed or tuberculin type)
Antigen-specific sensitization effector T cell-mediated
The immune substances involved in causing the reaction are not humoral antibodies but sensitized lymphocytes
Type I allergic reaction
angioedema
Also known as angioneurotic edema, also known as giant urticaria or Kunkel's edema
Loose tissue under the skin
Good hair on upper lip
Occurs in the epiglottis causing suffocation
Lips, tongue, cheeks, eyes, face, earlobes, throat, etc.
The vulva and gastrointestinal tract mucosa can also be involved
hereditary or acquired
reason
food
Fish, shrimp, crab, eggs, milk
drug
Non-steroidal anti-inflammatory drugs
Sulfonamide antibiotics
Captopril
flora and fauna
physical factors
cold, heat, light, friction, pressure
Mental factors such as emotional excitement
Viruses, bacteria, parasites
genetics
Chang Xian
CL esterase
diagnosis
History of exposure or recurrence
Differential diagnosis
periapical abscess
No allergens
Chief complaint of toothache
cellulitis
No allergic substances, no systemic symptoms, fever up to 38°C
Antibiotics are effective
treat
A large amount of vitamin C 500~1000mg
10% calcium gluconate
Dexamethasone 5~10 mg intravenously
Oral anti-allergy medications
Chlorpheniramine maleate
diphenhydramine hydrochloride
For severe cases, hormones can be used
Prednisone 5~10mg three times a day
When larynx is edema
Adrenaline
hydrocortisone
Hold ice cubes in mouth
Tracheotomy if necessary
drug allergic stomatitis
allergen
antibiotics
Penicillin, streptomycin, tetracycline
antipyretic analgesics
aspirin
Hypnosis and anti-epilepsy
Phenobarbital, phenytoin, carbamazepine
Sulfonamides
A small number of Chinese patent medicines
clinical manifestations
The first time requires an incubation period (4~20 days)
blister rupture erosion ulcer
Skin: Commonly occurs around the mouth
The most common lesions are round erythema
The appearance of blisters on top of erythema is called vesicular erythema
The location of the lesion is fixed
Fixed drug eruption
diagnosis
Medication history, allergy history
sudden acute inflammation
Improvement after stopping medication
Differential diagnosis
polymorphous exudative erythema
target erythema
self-limiting
Large area erosion, false membrane, blood scab
herpetic stomatitis
infants
treat
Discontinue medication
High dose vitamin C
Intravenous injection of 10% calcium gluconate plus vitamin C can increase the density of blood vessels to reduce exudation and inflammation.
anti-allergy medicine
antihistamines
Oral loratadine (Claritan) is available for adults
Chlorpheniramine (Chlorpheniramine)
hormone therapy
The application of glucocorticoids depends on the severity of the disease. Prednisone can be given to patients with mild symptoms.
Severe cases may be given hydrocortisone
When the condition is particularly severe, epinephrine 0.25 ~ 0.5 mg subcutaneous injection or isoproterenol should be given
Antibiotics fight infections?
Ethacridine and chlorhexidine topical application
contact stomatitis
delayed allergic reaction
It takes at least 7 to 10 days for local antibodies to form after a certain incubation period after exposure to the substance.
Reaction usually takes 48 to 72 hours after repeated exposure.
After the body is exposed to allergens, it takes 2 to 3 days for local oral mucosal congestion and edema to appear.
Cause
Denture base (methacrylic acid, engraving alloy, diamond alloy)
Dental fillings (silver alloy, resin)
Inlay (gold, silver)
Toothpaste, lipstick, chewing gum, clove oil, dish detergent, etc.
Histopathology
Histopathology shows acute inflammation
Tissue edema, blood vessel dilation, and inflammatory cell infiltration can be seen
When showing a fresh-like reaction, mild partial hyperkeratosis of some epithelium can be seen, the granular layer is obvious, the basal layer is thickened or thinned, the basal cells are liquefied and degenerated, lymphocyte infiltration can be seen under the epithelium, and a small amount of eosinophils and neutrophils can be seen. Granulocyte, plasma cell infiltration and infiltration around small blood vessels.
disease management
Remove suspected allergens first
Such as replacing denture repair materials or dental filling materials
Stop using suspicious drugs or cosmetics, etc.
medical treatement
See Drug-allergic stomatitis
prevention
Try not to use drugs, foods or cosmetics that may cause allergic reactions
erythema multiforme
Histopathology
nonspecific inflammation
Intraepithelial and intercellular edema
There may be holes or fissures formed in the epithelium, or large scars may form under the epithelium.
No acantholysis
There is edema in the connective tissue and infiltration of inflammatory cells
In the early stage, eosinophils predominate, and gradually neutrophils predominate.
Dilation of blood vessels, swelling of vascular endothelial cells and thickening of blood vessel walls, and infiltration of mixed inflammatory cells mainly composed of lymphocytes around blood vessels
Sometimes red blood cells migrate out of the blood vessels
ulcerative disease
Recurrent oral ulcers (ROU) also known as recurrent aphthous ulcers (RAU)
The prevalence rate of oral mucosal diseases ranks first
Periodic, recurring, self-limiting
Cause
The cause is unknown, but there are obvious individual differences
The triple factor theory of genetics, environment and immunity
"Double factor theory", that is, exogenous infectious factors (viruses and bacteria) and endogenous inducing factors (hormone changes, mental and psychological factors, nutritional deficiencies, systemic diseases and immune dysfunction) interact to cause disease.
clinical manifestations
Red (redness and swelling at the end of the year) yellow (yellow pseudomembrane) concave (sunken in the middle of the lesion) pain (pain is very obvious)
Attack phase (- prodromal phase - ulcer phase) - healing phase - intermittent phase
Classification
Mild aphtha
Severe aphtha
stomatitis type aphtha
Lightweight
l0~l4 days
herpetiform
l0~l4 days
Heavy duty
>14 days, can be 1~2 months or longer
Differential diagnosis
Behcet's disease
Oro-eye-genital triad
Erythema nodosum, folliculitis, positive acupuncture reaction
Systemic immune system diseases
traumatic ulcer
Consistent with mechanical trauma factors
malignant tumor ulcer
Deep, large, crater-shaped ulcer with raised edges
progress rapidly
no self-limiting
tuberculous ulcer
The edges are uneven, rat-like, and curled toward the center.
Exudate, mulberry granuloma beneath the exudate
Acidophilus bacteria were seen under the microscope, not self-limiting
herpetic stomatitis
child
treat
Anti-inflammatory and analgesic
Occluded therapy ( )
Traditional Chinese Medicine
Behcet's disease
Histopathology
nonspecific perivasculitis
All large, medium and small blood vessels throughout the body, of which veins are the most affected
Perivascular lymphomonuclear cell infiltration
clinical manifestations
Oral ulcers
Similar to recurrent aphthous ulcer
It usually manifests as mild or scar-like type, and may also appear severe.
70%~99% of the first symptoms will eventually occur in 100% of patients
genital ulcers
Approximately 75% of patients develop
The lesions are basically similar to oral ulcers
The ulcer is deep and large, causing severe pain and slow healing.
skin damage
The incidence rate is high, up to 80%, and the manifestations are diverse
Erythema nodosum, eruptions, papules, scablike rashes, erythema multiforme, annular erythema, necrotizing tuberculosis eruption-like lesions, large scar necrotizing vasculitis, Sweet's disease-like skin lesions, pyoderma, etc.
Particularly valuable for diagnosis
Erythema nodosum-like skin lesions
It usually occurs in the limbs, especially the lower limbs.
Inflammatory response after minor trauma (acupuncture)
After intramuscular injection, rashes and small pus spots may appear at the needle insertion site, or thrombophlebitis may occur after intravenous injection, which will subside within 3 to 7 days.
ophthalmia
Approximately 50% of patients are affected
The most common eye disease is uveitis
Keratitis, exanthematous conjunctivitis, scleritis, choroiditis, retinitis, optic nerve papillitis, necrotizing retinal vasculitis, fundus hemorrhage, etc.
joint damage
25% to 60% of patients have
Presents as relatively mild localized, asymmetric arthritis
nervous system damage
The incidence rate is about 5%~50%
Neuroautotic disease
digestive tract damage
The incidence rate is 10%~50%
Also known as intestinal Behcet's disease (
The entire digestive tract from the mouth to the anus can be affected. Ulcers can be single or multiple and vary in depth.
More common in ileocecal part
vascular damage
About 10% to 20% of patients are complicated by large and medium vasculitis, which is the main cause of death and disability.
The basic lesion of this disease is vasculitis, which can affect both large and small blood vessels throughout the body.
9. Lung damage
About 5%~10%
Kidney, heart and other damage
Diagnostic criteria
This disease has no specific serological and pathological characteristics, and diagnosis is mainly based on clinical symptoms.
Reiter syndrome
non-organ-specific autoimmune disease
Highly relapsing
triad
arthritis
most prominent symptoms
Acute attacks are more common in large joints of the lower limbs, often in the knee joint.
urethritis
starter
conjunctivitis
second
Other symptoms
Oral ulcers, balanitis, cervicitis
More common in men aged 15-35
diagnosis
triad
bullous disease
pemphigus
Chronic mucocutaneous autoimmune macroscar disease
antigen
Desmoglein (Dsg)
desrnoglein 3 (Dsg3)
Level far higher than thousand Dsgl
basal and parabasal layers
desrnoglein 1 (Dsg 1)
Expresses all layers of epidermis, more abundant in superficial layers
Transmembrane glycoproteins of the desmosomal cadherin family
More common in people aged 40 to 60 years old
Chronic onset, most cases last 4 to 7 months from onset to diagnosis
Antigen-antibody reactions against adhesive components exist between spiny cells, leading to acantholysis and water scar formation.
Hemorrhoids vulgaris
clinical manifestations
Oral mucosa
About 70% of patients are affected first in the oral mucosa, and about 90% of patients develop oral mucosal damage during the course of the disease.
Irregular erosion surface left after boils break
Erosed surfaces are difficult to heal
The surface of old eroded surfaces may be covered with yellow-white pseudomembrane
Nikolsky's sign, that is, positive Nikolsky's sign
Use a cotton swab to rub the normal-looking tooth and heel mucosa. Water sores or hematomas may appear on the mucosal surface, or the normal-looking mucosal surface may fall off.
Peel test positive
After the water scar is broken, the scar wall can be left behind and shrink around. If the scar wall is torn off or lifted, it is often torn off painlessly along with the adjacent normal-appearing mucosa, leaving a bright red wound.
Probe test positive
If the probe is gently inserted parallel to the mucosa at the edge of the erosion surface, the probe can be inserted painlessly.
skin
Hydrorrhea often appears in areas prone to friction such as the chest, scalp, neck, armpits, and groin.
The scabies are easy to break. After breaking, a red and wet eroded surface will be revealed. Ascariae may form, heal and leave pigmentation.
Using your fingers to push sideways on normal-looking skin can cause boils to form quickly; pushing against the skin can cause it to move on the skin. These phenomena are also positive for Chienie's sign.
Mild itching and pain. During the course of the disease, patients may develop systemic symptoms such as fever, weakness, anorexia, etc.
Other parts
In addition to the oral cavity, the mucous membranes of the nasal cavity, eyes, external genitalia, anus, etc. can be damaged similar to those of the oral mucosa, and most of them are difficult to heal.
proliferative scarring
It is rare. Because its antigenic components are mostly consistent with those of vulgaris, it is also considered to be a subtype of vulgaris.
Before the use of glucocorticoids to treat the disease, the mortality rate was 75%. After the use of glucocorticoids, the mortality rate dropped to 5% to 10%.
Deciduous grass sore
Oral mucosa
Damage is rare, and even if it occurs, it is mostly small and superficial erosion that is not obvious.
skin
It usually occurs on the head, face and upper chest and back. Water scars often occur on the basis of erythema, Nissl's sign is positive, the walls are thinner and more susceptible to rupture, and the superficial erosion surface is covered with yellowish-brown, greasy roundworms and scales, such as fallen leaves.
Erythematous scarring
The original ingredients are consistent with those of the deciduous type, and the disease is considered to be a subtype of the deciduous type.
Other types of acne
proliferative scarring
Erythematous psoriasis
paraneoplastic scarring
pimple-like psoriasis
Drug-induced peptic ulcer
Histopathology and Immunopathology
Acantholysis, epithelial lining (or fissure)
Loose single spiny cells or spiny cells distributed in clusters
Tzanck cells, acne cells or acantholytic cells
Direct immunofluorescence (DIF) examination shows IgG (or C3) deposition between the spiny cells, which is distributed in a network.
According to indirect immunofluorescence (IIF) examination, about 80% of patients have anti-Dsg antibodies in their serum, mostly of the IgG type.
Consistent with direct immunofluorescence display
network deposition
disease management
Glucocorticoids
The drug of choice for treating hemorrhoids
Early application, adequate dosage control, reasonable reduction, and appropriate maintenance
The initial control stage should be "large amount and fast", and the reduction and maintenance stage should be "decrease and avoid impatience".
If no new damage occurs within 1 to 2 weeks of treatment, it indicates that the dose is sufficient. Otherwise, the dose needs to be increased or other immunosuppressants need to be combined.
If the dose of prednisone is high, reduce the original dose by 10% every 1 to 2 weeks.
When the dose is as low as 30 mg/d, the dose reduction should be more cautious and the speed of dose reduction should be slowed down to prevent recurrence of the disease.
When the dose of glucocorticoids is reduced to a very small dose, it can be maintained for a long time. The maintenance dose is prednisone 0.2 mg/(kg · d) or 10 mg/d.
If the condition remains stable, a lower dose can be maintained
immunosuppressant
Patients who do not respond well to glucocorticoids
Patients with diabetes, hypertension, osteoporosis and other diseases
Commonly used first-line immunosuppressants include thiazolopine (AZA) and mycophenolate mofetil (MMF).
Pemphigoid
Autoantibodies are produced against structural proteins in the basement membrane zone at the junction between mucosal epithelium and subepithelial connective tissue (skin epidermis and dermis)
Autoimmune disease characterized by mucosal (skin) tension bleeds and erosions
Mucous membrane pemphigoid (MMP)
Cicatricial psoriasis
benign mucosal leukemia
It is more common in people over 60 years old. The incidence rate in women is twice that of men
target antigen
BP180
BP230
Laminin 332
Laminated eggs from 311
Two subunits of a6 positive integrin
clinical manifestations
Oral mucosa, especially the heel of the teeth, repeatedly scars for several months or years, and does not heal.
low risk type
The damage is limited to the oral mucosa or is accompanied by localized skin damage
High risk type
Damage involving the mucous membranes of any part of the eyes, genitals, esophagus, and throat
Oral mucosa
Any part of the mouth
Gums>Palate>Cheeks
The eroded surface has similar characteristics to the eroded surface of Tianbao.
The heel of the tooth may also be damaged like exfoliation
Nissl's sign, skin peel test, and probe test are generally negative.
Damage to the oral mucosa is less likely to cause scarring. However, if damage occurs to the uvula, soft tissue, cheek, tongue, and pharyngeal arches, scars may appear after healing and may adhere to adjacent tissues to cause deformity.
Eye
65% of patients with mucosal leprosy are accompanied by eye damage
Eye symptoms appear earlier
Simple conjunctivitis with early and persistent damage
recurring damage
Adhesions on the ball of the face
further damage
Facial entropion, trichiasis and corneal damage
skin
Skin lesions are rare
Tension water scars on skin with normal appearance, negative Nissl sign, thick walls and difficult to break; erosion and scab formation after scar breakage.
Other parts
The mucous membranes of the pharynx, larynx, trachea, esophagus, urethra, vulva, and anus are occasionally affected, and local fibrous adhesions can be formed.
Histopathology and Immunopathology
There is a sac or fissure between the epithelium and connective tissue, which is the subepithelial cavity.
The connective tissue is infiltrated by lymphocytes, plasma cells and eosinophils and dilated blood vessels are seen.
direct immunofluorescence
Linear deposits of IgG and/or C3 on the basement membrane
Occasionally lgA, lgM
Indirect immunofluorescence test
IgG can be deposited linearly in the basement membrane zone of the substrate (preferably healthy people's oral or vaginal mucosa as the substrate), but the sensitivity of this test is low, only 10%
paraneoplastic pemphigus
A fatal autoimmune disease associated with tumors
There is no gender predilection. The age of onset ranges from 7 to 76 years old, with an average age of 51 years.
Involves multiple tissues and organs, such as lungs, thyroid, kidneys, smooth muscles, and gastrointestinal tract
Some researchers have also called it paraneoplastic autoimmune multiple organ syndrome (PAMS)
It does not mean that scars and tumors simply coexist, but an autoimmune disease with special autoantibodies in the serum.
The occurrence is closely related to tumors
Especially lymphoproliferative tumors
antigen
Desmoglein Dsg3 and Dsgl
clinical manifestations
In most patients, the skin and mucosal lesions appear after the tumor is discovered, and in some patients, the tumor is not detected until the skin and mucosal lesions appear.
Mucous membrane
Oral mucosal damage is often the first clinical manifestation
Lipstick lesions often appear first
Erosions and thick ascariae often mimic the appearance of erythema multiforme and Sjohn's syndrome
Oral mucosal damage is similar to common pimples, such as large-scale erosion, positive Nissl sign, positive peel test and positive probe test, etc.
skin
Skin damage is often delayed from mucosal damage by days to months
polymorphism
Hematoma-like, hematospermoid-like, erythema multiforme-like, graft-versus-host disease-like and lichen-like skin lesions
Sore-like skin lesions manifest as flaccid lesions, erosions, ascariae, and erythema
Massive scar-like skin lesions manifest as erythema with scales and tense pus on the limbs.
Erythema multiforme-like skin lesions mainly manifest as target-shaped erythema, sometimes even accompanied by refractory erosion
Lichen planus-like skin lesions appear as flat, purple-brown, scaly papules and plaques
Graft-versus-host disease-like skin lesions manifest as scattered dark red scaly papules
Histopathology and Immunopathology
Acantholysis occurs in the epithelium (obvious in the oral mucosa). Fissures or basal cells are located immediately above the basal cell layer. The basal cells at the bottom of the basal cell form a tombstone-like structure.
Necrotic keratinocytes can appear in all layers of the epithelium and skin attachments. If they appear in the acantholysis area, it is an important reminder of paraneoplastic acne.
interface dermatitis
Basal cell layer liquefaction degeneration
Easily visible in oral mucosa), which may coexist with acantholysis or occur alone
Lymphocyte infiltration around the blood vessels in the lamina propria, sometimes with green-like changes
direct immunofluorescence
IgG (or with C3) is deposited between spinous cells, and some patients also have IgG (and/or C3) deposition in the basement membrane zone.
Lichen planus pemphigoid
An autoimmune macroscar skin and mucosal disease that has both typical flat lichen and macroscarlike scarring characteristics in terms of clinical manifestations, histopathology and immunofluorescence examination.
The main target antigen is BP180
clinical manifestations
Oral mucosa
When large tension scars appear on the oral mucosa, small white stripes can be seen in the form of a network. Water scars are scattered and can break down to form ulcers.
skin
Water scars often appear suddenly after an acute attack of generalized lichen planus
The water scar is transparent, the kitchen wall is tense, and Nissl's sign is often negative.
Histopathology and Immunopathology
Fresh-like characteristics of flat moss
Epithelial hyperkeratosis, thickening of the granular layer, irregular thickening or atrophy of the spinous cell layer, vacuolation or liquefaction degeneration of basal cells, band-like infiltration of lymphocytes in the superficial layers of connective tissue, and colloid bodies can be seen
Damage area of phlegm of flat lichen-like skin ulcer
In subepithelial ulcers, moderately dense infiltration of lymphocytes, histiocytes and eosinophils can be seen around the superficial blood vessels of the connective tissue, but the basal cells above them are mostly intact due to no liquefaction degeneration.
direct immunofluorescence
IgG and C3 are deposited linearly in the basement membrane zone in both leprosy and non-lethal lesions.
Linear IgA
An autoimmune macrophage disease characterized by linear lgA deposition in the basement membrane between mucosal epithelium and connective tissue (between the epidermis and dermis of the skin)
It can occur at any age. There are two peak incidences, namely in children as young as 5 years old and in elderly people as old as 60 years old. Females are slightly more common than males.
The most common hemorrhoid-like disease affecting children
Can occur spontaneously or induced by drugs
Vancomycin
Followed by non-anti-inflammatory drugs
The main target antigen is BP180
BP230 is also a target antigen for linear IgA disease
clinical manifestations
adult linear lgA disease
The specificity is not high and it is difficult to distinguish it from other subepidermal macroscopic diseases.
Skin lesions are mostly generalized and polymorphic
Erythema, papules, tension scars or large pimples, annular, sausage-like and bead-like erythematous rashes have certain characteristics.
Negative Nissl sign
May only cause oral damage without skin damage
linear lgA disease in children
Most of the disease occurs in preschool years, with an acute onset, periodic attacks and remissions, and a self-limiting course.
Skin lesions are widely distributed and symmetrical
Commonly seen around the mouth, extended sides of limbs, groin and vulva
Tension hydromas appears on normal skin or erythema, negative Nissl sign, accompanied by varying degrees of pain and itching
May be accompanied by mucosal damage, manifested as oral mucosal erosion, nasal congestion and bleeding, and conjunctivitis
Histopathology and Immunopathology
Mucosal epithelium/skin subepidermis
Eosinophilic infiltration may be seen in some cases
More neutrophil infiltration and micro-abscess formation can be seen in some parts
direct immunofluorescence
Uniform linear deposition of lgA on the skin or mucosal basement membrane, sometimes accompanied by deposition of IgG and C3
disease management
Ammonia maple
If the effect is not good, low-dose prednisone can be used in combination
Patients with mucosal damage can also be treated with local glucocorticoids
zebra disease
Oral flat lichen
Common chronic inflammatory diseases of oral mucosa
The most common oral mucosal disease after recurrent aphthous ulcer
Etiology and pathogenesis
immune factors
There are a large number of T lymphocytes infiltrating in the epithelial lamina propria in a dense band-like manner.
mental factors
history of trauma
endocrine factors
Middle-aged women have a higher incidence of OLP
Infectious factors
Viral infection may be one of the causative factors
Microcirculatory disorders factors
Microcirculation disorders and hyperviscosity are related to OLP
There are inclusion bodies within the lesion
genetic factors
The disease has been found in several people in a family; some patients have a family history
other
Diabetes, hepatitis, hypertension, digestive tract disorders
clinical manifestations
Small papules connected into linear white and gray-white patterns
Wickham striae similar to skin lesions
The lesions are mostly symmetrical
Cheeks are most common
The mucosa in the lesion area may be normal, or may suffer from congestion, erosion, ulcers, atrophy, and water scars, etc.
After subsidence, pigmentation may remain on the mucosa
Consciously, the mucous membranes are rough, woody, burning, dry mouth, and occasionally crawling insects and itching.
When irritated by spicy, hot, sour, or salty food, the affected area may become sensitive and burn.
1. According to the morphological characteristics of the lesion
Reticulated type
Thousands of pairs of cheeks are common
plaque type
It mostly occurs on the back of the tongue and is slightly light blue.
atrophic
Water scar type
erosion type
Papular type
Characteristics of OLP lesions in different parts of the oral mucosa
Tongue
Often manifests as atrophic and plaque type
lips
Red lips are more common on the lower lip, mostly with mesh or ring-shaped white stripes
Heel
Atrophic and erosive type is common
palate
Relatively rare, the lesions are often located near the heel edge of the hard bone
(2) Skin lesions
Flat polygonal papules, purple-red in color, with thin scales on the surface and a waxy sheen
(3) Finger (toe) nail lesions
It is often symmetrical, but it is rare for patients to have ten finger (toe) nails affected at the same time. The nail body becomes thin and dull, and there are dents when pressed.
Histopathology and Immunopathology
Well-demarcated lymphocyte-predominant band-like inflammatory cell infiltrate, limited to the superficial layers of connective tissue
Basal cell liquefaction degeneration occurs
No epithelial dysplasia
Mitochondria and rough endoplasmic reticulum swell in basal cells, and vacuoles appear in the cytoplasm.
Degeneration and degeneration of desmosomes between basal cells and hemidesmosomes between basal cells and the basement membrane, proliferation, degeneration, and destruction of basal cells
There are immunoglobulin deposits in the epithelial basement membrane area, mainly lgM, and there may also be deposits of colloid bodies of lgG and C3.
Direct immunofluorescence method shows fine granular fluorescence, forming a fluffy fluorescent band along the basement membrane area.
Differential diagnosis
Oral lichen-like lesions
Drugs that cause drug-induced liver damage
Methyldopa, Clovax, Captopril
contact lichen-like lesions
After oral treatment, radial white stripes or white patches appear on the oral mucosa corresponding to the filling and restoration materials, similar to OLP-like lesions.
graft-versus-host reaction liver-like lesions
patients after bone marrow transplant
At present, the differential diagnosis of OLP and OLL is mainly based on clinical criteria and histopathological criteria.
Oral leukoplakia
Plaque OLP and leukoplakia are sometimes difficult to differentiate, especially lesions on the back of the tongue
Histopathological examination is of great significance in the identification of
Oral erythema
Mixed oral erythema is easily confused
Diagnosis often relies on histopathological examination
Vulgaris, mucous membrane scabies
Lacks distinct white stripes
erythema multiforme
Erythema multiforme appears on the skin. There is a small puddle in the center of the erythema. The appearance of the lesion looks like an "iris" or a "target ring".
disease management
topical treatment
Glucocorticoids: 0.05% azolone acetate and 0.05% clobetasol gel are highly safe and effective when applied locally.
Injection into the base of the lesion area has a good effect on erosion and ulcer type
Vitamin A acid
Suitable for patients with lesions with high degree of keratinization
antifungal drugs
For OLP that does not heal, attention should be paid to the possibility of Candida albicans infection
systemic treatment
Glucocorticoids
For acute large-area or multifocal erosive OLP, low-dose, short-course treatment regimens may be carefully considered.
Oral prednisone
immunosuppressant
Hydroxychloroquine
The more common adverse reactions include dizziness, nausea, vomiting, reduced visual field, retinopathy, tinnitus, and leukopenia. The rare serious toxic reactions include arrhythmia, cardiac arrest, and cardiogenic cerebral ischemic syndrome. Failure to rescue in time can lead to death
Thiopsin or cyclophosphamide
For individual stubborn cases that are not sensitive to glucocorticoids
immune booster
Thymosin enteric-coated tablets and transfer factors, etc.
Antioxidants
B-carotene
Vitamin E
Effective in treating OLP lesions and relieving pain
Chinese patent medicine
Tripterygium wilfordii
Strong anti-inflammatory effect
other
White peony root
Has anti-inflammatory and immunomodulatory properties
discoid lupus erythematosus
Chronic skin-mucosal connective tissue diseases
The lesions are characterized by persistent erythema with a central atrophied and concave disk shape.
Causes and pathogenesis
autoimmune disease
It is related to many factors such as ultraviolet radiation, trauma, infection, and drugs.
UV exposure, trauma
Infectious factors
other factors
certain drugs
Chloropropyl chloride, chloropropyl chloride, isopropyl chloride, penicillamine, etc.
certain foods
clover sprouts
Cold stimulation, mental stress
Histopathology and Immunopathology
Epithelial hyperkeratosis or hypokeratosis
The cornified layer may be exfoliated and the granular layer may be obvious
Cuticle plugs are sometimes seen in skin lesions
Atrophy and thinning of the spinous layer
Sometimes, epithelial nail process proliferation and elongation can also be seen
Significant liquefaction and degeneration of the basal cell layer
Fissures and small sores may form between the epithelium and the lamina propria, and the basement membrane is not clear.
The telangiectasia of the lamina propria are dilated, and hyaline thrombus can be seen in the blood vessels.
There are dense lymphocytes (mainly T cells) around blood vessels
(PAS) dyed red
Hyalinization, edema, and fracture of collagen fibers in connective tissue
direct immunofluorescence
There is a continuous green fluorescent band with uneven thickness in the basement membrane area, which is called the "lupus band"
clinical manifestations
Localized damage is limited to the skin and mucous membranes above the neck
The disseminated type can involve parts below the neck, such as the upper chest, arms, dorsums of hands and feet, and extensions, etc.
Higher odds of transition to SLE
Mucosal damage
Round or oval erythematous erosions are concave and disk-shaped, with slightly raised edges. There is redness or telangiectasia around the redness, and there are short white streaks arranged radially around the redness.
The vermilion mucosa of the lower lip is a common site for DLE
The boundary between lipstick and skin disappears, which is a characteristic manifestation of DLE lesions
Lesions are often asymmetrical
The typical lesions are surrounded by radiating thin short white lines.
skin damage
Good hair, face and other exposed parts
It initially appears as a rash, appearing as long-lasting round or irregular red spots, slightly raised, with clear borders, covered with telangiectasia and gray-brown adherent scales on the surface.
The scales look like "thumbtacks", that is, "keratin plugs"
Differential diagnosis
systemic lupus erythematosus
Compared with discoid lupus erythematosus, the diagnosis of SLE requires a combination of clinical diagnostic criteria and immunological criteria
clinical diagnostic criteria
Tremorous erythema, discoid erythema of the skin, oral or nasopharyngeal ulcers, non-scarring alopecia, synovitis, serositis, kidney damage, nervous system damage, blood system damage, etc.
immunological standards
Antinuclear antibody positive, ds-DNA antibody positive, Sm antibody positive, phospholipid antibody positive, low complement, etc.
flat moss
The skin lesions of lichen planus are symmetrical and occur on the extensor sides of the limbs or the trunk.
Light purple polygonal flat papules, the patient feels strong itching
Oral mucosal lesions are irregularly shaped self-colored stripes or plaques, and the lesions on the vermilion area will not exceed the vermilion border.
disease management
Try to avoid or reduce sunlight exposure
For non-erosive lesions on the lipstick area, 5% zinc dioxide ointment, 5% para-aminobenzoic anhydride, zinc oxide paste, etc. can be applied for shading.
Avoid cold stimulation
2. Local treatment
Topical corticosteroids
For extensive erosive damage, ultrasonic atomization treatment can be supplemented
For focal congestion and erosion, local sealing therapy with glucocorticoids may also be considered.
Various intraoral preparations containing glucocorticoids, antibiotics, local anesthetics, traditional Chinese medicine, etc. can be applied to the intraoral mucosal lesions.
When there are blood or pus ascarids on the lower lip, first wet compress with 0.2% pyrancillin solution, remove the ascaris skin, and then apply a topical glucocorticoid preparation
Immunosuppressants such as cyclosporin and tacrolimus
systemic treatment
Hydroxychloroquine
First-line drugs for treating DLE
Less toxic and side effects than chloroquine
Tripterygium wilfordii and Kunmingshan crabapple
Glucocorticoids
When the effects of chlorine and tripterygium wilfordii are not obvious
thalidomide
It is used for refractory or relapsed and worsening DLE that is ineffective in conventional treatments such as clofenac and glucocorticoids.
Oral leukoplakia
Occurrence of predominantly white lesions on the oral mucosa that cannot be wiped off and cannot be clinically and histopathologically diagnosed as other definable lesions
Cause
Tobacco and other physical and chemical irritants
ethanol
tobacco
Local irritating factors such as cheek-biting habits, misaligned teeth, sharp edges formed by uneven wear of teeth, residual roots and crowns, dental calculus, etc., can all irritate the oral mucosa and are related to the occurrence of oral leukoplakia.
Candida infection
human papillomavirus infection
systemic factors
trace elements
microcirculatory changes
genetic susceptibility
fat-soluble vitamin deficiency
diagnosis
The diagnosis of oral leukoplakia requires a comprehensive judgment based on clinical and pathological manifestations.
Diagnostic certainty (certainty, C) can be divided into the following four levels
disease management
health education
Remove irritants
medical treatement
Vitamin A
Vitamin A acids
It is forbidden for pregnant women and should be used with caution by women of childbearing age.
Systemic application has serious side effects
Topical preparations for the treatment of oral leukoplakia
�Carotene
other
Lycopene
Vitamin E
Surgical treatment
Homogeneous oral leukoplakia in the danger zone as well as caressing, granular and ulcerative forms of oral leukoplakia
Physiotherapy
Photodynamic therapy, laser therapy, cryotherapy, etc.
Traditional Chinese Medicine Treatment
Regular follow-up
White spongy spots
Also known as white folded disease (soft leukoplakia), white fold mucosal hyperplasia of the family
clinical manifestations
Commonly occurs in the mucosa of the cheeks, floor of the mouth and tongue
Gray-white water-like wrinkles or grooves, with a special pearlescent color
The folds can sometimes be scraped or peeled off. It is painless and does not bleed when peeled off. The underlying surface is smooth and similar to normal epithelium.
The same lesions can also occur in mucous membranes other than the oral mucosa, such as the nasal cavity, vulva, anus, etc.
family genetic history
Histopathology
The epithelium is significantly thickened, with incomplete keratinocytes on the surface
The spine cells enlarge and the layers increase, sometimes reaching more than 40 to 50 layers.
Vacuolar degeneration of acanthocytes, pyknosis or disappearance of nuclei
Increased basal cells but well differentiated
There is a small amount of inflammatory cell infiltration in the connective tissue
Under the electron microscope, a large number of Odland bodies were found in the cells.
In this disease, there are insufficient Odland bodies between cells and an increase in desmosomes in the lesion area, which may be the reason for the accumulation of cells on the epithelial surface and the spongy appearance.
disease management
The disease does not require treatment when it is asymptomatic. Oral retinoic acid has a certain effect during treatment
Oral leukokeratosis
Also known as oral leukokeratosis, benign hyperkeratosis, and anterior leukoplakia.
Local white keratinized plaques or patches on the oral mucosa caused by long-term mechanical or chemical stimulation.
Cause
Prolonged mechanical or chemical irritation
Residual roots, residual crowns, and sharp edges of maxillary and mandibular posterior teeth
Malocclusion
Bad restoration
smoking
After the irritating factors are removed, the lesions can gradually become thinner or disappear
clinical manifestations
Most common on cheeks, lips, and tongue
It is a grey-white or milky-white patch or patch with ill-defined boundaries, not higher than or slightly higher than the mucosal surface, with a smooth surface and a soft base without nodules.
There is no obvious change in the texture and elasticity of the mucosa in the leukokeratosis area.
Nicotinic (nicotine) leukokeratosis
Occurs in the mucosa of the hard cheeks and the heels of the teeth, and is diffusely distributed as gray-white or milky-white lesions with scattered red dots, mostly caused by long-term smoking.
The red dots on it are the openings of the parotid glands
Nicotinic (nicotine) stomatitis
Patients may have subjective symptoms such as dryness and roughness
Histopathology
Epithelial hyperkeratosis or partial parakeratosis
The epithelial layer is slightly thickened, the spinous layer is thickened or not, the epithelial nails are elongated, the basal layer cells are normal, the basement membrane is clear and complete, and there is no inflammatory cell infiltration or a small amount of plasma cell and lymphocyte infiltration in the lamina propria.
diagnosis
Local molar-colored or gray-white plaques and patches on the oral mucosa. The patient has a long-term smoking history or bad restorations (such as unqualified clasps, rough and overly long base edges), residual roots, and residual parts are found in the corresponding areas. The diagnosis can be made by looking at the sharp edges of crowns, caries or tooth fractures, and excessively steep cusps. Usually 2 to 4 weeks after the stimulation is removed, the white lesions become lighter in color, significantly reduced in scope, or even disappear. Perform tissue biopsy on suspected cases and pathological examination to confirm diagnosis.
Differential diagnosis
disease management
Remove irritating factors and observe; for severe keratosis, topical retinoic acid preparations can be used
Oral erythema
Also known as proliferative erythema, red proliferative lesion
Also called Quelett's erythema
Bright red patches on the oral mucosa, velvet-like, with clear borders, which cannot be diagnosed as other diseases clinically and pathologically
Potentially malignant disease
Cause
clinical manifestations
More common among middle-aged patients, slightly more men than women
The margin of the tongue is the most common, followed by the calcaneus, buccal groove, floor of the mouth, tongue belly, and apex.
three types
Homogeneous erythema
Velvet-like bright red surface, smooth and shiny, resembling "loss of epithelium"
intermittent erythema
There are scattered white spots in the erythema lesion area, red and white.
Difficult to distinguish from flat moss
granular erythema
There are tiny granular nodules in the erythema lesion area, which are like mulberry-like or granular granulations, slightly higher than the mucosal surface, and the tiny nodules are red or white.
This type is often carcinoma in situ or early squamous cell carcinoma
Histopathology
Epithelial parakeratosis or mixed keratosis
Epithelial atrophy, extremely thin or even absent cornified layer
The epithelial nail process increases and elongates
The spiny cells in the papillary area between the nail processes atrophy and become thinner, bringing the papillary layer very close to the epithelial surface.
The capillaries in the connective tissue papilla are significantly expanded, so the lesions appear bright red.
The mechanism of granule formation is that the surface of the enlarged nail process forms a depression, and the high-protruding connective tissue papilla forms red granules.
Abnormal epithelial proliferation, disordered cell arrangement, loss of polarity, varying cell shapes and sizes, large and deeply stained nuclei, increased mitotic figures, etc.
Sometimes keratinized beads can be seen forming
There is obvious infiltration of inflammatory cells in the lamina propria, mainly lymphocytes and plasma cells
Granular erythema is mostly carcinoma in situ or early invasive cancer that has protruded from the basement membrane.
diagnosis
The formal diagnostic procedure is to remove possible traumatic factors such as sharp cusps and restorations and observe them for 2 weeks. If the lesion does not improve significantly, biopsy of the lesion is performed to confirm the diagnosis and rule out malignant transformation.
Biopsy to determine the malignancy of the lesion
Oral mucosa autofluorescence
Lesions show loss of autofluorescence
Indicates the malignant tendency of the lesion
Oral mucosal biopsy staining (such as toluidine blue staining)
Positive toluidine blue staining indicates the malignant tendency of the lesion.
disease management
Once oral erythema is diagnosed, radical surgery should be performed immediately
Surgical resection is more reliable in clinical efficacy than cryotherapy
Oral submucosal fibrosis
Oral submucosal fibrosis (OSF) is a chronic oral disease that can affect any part of the oral cavity.
The occurrence of this disease is closely related to chewing palm coconuts
Cause
chewing palm
stimulus
Factors such as eating chili peppers, smoking, and drinking alcohol can aggravate submucosal fibrosis.
lack of nutritional factors
Deficiency of vitamins A, B and C, low serum iron and selenium and high serum zinc and copper
immune factors
It may be related to allergic reactions caused by exogenous antigen stimulation such as palm alkaloids
genetic factors
other factors
Some patients have microcirculatory disorders and blood rheology abnormalities, etc.
clinical manifestations
Whitening of the oral mucosa with leathery texture changes
The common symptom is a burning sensation in the oral mucosa, especially when eating spicy food.
Symptoms such as dry mouth, loss of taste, numbness of the lips and tongue, mucous membrane swelling, and ulcers may also occur.
The mucous membranes of the cheeks, soft cheeks, lips, tongue, pterygomandibular ligament, and dental limits can all be affected. Cheeks often occur symmetrically, with pale buccal mucosa and vertical fibrous cords.
Histopathology
Epithelial atrophy, accumulation and degeneration of collagen fibers in the mucosal lamina propria and submucosa, and vascular occlusion and reduction, etc.
In the early stage, some small collagen fibers appear under the epithelium with edema.
Blood vessels may be dilated and congested, with neutrophil infiltration.
Then a hyaline degeneration band of collagen fibers appears below the epithelium, and the collagen fibers below it are edematous and have lymphocyte infiltration.
In the middle stage, hyaline degeneration of collagen fibers gradually worsens, with infiltration of lymphocytes and plasma cells.
In the late stage, all collagen fibers become hyaline-like, the structure completely disappears, and the refractive index is strong. narrowing or occlusion of blood vessels
disease management
health education
Remove causative factors
medical treatement
Including anti-inflammation, anti-fibrosis, improvement of ischemic state and antioxidant, etc.
Glucocorticoids
Short-acting glucocorticoids (hydrocortisone), intermediate-acting glucocorticoids (triamcinolone acetonide), and long-acting glucocorticoids (betamethasone and dexamethasone) can all be used to control OSF.
Antifibrotic drugs and proteolytic enzymes
Hyaluronidase is often used in combination with hormones
peripheral vasodilators
Mainly include pentoxifylline, buflodil, bufenin hydrochloride and isoxurin, etc.
Antioxidants and nutrients
The most commonly used antioxidant at present is lycopene
Vitamins A, B, C, D, E
hyperbaric oxygen therapy
Chinese medicine treatment
The main medicines are Salvia miltiorrhiza, Scrophulariaceae, Angelica sinensis, Radix Rehmanniae, Astragalus, Safflower, etc.
Granuloma
orofacial granulomatous disease
Rare idiopathic granulomatous disease localized to facial tissues
Mainly manifests in the oral cavity and face, similar to the orofacial manifestations of sarcoidosis and Crohn's disease, except for systemic granulomatous diseases (such as Crohn's disease, sarcoidosis, leprosy, tuberculosis, deep fungal infections wait)
May-Lo syndrome
granulomatous cheilitis
Etiology and pathogenesis
genetic factors
Infectious factors
Allergy factors
clinical manifestations
Swollen lips, cheeks, heels, tongue, etc., oral mucosa thickening, tooth heel hyperplasia, and nodules forming under the mucosa
lip
It often occurs on the upper lip or lower lip alone, but it can also occur on both lips, but it is rare.
Sometimes the swelling gives the lip a lobed appearance. Lips and surrounding skin may appear red or dark red
oral cavity
The buccal mucosa is swollen and proliferated, showing lobulation or thickening. The thickened mucosa can easily be bitten and form traumatic ulcers.
The heel tissue can be extensively proliferated and swollen, and the surface may be smooth or have small nodules.
face
The swelling is mostly in the lower half, with a few visible swellings in the eyes, face, cheeks, and nose.
Swelling can be persistent or temporary
In addition to neurological symptoms, there are rarely other systemic symptoms
Facial nerve paralysis often occurs before facial swelling
Histopathology
noncaseating necrotizing granuloma
Histiocytes and lymphocytes form focal nodules, with blood vessels passing through the center of the granuloma.
When the lesions are atypical, the tissue is edematous and lymphocytes may diffusely infiltrate.
diagnosis
noncaseating necrotizing granuloma
Crohn's disease
A chronic recurrent granulomatous inflammation of the gastrointestinal mucosa
All segments of the digestive tract from the mouth to the anus can be affected
The terminal ileum and adjacent colon are most commonly affected
Also known as Crohn's disease, Crohn's disease
The main symptoms are abdominal pain, diarrhea, and intestinal obstruction, and there are extraintestinal manifestations such as fever and nutritional disorders.
Etiology and pathogenesis
genetic factors
immune factors
Infectious factors
other
mental factors
abdominal trauma
envirnmental factor
clinical manifestations
CD starts slowly and progresses gradually, usually lasting several years.
Systemic manifestations
There are systemic symptoms such as low fever, fatigue, and weight loss in the afternoon. Anemia may also be caused by malabsorption of iron, vitamin B12, and folic acid due to lesions and dysfunction of the digestive tract.
Gastrointestinal manifestations
The patient had recurrent abdominal distension, abdominal pain, abdominal masses, increased stool frequency, and paroxysmal cramps, diarrhea, and bloody and purulent stools in the right lower abdomen.
In the late stage, intestinal obstruction or even intestinal perforation may occur, resulting in severe abdominal pain, bloating, vomiting, constipation, etc.
Oral manifestations
Oral lesions occur in about 10% of cases
Formation of linear or aphthous ulcers
Linear ulcers are like knife incisions with raised edges, rather like ulcers caused by irritation on the edge of a dental tray
Granulomas, small nodules and heel hyperplasia may also form
Oral mucosa may also undergo cord-like hyperplasia, folds, granular, and gravel-like nodular hyperplasia.
The lips may become diffusely swollen and indurated
The heel of the tooth may also appear visibly red and granular on the surface.
Other extraintestinal manifestations
Other lesions outside the digestive tract may include osteoarthritis, spondylitis, uveitis, skin erythematous nodules, pyoderma gangrenosum, etc. Disorders of intestinal function may also lead to disorders of uric acid metabolism and the formation of kidney stones.
Histopathology
Noncaseating epithelioid cell granuloma with lymphocyte and plasma cell infiltration
Intestinal lesions include intestinal edema, muscle layer thickening and granuloma formation, and cause intestinal stenosis
Auxiliary inspection
laboratory tests
Intestinal barium angiography
CT examination
MRI examination
Ultrasonography
endoscopy
sarcoidosis
Sarcoidosis is a systemic granulomatous disease that affects multiple systems and organs.
Almost every organ in the body can be affected
self-limiting disease
Clinically, more than 90% have lung changes
It is more common among young and middle-aged people, but children and the elderly can also suffer from it.
clinical manifestations
Oral manifestations
It often occurs on the lips, cheeks, cheeks, teeth and heels, head and neck lymph nodes, jaws, salivary glands, etc.
The lip tissue thickens and swells, forming a giant lip. The skin in the swollen area is dark red, and nodules can be palpated, with a hard feeling.
Nodular swelling may also occur on the cheeks
Mucosal hyperplasia without conscious symptoms may also occur in the parotid mucosa.
Granulomatous lesions in the alveolar bone can also cause bone destruction and loose teeth.
Parotid glands are often affected bilaterally
Palpable induration, painless, with symptoms of dry mouth
Manifestations of extraoral tissue and organ involvement
All systems of the body can be affected, with the lungs most commonly affected, followed by the eyes, skin, and lymph nodes.
Patients may have a cough or be asymptomatic, and in severe cases may develop pulmonary insufficiency.
Eye diseases include chronic iridocyclitis and uveitis
The liver and spleen are enlarged, and organs such as the heart and kidneys are also damaged.
When the nervous system is invaded, paralysis occurs, mostly in the facial nerve.
Skin lesions often appear as dark red papules, nodules or erythema nodosum, distributed on the face and limbs
The course of the disease is slow, and it may gradually subside over several months or years, leaving behind pigmented spots.
Chronic swelling of cervical lymph nodes is a common symptom of sarcoidosis. The swollen lymph nodes have no adhesions, fluctuations, and no history of inflammation.
Histopathology and Immunopathology
Epithelioid cell nodules can be seen under the microscope, in which there are many epithelioid cells, few or no giant cells, and few lymphocytes.
There are small blood vessels in the nodule, and there is no caseation in the center, which is different from tuberculosis nodules.
Reticular fiber staining reveals a large number of argyrophilic reticular fiber frameworks
Star-shaped bodies, which are star-like inclusions contained within giant cells, are occasionally seen within granulomas.
Visible Schumann body
Round or oval body with lamellar calcification on the periphery, dark blue in HE staining
Immunofluorescence examination shows immunoglobulin deposition, mainly IgG, in the granulomas.
granulomatosis with polyangiitis
Diseases of the lips and tongue
Cheilitis
Glandular cheilitis
Cheilitis characterized by hyperplasia and hypertrophy of labial glands, swelling of the lower lip, or occasionally swelling of the upper and lower lips at the same time
Etiology and pathogenesis
autosomal dominant inheritance
Toothpaste or mouthwash containing allergenic substances, trauma, smoking, poor oral hygiene, bad mood, periapical lesions, excessive ultraviolet exposure
Histopathology
Characterized by marked hyperplasia of small glands
Hypertrophic and dilated labial gland ducts
Periductal inflammatory cell infiltration in glands and lobules
Eosinophilic material in the duct
Mucosal epithelial cells have mild intracellular edema
Ectopic mucus glands are seen in the submucosa
In purulent cheilitis glandularis, small abscess formation can be seen in the subepithelial connective tissue.
clinical manifestations
Good luck in middle age
simple glandular cheilitis
The most common type
Infiltrative hypertrophy of the lips, which can be several times thicker than normal
There is obvious swelling
Small nodules of varying sizes can be rubbed
On the mucosal surface of the lips, small salivary gland duct openings as large as needles can be seen arranged like sieve holes. The center is sunken and the center is expanded. Transparent mucus is discharged from the duct opening. When the lips are squeezed, more mucus is seen in the shape of dewdrops.
Sticky lipstick on upper and lower lips
When awake, it becomes thin and light white and becomes sticky due to dryness.
Superficial suppurative cheilitis glandularis
Baelz disease
Caused by simple secondary infection
Superficial ulcers and scabs on the lips
Purulent secretions accumulate under the scab. After removal of the ascariae, the red moist base is exposed, and purulent fluid can be discharged from the gland opening when squeezed.
Deep suppurative cheilitis glandularis
Simple or superficial suppurative abscesses are caused by repeated abscesses that cause deep infection. Deep mucus glands suppurate and develop ducts. If they do not heal for a long time, cancer may occur. This is a serious form of glandular cheilitis.
The lips gradually become diffusely thickened and enlarged.
benign lymphoproliferative cheilitis
Based on localized damage, recurrent severe itching, discharge of light yellow mucus and ascariasis
granulomatous cheilitis
noncaseating epithelioid granuloma
Based on the typical symptoms of diffuse and repeated swelling of the lips, we found a mattress feeling, a history of recurring attacks, and irreversible swelling and lesions.
It mainly uses corticosteroids to partially seal the lesion, plus systemic treatments such as anti-inflammatory and anti-allergic treatments.
Local injection of adrenocortical hormone drugs can be used in the swollen area of the lip
actinic cheilitis
clinical manifestations
acute actinic cheilitis
The onset is sudden, often preceded by a history of exposure to the sun
Extensive edema, congestion, and erosion in the lipstick area
The surface is covered with yellow-brown blood ascarids or ulcers are formed, with obvious burning sensation and severe itching.
If there is secondary infection, purulent secretions may appear, forming pus ascarids, and the pain will worsen.
Deep lesions may leave scars after healing
chronic actinic cheilitis
Desquamative cheilitis
Insidious onset or evolution from acute
In the early stage, the lower lip is dry and has no secretions, and small, molten-colored scales appear constantly, varying in thickness and easy to peel off. New scales will appear after the scales fall off.
If it does not heal for a long time, localized lipstick, mucosal thickening, and hyperkeratosis may occur.
Infiltrating milky white patches, called actinic leukoplakia, eventually develop into caressing nodules, which can easily evolve into squamous cell carcinoma
The patient does not feel obvious pain and itching, but often uses his tongue to touch his lips due to dryness and discomfort.
Causes perioral band dermatitis 1 to 2 cm wide around the mouth, resulting in depigmentation and lightening of the perioral skin, accompanied by gray-white keratinized streaks and swelling.
disease management
Diagnosis and treatment as early as possible
Immediately reduce UV exposure, stop using suspicious drugs and foods, and treat other diseases that affect leaf metabolism.
topical treatment
Sunscreens that absorb, reflect and block light
3% Hydroxychloroquine Ointment
5% Chin Dioxide Ointment
Wet compress with anti-infective solution or mouthwash
Remove the tapeworm membrane and keep it dry and clean
For dry and desquamated patients, retinoic acid, hormones or antibiotic ointments can be applied topically.
systemic treatment
Hydroxychloroquine sulfate
Nicotinamide
para-aminobenzoic acid
Vitamin B complex
physical therapy
Carbon dioxide laser irradiation, cryotherapy, photodynamic therapy, etc.
Surgical treatment
Patients who are suspected of being cancerous or already have cancer should undergo surgery as soon as possible, but attention should be paid to the repair of the vermilion resection margin.
prevention
Avoid sun exposure as much as possible.
5% quinine light-protecting ointment
allergic cheilitis
chronic nonspecific cheilitis
also known as chronic cheilitis
It cannot be classified into the aforementioned cheilitis with special pathological changes or causes. The course of the disease is prolonged and recurring.
Etiology and pathogenesis
The cause is unknown. May be related to long-term and sustained stimulation by temperature, chemical, and mechanical factors
Histopathology
non-specific inflammatory manifestations
Normal arrangement of intraepithelial cells or edema
Infiltration of lymphocytes and plasma cells in the lamina propria, dilation and congestion of blood vessels
The mucosal epithelium may have parakeratosis or hyperkeratosis, or may have exfoliative defects.
clinical manifestations
chronic desquamative cheilitis
Women before 30 years old
It often affects the vermilion area of the upper and lower lips, but is more severe on the lower lip.
Lipstick is dry and cracked, with yellowish or brown scaling
In mild cases, there is single layer of scattered desquamation.
In severe cases, the scales overlap and form dense sheets.
The skin scales can be easily and painlessly torn off, exposing the bright red "skinless" tissue underneath the scales.
Have secondary infection
Mild edema and congestion, local swelling, itching, stinging or burning pain
The condition relapses and can last for months or even years without recovery.
chronic erosive cheilitis
Repeated erosion of the upper and lower lip vermilion, obvious oozing, and peeling of scabs
Thin yellow ascarids will form when there is inflammatory exudation, blood will coagulate when there is bleeding, and pus will form when there is secondary infection.
Ascaris peels off and forms a bleeding wound, causing burning pain or swelling and itching.
Patients often bite their lips, chew their tongues or rub their hands unconsciously, causing the lesion to become cracked, the pain to worsen, and the oozing to become more obvious.
Ascaris on top of ascarids
Swelling or chronic mild hyperplasia of the vermilion area, swollen submandibular lymph nodes
diagnosis
Lipstick is repeatedly dry, desquamated, painful, itchy, oozing and crusted
diagnosis
Depending on the course of the disease, it may be mild or severe, and is more likely to occur in cold and dry seasons.
Differential diagnosis
Sjogren's syndrome
Cheilitis caused by diabetes
chronic actinic cheilitis
Differentiation of Candida cheilitis
disease management
Avoiding irritants is the primary treatment measure
For example, change bad habits such as lip biting and lip caress, quit smoking and drinking, avoid spicy food, avoid wind and cold stimulation, and keep lips moist, etc.
Chronic desquamative cheilitis requires lip moisturizing
Angular stomatitis
Also known as cheilitis of the corners of the mouth and erosion of the corners of the mouth
The main symptoms are fissures, erosions at the corners of the mouth and ascariasis.
A general term for inflammation of the corners of the mouth at the junction of the upper and lower lips
dystrophic angular stomatitis
Those who have been deficient in vitamin B2 (riboflavin) for 1 year
Based on the clinical manifestations of non-specific inflammation in the corner of the mouth combined with other symptoms such as tongue, lip lesions and systemic symptoms
infectious angular stomatitis
Etiology and pathogenesis
Caused by pathogenic microorganisms such as fungi, bacteria, and viruses
Candida, Streptococcus and Staphylococcus aureus
Too many teeth are missing or the entire mouth is severely worn
Patients suffering from long-term chronic diseases or weak constitution after radiotherapy or chemotherapy
Candida
scarlet fever in children
Herpes virus infection, Treponema pallidum infection, HIV infection
clinical manifestations
In the acute stage, the corners of the mouth are congested, red and swollen, with bloody or purulent secretions exuding, layers of dirty blood or pus, and obvious pain.
In the chronic stage, the skin and mucous membranes at the corners of the mouth are thickened and gray-white, accompanied by small horizontal lines or radial cracks, and the lips are red and cracked, but the pain is not obvious.
There are also other corresponding symptoms of primary diseases such as scarlet fever, rash, syphilis, and AIDS.
diagnosis
Based on the clinical manifestations of inflammation in the corner of the mouth and the results of microbiological examinations such as bacterial culture and candida direct microscopy
Fungal angular cheilitis often occurs simultaneously with fungal cheilitis
disease management
Targeted at different pathogenic microorganisms that cause infectious angular stomatitis, local treatment is mainly used
Fungal angular stomatitis can be treated with 2% sodium bicarbonate solution wet compress
Bacterial infectious angular stomatitis can be treated with chlorhexidine solution as a wet compress
Topical chlorhexidine solution can be used for eruptive angular stomatitis
Measures should be taken to eliminate the adverse environment that causes infectious angular stomatitis
Traumatic angular stomatitis
Etiology and pathogenesis
Caused by iatrogenic trauma to the corner of the mouth, severe physical stimulation or certain bad habits
clinical manifestations
Unilateral damage to the corners of the mouth, fresh wounds of varying lengths
Cracks often have bleeding and bloody worms
Old wounds may have ascariae, edema, and erosion.
Those caused by trauma may be accompanied by local tissue edema and subcutaneous congestion.
diagnosis
Clear history of trauma or prolonged oral treatment experience
disease management
Mainly local treatment
Use anti-inflammatory solutions such as compound acid solution, hydrogen peroxide solution, normal saline, ethanol solution, and chlorhexidine solution for local flushing or wet compress. After flushing and wet compress, apply povidone analgesic locally.
Tongue disease
lingual papillitis
Etiology and pathogenesis
Local factors include sharp tooth tips, dental calculus, poor restorations, irritation such as eating spicy or hot food, and pharyngeal infection
Systemic factors include malnutrition, anemia, blood diseases, fungal infections, abuse of antibiotics, endocrine disorders, vitamin deficiency, etc.
geographical tongue
Superficial non-infectious tongue inflammation
clinical manifestations
It usually occurs on the back, tip and edge of the tongue. The lesions are mostly in the front 2/3 of the tongue and generally do not cross the lambdoid groove.
The central area shows filiform papillary atrophy and exfoliation-like appearance, and the mucosal surface is smooth, congested, red, and slightly concave.
The peripheral area shows thickening of the filiform papillae, which is distributed in the shape of yellow strips or arcs, about several millimeters wide, and forms a clear boundary with the surrounding normal mucosa.
Histopathology
non-specific inflammatory manifestations
Divided into atrophic zone and marginal zone
Intraepithelial spinous cell degeneration and edema, with microabscess formation similar to psoriasis
grooved tongue
cerebriform tongue or wrinkled tongue
The cause is unknown and may be related to age, viral infection, delayed allergic reactions, systemic diseases, genetics
clinical manifestations
The shape is like gyri, leaf veins or branches, and can also occur on the lateral edge of the tongue
The mucosa at the bottom of the sulcus is continuous and complete, with no bleeding
The filiform papillae at the bottom of the sulcus are absent, and the filiform papillae at the lateral walls of the sulcus are sparse.
It may worsen with age, but progresses slowly
Often no symptoms
hairy tongue
Median rhomboid glossitis
Lingual tonsil hypertrophy
Benign proliferative changes. The incidence rate is higher in women than in men.
Nodular bulges appear on one or both sides of the base of the tongue, which are dark red or light red and soft in texture.
Several lymphoid follicles are formed in the lamina propria and submucosa of the mucosa.
burning mouth syndrome
The tongue is the main site of attack, with burning pain being the main symptom.
Also known as glossodynia, tongue paresthesia, oral mucosal paresthesia
Often there are obvious mental factors
The incidence is higher among women who are menopausal or premenopausal or late.
Etiology and pathogenesis
Mental factors play an important role
local factors
System factors
neurological disease
clinical manifestations
Burning tongue pain is the most common clinical symptom
It may manifest as numbness, tingling, skinlessness, dull taste, dull pain and discomfort, etc.
The pain is mostly at the base of the tongue
Followed by the tongue edge, tongue dorsum and tongue tip
The pain does not worsen when drinking, eating, or being distracted, or the pain decreases or even disappears.
sexually transmitted diseases
syphilis
Treponema pallidum
Chronic, systemic sexually transmitted diseases
Cause
Treponema pallidum also known as Treponema pallidum subsp. pallidum
Artificial cultivation is difficult to succeed
But it can reproduce in apes, guinea pigs, and rabbits
Reproduction is slow, taking 30 to 33 hours to divide once
Anaerobic microorganisms cannot easily survive without the human body
Particularly sensitive to temperature and drying
It will die after drying for 1~2 hours or heating at 50°C for 5 minutes.
Strong cold tolerance
Sensitive to chemical disinfectants
Syphilis patients are the only source of infection for syphilis
clinical manifestations
Route of infection
Acquired (acquired) syphilis
primary syphilis
Hard gangrene
The incubation period is 1 week to 2 months, with an average of 2 to 4 weeks.
Labial gangrene
Glossary gangrene
painless inflammatory reaction
Mainly in external genitalia
It starts as a small patch of erythema, then develops into a papule or nodule, with necrosis on the surface, and develops into a round or oval shallow ulcer with a diameter of about 1 to 2 cm, with clear boundaries, a slightly raised edge, a flat base, and a cartilage-like hardness upon palpation. , no obvious pain or mild tenderness.
It can heal spontaneously without treatment in about 3 to 8 weeks.
swollen lymph nodes
secondary syphilis
It usually occurs 3 to 4 weeks after the subcutaneous gangrene subsides.
Treponema bacteremia
Fever, headache
Dizziness, general joint pain, lack of appetite, swollen lymph nodes throughout the body, etc.
skin damage
main performance
Macular rash, maculopapular rash, papule, scaly skin lesions, follicular rash and pus scar rash, etc.
Often manifests as mucosal plaques and mucositis
Mucosal plaque
Gray-white, shiny and slightly raised spots, round or oval
Tertiary syphilis
late syphilis
nodular syphilitic rash
gumma
syphilioma
Glossitis and tongue stains
It also invades internal organs, especially cardiovascular and central nervous system
Prenatally transmitted (congenital) plum blossoms
early congenital syphilis
late congenital syphilis
Late congenital syphilis mostly develops after the age of 2 years, and multiple symptoms appear one after another until the age of 13 to 14 years old. Most of them are asymptomatic infections, among which keratitis, bone damage and nervous system damage are common.
Cardiovascular syphilis is rare
congenital latent syphilis
Similar to acquired syphilis, but no gangrene occurs
iconic damage
Hutchinson teeth
Hutchinson's tooth, neurological deafness, and interstitial keratitis
Hutchinson's triad
Sang Qiya
latent syphilis
Anyone with a history of syphilis infection, no clinical manifestations or clinical manifestations that have disappeared, no positive signs other than positive anti-syphilis serology, and normal cerebrospinal fluid examination is called latent syphilis.
Its occurrence is related to the body's strong immunity or the temporary suppression of Treponema pallidum through treatment.
duration of disease
early syphilis
late plum
Histopathology
Endovascular and perivasculitis
It manifests as swelling and proliferation of vascular endothelial cells, and infiltration of a large number of lymphocytes and plasma cells around the blood vessels.
late regret
Granulomatous infiltrate with epithelioid cells and multinucleated giant cells, sometimes with necrotic tissue
syphilis serology test
Inspection methods are necessary for diagnosing syphilis, and serological diagnosis of latent syphilis is particularly important.
disease management
Treatment principles
Early detection, timely and regular treatment, the earlier the treatment, the better the effect.
The dosage is sufficient and the treatment course is regular
Sufficient time of follow-up observation is required after treatment
Examine and treat all sexual partners simultaneously
early syphilis
procaine penicillin
or jasmine penicillin
If you are allergic to penicillin, use the following medicines: doxycycline
Tetracycline hydrochloride
late syphilis
procaine penicillin
or jasmine penicillin
If you are allergic to penicillin, use the following medicines: doxycycline
Tetracycline hydrochloride
gonorrhea
Neisseria gonorrhoeae
Gram-negative diplococci, oval or round, often arranged in pairs
Neisseria gonorrhoeae is often located within neutrophils, but in the chronic phase it is extracellular
The optimal growth temperature is 35~36
The optimal pH is 7.5
Humans are the only natural host of Neisseria gonorrhoeae
Mainly invades mucosa
Mainly spread through sexual contact
urogenital infection
clinical manifestations
The incubation period is generally 2 to 10 days, with an average of 3 to 5 days.
Sexually active young and middle-aged people
Gonorrhea in men mainly manifests as gonococcal urethritis, and 90% of infected people have symptoms
The most commonly affected parts of gonorrhea in women are the endocervix and urethra, and the symptoms are mild.
gonococcal stomatitis
Mainly occurs in patients with a history of oral sex
It manifests as congestion and redness of the oral mucosa, which may have erosion or superficial ulcers, and is covered with a yellow-white pseudomembrane. The pseudomembrane is easy to wipe off, presenting a bleeding wound.
gonococcal pharyngitis
Common oral sex performers
More than 90% of infected people have no obvious symptoms, and a few patients experience dry throat, throat discomfort, burning or pain
Examination shows congestion of the pharyngeal mucosa and mucus or purulent secretions on the posterior pharyngeal wall.
Auxiliary inspection
direct smear
It is suitable for the diagnosis of gonorrhea in men without complications. It is not recommended for pharyngeal, rectal and female cervical infections.
Bacterial culture
Currently the only recommended method for diagnosing gonorrhea
Typical colonies may appear, and the oxidase test is positive
Nucleic acid amplification testing
Use PCR and other techniques to detect gonococcal nucleic acid positivity in various clinical specimens
disease management
Treatment principles
The principle of timely, sufficient and regular medication use
Adopt different treatment plans according to different conditions
Follow up
Sexual partners should be examined and treated at the same time
uncomplicated gonorrhea
Ceftriaxone 250mg, single intramuscular injection
Spectinomycin 2g, single intramuscular injection
Chlamydia infection cannot be ruled out, add anti-Chlamydia trachomatis infection drugs
sharp wet caress
human papillomavirusHPV
spherical
Man is the only natural host
It is mainly transmitted through sexual contact, and a few are transmitted through indirect contact.
Sexually transmitted diseases, mainly verrucous lesions
clinical manifestations
The incubation period is approximately 3 weeks to 8 months, with an average of 3 months
The skin around the external genitalia and anus
Oral sex can occur in the mouth
The initial manifestation is localized fine papules.
gradually increase or increase
Gradually develop into papillary, comb-shaped, cauliflower-shaped or mass-shaped vegetations
Color can range from pink to deep red, gray or brown-black
A few patients develop macrosomia due to low immune function or pregnancy
giant sharp
Generally there are no conscious symptoms. A few patients may experience itching, foreign body sensation, pressure or burning sensation.
Subclinical and latent infections
The appearance of subclinical infected skin and mucous membranes is normal. If 5% acetic acid solution is applied (acetic acid whitening test), a clearly defined area of origin may appear.
Latent infection means that tissues or cells contain HPV but the appearance of the skin and mucous membranes is normal, the lesions are not hyperkerated and the acetic acid white test is negative.
Sharp wet stroking in the mouth is mostly caused by oral sex infection, and it often occurs on the back of the tongue, lips, teeth, cheeks, cheeks, etc.
It manifests as single or multiple small nodules, pedunculated or sessile, which can gradually enlarge or merge to form cauliflower-like or papillary excrescences, which are flesh-colored or pale in color.
Histopathology
Papillomas or verrucous growths
Hyperkeratosis, flaky parakeratosis, epidermal acanthosis, basal cell hyperplasia, dilation of superficial dermal blood vessels, and infiltration of inflammatory cells mainly lymphocytes.
Superficial layer of epidermis
Focal, flaky and scattered vacuolated cells
Sometimes densely stained granular substances of varying sizes can be seen in keratinocytes, namely viral inclusion bodies.
Auxiliary inspection
Pathological examination
Nucleic acid amplification test
HPV-specific genes (Ll, E6, E7 region genes)
disease management
There is currently no method to eradicate HPV infection, and treatment mainly focuses on removing exogenous HPV.
Laser, freezing, microwave, photodynamic, surgical resection and other methods
Topical drug treatment mainly includes 0.5% podophyllotoxin anhydride, 5% imimod cream, and 30% to 50% trichloroacetic acid solution.
Systemic interferon and antiviral options
AIDS
HIV has weak survivability in the external environment, low resistance to physical and chemical factors, and is sensitive to heat
Process at 56°C for 30 minutes
HIV loses infectivity on human T lymphocytes in vitro but cannot completely inactivate HIV in serum
Process at 100°C for 20 minutes
HIV is completely inactivated
70% ethanol
0.2% sodium hypochlorite
1% glutaraldehyde
20% acetaldehyde
However, HIV is not sensitive to ultraviolet and gamma ray treatment
clinical manifestations
(1) Acute stage
(2) Asymptomatic period
(3) AIDS stage
Common opportunistic infections and tumors in various systems
oral cavity
acute pseudomembranous oral candidiasis
hairy leukoplakia
recurrent oral ulcers
Follow Yan
Kaposi's sarcoma
Oral manifestations of HIV infection
fungal infection
Oral candidiasis
Histoplasmosis
Chronic granulomas or large ulcers or necrosis on the tongue, cheeks, and cheeks
The pathological changes are granulation inflammatory hyperplasia, ulcer exudate smear and staining microscopy, and yeast-type capsular spores can be found inside and outside the mononuclear cells and polymorphonuclear cells (no coloring around the bacteria).
A fungal disease caused by Histoplasma capsulatum
Viral infection
hairy leukoplakia
It is considered to be one of the signs of severe systemic immune suppression in patients, mainly seen in HIV-infected patients.
Its occurrence is related to Epstein-Barr virus infection and is initially more common in gay men.
simple rash
Shingles
cytomegalovirus infection
Papilloma, focal epithelial hyperplasia
Kaposi's sarcoma
HIV-related periodontal disease
linear erythema on teeth
HIV-associated periodontitis
acute necrotizing ulcerative inflammation
necrotizing periodontitis
necrotizing stomatitis
ulcerative lesions
Salivary gland disease
non-hodgkin lymphoma
Oral manifestations in children with HIV are common: oral candidiasis, angular stomatitis, parotid gland enlargement, and simple pap rash; oral Kaposi sarcoma and hairy plaques are rare.
Diagnosis can be made if there is a history of epidemics, laboratory HIV antibody positivity, and any of the following:
(1) Unexplained and persistent irregular fever above 38°C for >1 month;
(2) Persistent diarrhea (more than 3 stools per day), >1 month;
(3) Lose more than 10% of body weight within 6 months;
(4) Recurrent oral fungal infections;
(5) Recurrent herpes simplex virus infection or herpes zoster virus infection;
(6) Pneumocystis pneumonia (PCP);
(7) Recurrent bacterial pneumonia;
(8) Active tuberculosis or non-tuberculous mycobacteriosis;
(9) Deep fungal infection
(10) Space-occupying lesions of the central nervous system;
(11) Dementia occurs in young and middle-aged people;
(12) Active cytomegalovirus infection;
(13) Toxoplasmic encephalopathy;
(14) Manilfei penicilliosis;
(15) Recurrent sepsis
(16) Kaposi sarcoma and lymphoma of skin, mucous membranes or internal organs
Treatment of oral diseases caused by HIV infection
Oral candidiasis
Use topical and systemic antifungal medications. For example, apply nystatin topically and rinse with sodium bicarbonate solution.
hairy leukoplakia
If there are no symptoms, no treatment is needed
In severe cases, use acyclovir
Kaposi's sarcoma
Mild or moderate Kaposi's sarcoma treated with highly active antiretroviral therapy
Severe Kaposi's sarcoma may be treated with a combination of antiretroviral therapy and chemotherapy
simplex and varicella zoster
Acyclovir can be used for simple lip rash
Shingles can be treated with famciclovir
HIV related periodontal disease
Carry out periodontal treatment as usual, such as local removal of calculus and plaque, and be careful to do so gently.
Rinse or gargle with 0.1% chlorhexidine solution or polyvinyl dish after surgery
If the condition is serious, take oral acetaminophen
recurrent aphthous ulcer
Topical use of glucocorticoid preparations and anti-inflammatory and antiseptic rinses. Optional thalidomide
xerostomia
Use a saliva secretion stimulant such as pilocarpine
papilloma
Treatments such as surgical resection and laser can be used, but there is a possibility of recurrence.
systemic disease
blood system diseases
iron deficiency anemia
clinical manifestations
Oral manifestations
Oral mucosa is pale, especially the lips, tongue, and teeth
The sensitivity of the mucous membrane to external stimuli increases, often causing foreign body sensation, dry mouth, burning tongue, etc. Some patients may suffer from recurring oral ulcers.
The filiform papillae and fungiform papillae on the back of the tongue atrophy and disappear, resulting in a smooth and pale back of the tongue.
Angular stomatitis may also occur. In severe cases, the oropharyngeal mucosa atrophies, causing difficulty in swallowing.
Plummer-Vinson syndrome or Plummer-Vinson syndrome, also known as iron deficiency dysphagia syndrome
It is a special type of iron deficiency anemia, with iron deficiency anemia, dysphagia and glossitis as the main manifestations. It is more common in middle-aged white women.
A potentially malignant disorder associated with a high risk of upper gastrointestinal squamous cell carcinoma that warrants regular follow-up
aplastic anemia
Insufficient bone marrow hematopoietic function, pancytopenia, and resulting anemia, bleeding, and infection syndromes.
Leukopenia and agranulocytosis
Leukopenia refers to the total number of white blood cells in peripheral blood remaining below 4.0xl09/L
Neutropenia refers to the absolute count of peripheral blood neutrophils, which is less than 2.0x109/L in adults, less than 1.8x109/L in children ≥10 years old, or less than 1.5x109/L in children <10 years old.
; In severe cases, when it is less than 0.5xl09 /L, it is called agranulocytosis.
Idiopathic thrombocytopenic purpura
Complex acquired autoimmune diseases involving multiple mechanisms
It may be related to excessive destruction of platelets mediated by humoral immunity and cellular immunity or abnormal quality and quantity of megakaryocytes mediated by humoral immunity and cellular immunity, and insufficient platelet production.
clinical manifestations
Systemic manifestations
Adult ITP generally has an insidious onset, and fatigue is one of its clinical symptoms.
Bleeding of skin and mucous membranes, such as spots, purple scars, spots, difficulty in stopping bleeding after trauma, etc. Nose bleeding is also common
The patient's condition may suddenly worsen due to infection, etc., resulting in extensive and severe bleeding of the skin, mucous membranes and internal organs.
Oral manifestations
Spontaneous heel bleeding is often an early manifestation of this disease.
The oral mucosa, especially the lipstick, tongue edge, floor of the mouth and cheeks, is prone to spots, ecchymoses, and hematomas.
The hematoma may rupture on its own or rupture and bleed due to food friction, leaving a round or oval erosion surface with clear edges.
diagnosis
Multiple tests revealed thrombocytopenia, an enlarged spleen, positive capillary fragility test, prolonged bleeding time, and coagulation. Blood time is normal
disease management
Glucocorticoids are the treatment of choice. Splenectomy and immunosuppressants can also be used for treatment
Digestive system diseases
ulcerative colitis
immune system diseases
Sjogren's syndrome
Sjögren syndrome (SS), also known as Sjögren syndrome
A diffuse connective tissue disease characterized by invasion of lacrimal glands, salivary glands and other exocrine glands, lymphocyte infiltration and specific autoantibodies (anti-SSA/SSB)
The disease is divided into two categories: primary SS (pSS) and secondary SS (sSS). The latter refers to Sjögren's syndrome secondary to another clearly diagnosed connective tissue disease or special viral infection.
clinical manifestations
Clinical manifestations are diverse, mainly related to glandular hypofunction
Systemic manifestations
Oral manifestations
Dry mouth, sticky mouth, abnormal taste, and in severe cases, difficulty in speech, chewing and swallowing
Oral mucosa: dry and dull, prone to candida infection
Rampant caries is one of the characteristics of this disease
Salivary gland enlargement: Parotid gland enlargement is the most common
It is usually a painless swelling, which can involve one or both sides, squeezing the gland, and there is no obvious saliva secretion at the duct opening.
Kawasaki disease
Kawasaki disease (KD), formerly known as mucocutaneous lymph node syndrome
An acute febrile and rash pediatric disease with systemic vasculitis as the main lesion
Clinical features include acute fever, skin and mucosal lesions, and lymphadenopathy. About 15% to 20% of untreated children develop coronary artery damage
It is more likely to occur in infants and young children under 5 years old, with more males than females.
Systemic manifestations
fever
Conjunctival hyperemia
hand and foot symptoms
Acute phase of hard edema of hands and feet and palmar erythema
Skin manifestations
cardiac manifestations
Pericarditis, myocarditis, endocarditis, and arrhythmia occur in 1 to 6 weeks
Other accompanying symptoms: Patients may develop pyuria and urethritis, or diarrhea, vomiting, and abdominal pain. A few children may develop hepatomegaly, mild jaundice, and elevated serum aminotransferase activity. Pulmonary infection is rare, and aseptic meningitis occasionally occurs.
Oral representation
Lip and perioral manifestations: red, swollen, dry and cracked lips, diffuse congestion of oral mucosa, red and swollen tongue papilla, strawberry tongue
Cervical lymph node enlargement: unilateral or bilateral, hard and tender, but the surface is not red or purulent. The disease appears initially and subsides when the fever subsides
The basic pathological change is systemic vasculitis, which mostly occurs in coronary arteries.
systemic lupus erythematosus
Endocrine system diseases and nutritional and metabolic diseases
diabetes
Cushing's syndrome
vitamin deficiency
Vitamin B2 deficiency
clinical manifestations
Systemic manifestations
Scrotal inflammation is the early and most common manifestation of the disease
The skin mainly manifests as dry itchy dermatitis and seborrheic dermatitis
Dry nasal mucosa, burning sensation, nasal vestibule scabies, and military skin fissures
Conjunctivitis, corneal congestion and vascular proliferation, turbidity, ulcers, photophobia and tearing, blurred vision, etc. appear in the eyes.
Oral manifestations
Angular stomatitis, cheilitis and glossitis are often early manifestations of the disease
Angular stomatitis: Bilateral symmetrical moist white skin at the corners of the mouth is soaked, eroded, and cracked and knotted.
Cheilitis
It is more common on the lower lip, and the lips vary from bright red, fiery red to dark purple.
Lips are slightly swollen, dry and flaky, cracked, and have a burning or stinging sensation
Glossitis
In the early stage, there are dry tongue, burning or tingling sensation, the tongue body is bright red, and the fungiform papillae are red and swollen. In the long term, the disease manifests as atrophic glossitis, the tongue papilla atrophies, and the tongue surface is smooth and bright red. Sometimes there may be a geographic tongue, and grooves or ulcers may appear on the back of the tongue.
disease management
Eat more foods rich in vitamin B2, such as milk, eggs, animal offal, lean meat, beans, etc.
Niacin deficiency
pellagra
Niacin and nicotinamide are both pyridine derivatives and are water-soluble vitamins
Found in animal and plant foods such as meat, milk, liver, beans and vegetables
clinical manifestations
Systemic manifestations
Dermatitis, diarrhea and dementia, dermatitis and diarrhea are more common
Oral manifestations
In the early stage, the tip of the tongue and the edges of the tongue are congested, and the fungiform papillae are red and swollen, and then the whole tongue becomes red with burning pain. In longer-term cases, the tongue filiform papillae and fungiform papillae atrophy, and the tongue surface becomes red, shiny, and beef-red, which is harmful to trauma. Or other irritating sensations, prone to ulcers.
The oral mucosa and pharynx may also become red and burning, and erosion or superficial ulcers may occur.
Moisture, whiteness or erosion at the corners of the mouth
Prone to inflammation and periodontitis
Vitamin C deficiency
scurvy
Clinical features are bleeding and bone lesions
clinical manifestations
Systemic manifestations
Bone joint muscle pain
Slow onset, general fatigue, loss of appetite, weight loss, depression, pale complexion, and tired skin
Oral manifestations
People who are deficient in vitamin C are prone to involvement of the dental caps and periodontal tissue.
amyloidosis
A group of diseases that cause tissue and organ damage at the deposition site due to amyloid deposits in the extracellular matrix.
Lingual amyloidosis is a common manifestation of amyloid deposits in the oral cavity
Divided into the following types
Immunoglobulin light chain amyloidosis
Amyloid A amyloidosis
β2 microglobulin amyloidosis
transthyretin amyloidosis
clinical manifestations
Systemic manifestations
Initial symptoms are mostly fatigue and weight loss
Oral manifestations
The tongue is the site most commonly affected by AL amyloidosis in the head and neck region, and can form a typical progressive macroglossia.
In addition to the tongue, it can also appear as yellowish nodules or raised white lesions on the oral mucosa (mainly the floor of the mouth, heels, cheeks, and very rarely the cheeks); or extensive blue-purple scar-like protrusions; or Spots, papules, ulcers, etc.
infectious diseases
scarlet fever
Acute respiratory infectious diseases caused by group A hemolytic streptococci type B
clinical manifestations
Systemic manifestations
The incubation period is 2 to 5 days. The onset is sudden, with high fever, mostly persistent, and sore throat. Rash started 1 day after onset of illness
Oral manifestations
The facial skin is congested and flushed without rash, and the congestion around the mouth and nose is not obvious. Compared with the congested face, it looks Whitening, called "perioral pale circle"
measles
a highly contagious disease caused by the measles virus
Transmitted through respiratory tract
The onset season is mainly winter and spring
Measles patients are the only source of infection
clinical manifestations
Systemic manifestations
Oral manifestations
1 to 2 days before the rash occurs, 0.5 to 1mm needle-sized gray-white or purple spots appear on the buccal mucosa corresponding to the patient's bilateral second molars, surrounded by redness, called measles mucosal spots or Koplik spots. (Koplik spots), these spots gradually increase in the rash stage, and can spread to the entire buccal mucosa and inner lip, merging with each other, and sometimes expanding into patches, like thrush
diphtheria
Pigmentation abnormalities
Endogenous pigmentation abnormalities
melanosis
dark spots on mucosa
Melanotic macules refer to melanotic spots that are not related to oral mucosal pigmentation caused by ethnicity, systemic diseases, or exogenous substances. The reason is unknown
Mucosal dark spots are currently considered benign lesions and generally do not require treatment.
If there are changes in color and size, ulcers, or swellings, you should be wary of malignant transformation.
pigmented polyposis syndrome
Pudji's disease
autosomal dominant inheritance
family inheritance
Melanotic spots on oral mucosa, perioral skin and other parts of the body
Multiple polyps in the gastrointestinal tract
The main symptoms and complications of this syndrome are caused by polyps. Patients often suffer from chronic abdominal pain, vomiting, diarrhea, anemia and melena.
In severe cases, complications such as intestinal obstruction and intussusception may occur. Intestinal polyps in this disease have a tendency to become malignant
Pigmented spots may increase with age
Histopathology
Mucosal skin damage manifests as an increase in melanocyte melanin granules in the basal cell layer, or accompanied by melanocyte hyperplasia
Intestinal polyps appear as hamartomas, and under the microscope, dendritic hyperplasia and non-specific glandular duct hyperplasia can be seen in the mucosal muscle layer.
For perioral and oral pigmentation, treatment is generally not required. Gastrointestinal polyps can be treated surgically
Primary chronic adrenal insufficiency
original
Addison's disease
It is caused by defects in the structure or function of the adrenal cortex caused by various reasons, resulting in insufficient secretion of adrenocortical hormones and often accompanied by increased plasma adrenocorticotropic hormone (ACTH) levels.
Secondary
Hypothalamic or pituitary disease causes reduced ACTH secretion, resulting in adrenocortical hormone deficiency, which is often accompanied by reduced plasma ACTH levels, but in a few cases it can be normal.
More common in middle-aged people, less common in the elderly and young children, especially gender differences
Autoimmune (including idiopathic adrenocortical atrophy and autoimmune polyendocrine hypofunction syndrome) is the main cause, followed by tuberculosis, and other causes (tumors, fungal infections, etc.)
clinical manifestations
The onset is slow, with deepening of skin and mucous membrane pigmentation, accompanied by fatigue, weakness, loss of appetite, weight loss, and lower blood pressure and blood sugar.
Pigmentation is one of the early symptoms of this disease and is also the most characteristic manifestation. It is seen in almost all cases.
People with secondary hypopituitarism often do not have this symptom
Pigmentation is systemic, bronze, brown or dark brown, more obvious in exposed and friction-prone areas
Oral mucosal pigmentation usually appears early on the skin, often in areas such as lipstick, cheeks, teeth, tongue edges and tongue tips.
Dot-like and flaky blue-black or dark brown pigmentation of varying sizes (Figure 12-1-3). Pigmentation areas without subjective symptoms
Fatigue, weakness, weight loss, decreased blood pressure, loss of appetite, mental disorder, weakened resistance to various stresses such as infection and trauma, etc. In severe cases, fainting, shock and adrenal crisis may occur.
Histopathology
Hyperpigmentation is the result of increased melanocyte activity without an increase in cell number
Within basal cells, also found above the basal layer
Auxiliary inspection
Hyponatremia and hyperkalemia can be found. Normocytic normochromic anemia, neutropenia, lymphocyte and eosinophilia are common
Basic ACTH measurement is helpful in the diagnosis and differential diagnosis of this disease.
Plasma ACTH is significantly elevated in primary patients
Most patients with secondary disease have low plasma ACTH levels
ACTH stimulation test is a method with diagnostic value for this disease, which can determine the functional status of the pituitary-adrenocortical axis.
In addition to the treatment of the cause, basic treatment is also required, that is, long-term use of adrenocortical hormone replacement supplements, usually oral prednisone or other corticosteroid drugs.
multiple fibrous dysplasia
acanthosis nigricans
A rare skin and mucosal disease characterized by hyperkeratosis, pigmentation and papilloma-like hyperplasia of the skin. It is divided into benign and malignant types according to the cause.
Common in insulin resistance, especially in obese patients
Secondly, it is related to other metabolic disorders, drugs, and malignant tumors.
Some patients lack a specific cause and may or may not have a familial history
At the beginning, the skin is dry and rough, with pigmentation, and is gray-brown or black. Later, the epidermis gradually thickens, with papilloma-like protrusions, and the pigmentation gradually deepens.
Skin lesions tend to occur in folds such as the neck, armpits, breasts and groin
The oral mucosa can be involved, and the cheeks, tongue dorsum, and pharynx may become thick and uneven or exhibit papillomatous hyperplasia, which may be accompanied by varying degrees of pigmentation.
Benign acanthosis nigricans occurs in newborns or early childhood and has a familial tendency
The most common malignancy associated with gastric adenocarcinoma
Often onset after the age of 40
Histopathology
Epidermal hyperkeratosis and papilloma-like hyperplasia, irregular thickening of the spinous layer, and mild increase in pigmentation in the basal cell layer
Diagnosis is based on clinical manifestations and combined with medical history and auxiliary examinations to help find the cause.
Disease management focuses on actively finding and treating the underlying disease
Pigmented nevus
It often occurs on the skin of the face and neck, and occasionally in the oral mucosa, facial conjunctiva, etc.
Melanocytes derived from the basal layer of the epidermis or embryonic neural crest precursor cells
Autosomal dominant inheritance, a developmental malformation, which can also be acquired later in life
Junctional hemorrhoids
Light brown, dark brown or brown-black macules, papules or nodules, flat or slightly higher than the surface of the skin, smooth and hairless, can occur in any part, and are highly pigmented on the palms and vulva, and are called junctional hemorrhoids
If it is located in an area that is often subject to friction, trauma or chronic irritation, there is a possibility of malignant transformation.
When the junction area is significantly enlarged, the pigment becomes darker, itching, pain, burning, ulceration, and bleeding occur locally, and small satellite spots, nodules, or radiating black lines appear around it, the possibility of malignant transformation should be considered.
Intradermal or intramucosal hemorrhoids
Light brown to dark brown, smooth or slightly raised skin surface, may also be papillomatous or symptomatic, smooth surface, may be hairy, more common on the head and neck
mixed hemorrhoids
Clinically, it is difficult to distinguish from the above two pigmented hemorrhoids. More common in teenagers, with raised skin surface, light brown and dark brown, smooth surface, may grow hair
Histopathology
Junctional hemorrhoids are located at the junction of the epidermis and dermis. Intradermal hemorrhoids are located in the dermis. Mixed hemorrhoids are intradermal hemorrhoids and junctional hemorrhoids that coexist.
malignant melanoma
High invasiveness, high metastasis rate, and extremely poor prognosis
Origin of embryonic neural crest
Abnormal melanocyte hyperplasia
malignant tumor
May occur on skin and mucous membranes
The average age of onset is older, with the peak incidence in the skin at 40 years old, and in the mucous membrane 15 to 20 years later than in the skin.
Malignant melanoma of the maxillofacial region often occurs on the basis of pigmentation
Ultraviolet rays, heredity, endocrine, chronic stimulation and damage are related to the onset of malignant melanoma.
Commonly found on scalp, cheeks, neck and ears
When malignant transformation occurs, it rapidly increases in size, becomes darker in pigment, expands radially, and ruptures and oozes blood. Satellite nodules appear around it, and the lymph nodes in the corresponding area suddenly enlarge.
Malignant melanoma in the oral cavity can occur anywhere in the mouth, and most commonly involves the parotid and maxillary alveolar mucosa. It is often asymptomatic in the early stages.
Malignant melanoma often occurs early and extensive lymph node metastasis
The hematogenous metastasis rate is high, up to 40%, mainly in the lungs, liver, bones, brain and other organs
Histopathology
Malignant melanoma tumor cells are round, oval, spindle-shaped and polygonal
Cytoplasm is clear and contains melanin
The nuclei are large, deeply stained, with obvious nucleoli, numerous mitotic figures, and multinucleated giant cells can be seen.
Sometimes the tumor cells may not contain melanin, which is amelanotic melanoma
Dopa reaction can be used to assist diagnosis
diagnosis
The ABCDE five manifestations of melanoma
Asymmetry (A, asymmetry)
Border irregularity (B, border irregularity)
Color change (C, color variartion)
Diameter (D, diameter) 5mm
Elevation (E, elevation)
Biopsy can promote tumor spread and metastasis, and it is generally not suitable to perform biopsy
Timely treatment and comprehensive treatment are very important
Cryotherapy of the primary tumor, chemical therapy, surgical treatment (selective neck dissection, extended resection of the primary tumor + tissue repair), biological therapy, rehabilitation therapy (rehabilitation therapy, speech training, dentition restoration), such as after cryotherapy The primary tumor was not controlled and additional surgical resection was performed.
Hemoglobinosis
hereditary
Autosomal recessive genetic disease caused by genetic abnormalities on chromosome 6
Acquisition
Long-term excessive iron intake, long-term massive blood transfusions, iron metabolism disorders caused by liver disease, and red blood cell growth disorders caused by various reasons
The clinical characteristics are bronze or gray-black skin, mainly occurring on the face, upper limbs, back of hands, armpits, and perineum.
The oral mucosa may have blue-gray or blue-black pigmentation, which mainly occurs on the hard edges, teeth and cheeks.
This disease can be treated with deferoxamine, iron complex therapy or bloodletting. Pigmentation of the oral mucosa does not require special treatment
Bilirubinosis
Jaundice
Exogenous pigmentation abnormalities
Heavy metal pigmentation
Chronic lead poisoning, bismuth poisoning, mercury poisoning
Lead lines, bismuth lines, and mercury lines form on the edges of the teeth, appearing as blue-black or gray-blue
Silver and gold poisoning will be different
Blue-gray pigmentation of oral mucosa and purple discoloration of tooth heels
amalgam tattoo
drug-induced pigmentation
Quinacrine, chlorine, chlorine, quinidine, zidovudine, tetracycline, minocycline, chlorpropanax, oral contraceptives, clofazimine, ketoconazole, acetaminophen, albumin doxorubicin, bleomycin, cyclophosphamide
post-inflammatory pigmentation
Chronic periodontitis, lichen planus, psoriasis, psoriasis, and lupus erythematosus
Smoking-induced melanosis
depigmentation
white scar wind