Mecanismos de defensa y casos - Vicky Alice

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Mecanismos de 
defensa de la encía
The gingival tissue is constantly subjected to 
mechanical and bacterial aggressions. 
The saliva, the epithelial surface, and the 
initial stages of the inflammatory response 
provide resistance to these actions
Liquido del surco 
The presence of sulcular fluid, or gingival 
crevicular fluid (GCF), has been known since 
the nineteenth century, but its composition 
and possible role in oral defense mechanisms 
were elucidated by the pioneering work of 
Waerhaug, and Brill and Krasse in the 1950s
The amount of GCF collected on a paper strip can be evaluated
in a variety of ways. 
The wetted area can be made more visible by staining with ninhydrin;
it is then measured planimetrically on an enlarged photograph
or with a magnifying 
glass or a microscope. 
An electronic method has been devised for measuring
the fluid collected on a “blotter”
(Periopaper), employing an electronic transducer
(Periotron, Harco Electronics, Winnipeg, Manitoba, Canada)
Composition
The components of GCF can be characterized according to individual proteins,73,85,103 
specific antibodies, antigens, and enzymes of several specificities.
The GCF also contains cellular elements.
Cellular Elements: bacteria, desquamated epithelial cells, and leukocytes (PMNs, 
lymphocytes, monocytes/macrophages), which migrate through the sulcular epithelium.
Electrolytes: Potassium, sodium, and calcium have been studied in GCF. Most studies have 
shown a positive correlation of calcium and sodium concentrations and the 
sodium/potassium ratio with inflammation
Organic Compounds: carbohydrates and proteins have been investigated. 
Glucose hexosamine and hexuronic acid are two of the compounds found in GCF. The total 
protein content of GCF is much less than that of serum. No significant correlations have been 
found between the concentration of proteins in GCF and the severity of gingivitis, pocket 
depth, or extent of bone loss. Metabolic and bacterial products identified in GCF include 
lactic acid, urea, hydroxyproline, endotoxins, cytotoxic substances, hydrogen sulfide, and 
antibacterial factors.
Clinical Significance
GCF is an inflammatory exudate. 
Its presence in clinically normal 
sulci can be explained because 
gingiva that appears clinically 
normal invariably exhibits 
inflammation when examined 
microscopically. 
The amount of GCF is greater 
when inflammation is present 
and is sometimes proportional 
to the severity of inflammation.
GCF production is not increased 
by trauma from occlusion but is 
increased by mastication of 
coarse foods, toothbrushing and 
gingival massage, ovulation, 
hormonal contraceptives, and 
smoking.
Drugs in Gingival Crevicular 
Fluid
Drugs that are excreted through the GCF may be 
used advantageously in periodontal therapy. 
Tetracyclines are excreted through the GCF, this 
finding triggered extensive research that showed 
a concentration of tetracyclines in GCF 
compared with serum.
Metronidazole is another antibiotic that has been 
detected in human GCF
SALIVA
Saliva exerts a major influence on 
plaque by mechanically cleansing the 
exposed oral surfaces, by buffering 
acids produced by bacteria, and by 
controlling bacterial activity
Salivary secretions are protective in 
nature because they maintain the oral 
tissues in a physiologic state 
Role in Periodontal Pathology
Saliva exerts a major influence on plaque initiation, maturation, and metabolism. Salivary flow 
and composition also influence calculus formation, periodontal disease, and caries. The 
removal of the salivary glands in experimental animals significantly increases the incidence of 
dental caries and periodontal disease and delays wound healing
In humans, an increase in inflammatory gingival diseases, dental caries, and rapid tooth
destruction associated with cervical or cemental caries is partially a consequence of
decreased salivary gland secretion (xerostomia).
Xerostomia may result from sialolithiasis, sarcoidosis, Sjögren’s syndrome, Mikulicz’s disease, 
irradiation, surgical removal of the salivary glands, and other factors
Inflamación gingival
Pathologic changes in gingivitis are associated 
with the presence of oral microorganisms 
attached to the tooth and perhaps in or near 
the gingival sulcus
STAGE IV GINGIVITIS: THE ADVANCED
LESION
Extension of the lesion into alveolar bone 
characterizes a fourth
stage known as the advanced lesion or 
phase of periodontal breakdown
Características Clínicas de la 
gingivitis
CHANGES IN GINGIVAL CONTOUR
Experimental gingivitis studies provided the first empiric evidence that accumulation of 
microbial biofilm on clean tooth surfaces results in the development of an inflammatory 
process around gingival tissue
The local inflammation will persist as long as the microbial biofilm is present adjacent to the 
gingival tissues and that the inflammation may resolve subsequent to a meticulous removal of 
the biofilm
CHANGES IN GINGIVAL CONTOUR
Prevalence-worldwide
Epidemiologic studies indicate that more than 82% of adolescents in the United States (US) 
have overt gingivitis and signs of gingival bleeding
Similar or higher prevalence of gingivitis is reported for children and adolescents in other 
parts of the world
CHANGES IN GINGIVAL CONTOUR
Clinical features of gingivitis may be characterized by the presence of any of the following 
clinical signs: redness and sponginess of the gingival tissue, bleeding on provocation, 
changes in contour, and presence of calculus or plaque with no radiographic evidence of 
crestal bone loss
COURSE AND 
DURATION
Gingivitis can occur with sudden onset and short 
duration and can be painful. A less severe phase of 
this condition can also occur
Recurrent gingivitis reappears after having been 
eliminated by treatment or disappeared 
spontaneously
Chronic gingivitis is slow in onset and of long 
duration. It is painless, unless complicated by acute 
or subacute exacerbations, and is the type most 
often encountered
Localizada
confined to the gingiva of a single tooth or group of teeth
Marginal 
gingivitis 
involves the 
gingival margin 
and may 
include a 
portion of the 
contiguous 
attached 
gingiva
Generalizada
involves the entire mouth
Color Changes in 
the Gingiva
Determined by several factors, including the number 
and size of blood vessels, epithelial thickness, quantity 
of keratinization, and pigments within the epithelium
Change in color is an important clinical sign of 
gingival disease. The normal gingival color is “coral 
pink” and is produced by the tissue’s vascularity and 
modified by the overlying epithelial layers
Metallic Pigmentation. Heavy metals (bismuth, arsenic, 
mercury, lead, and silver) absorbed systemically from 
therapeutic use or occupational or household 
environments may discolor the gingiva and other 
areas of the oral mucosa
Color Changes Associated with Systemic 
Factors
Endogenous oral pigmentations can be caused by melanin, bilirubin, or iron
The deposition of iron in hemochromatosis may produce 
a blue-gray pigmentation of the oral mucosa
Jaundice is best detected by examination of the sclera, 
but the oral mucosa may also acquire a yellowish color
Melanin oral pigmentations can be normal physiologic 
pigmentations and are often found in highly pigmented 
ethnic groups. 
Diseases that increase melanin pigmentation include the following:
• Addison’s disease is caused by adrenal dysfunction and produces isolated
patches of discoloration varying from bluish black to brown. 
• Peutz-Jeghers syndrome produces intestinal polyposis and melanin
pigmentation in the oral mucosa and lips. 
• Albright’s syndrome (polyostotic fibrous dysplasia) and von
Recklinghausen’s disease (neurofibromatosis) produce areas of oral melanin
pigmentation
Toothbrushing has various effects on the 
consistency of the gingiva such as promoting 
keratinizationof the oral epithelium, enhancing capillary 
gingival circulation, and thickening alveolar bone.
In animal studies, mechanical stimulation by 
toothbrushing was found to increase the proliferative 
activity of the junctional basal cells in dog gingiva by 2.5 
times compared with using a scaler.
These findings may indicate that toothbrushing causes an 
increased turnover rate and desquamation of the 
junctional epithelial surfaces. This process may repair 
small breaks in the junctional epithelium and prevent 
direct access to the underlying tissue by periodontal 
pathogens
Changes in Position of the Gingiva
Recession is exposure of the root surface by an apical 
shift in the position of the gingiva
The actual position is the level of the coronal end of the 
epithelial attachment on the tooth, whereas the apparent 
position is the level of the crest of the gingival margin
The severity of recession is determined by the actual 
position of the gingiva, not its apparent position
The following etiologic factors have been implicated in gingival recession: faulty
toothbrushing technique (gingival abrasion), tooth malposition, friction from soft tissues
(gingival ablation), gingival inflammation, abnormal frenum attachment, iatrogenic dentistry, 
oral piercings.
Orthodontic movement in a labial direction in monkeys has been shown to result in loss of 
marginal bone and connective tissue attachment, as well as in gingival recession.
Agrandamiento 
gingival
Increase in size of the gingiva is a common feature of 
gingival disease. Accepted current terminology for this 
condition is gingival enlargement or gingival 
overgrowth
The many types of gingival enlargement can be classified
according to etiologic factors and pathologic changes as 
follows:
I. Inflammatory enlargement
A. Chronic
B. Acute
II. Drug-induced enlargement
A. General information
B. Anticonvulsants
C. Immunosuppressants
D. Calcium channel blockers
III. Enlargements associated with systemic diseases or
conditions
A. Conditioned enlargement 1. Pregnancy 2. Puberty 3. 
Vitamin C deficiency 4. Plasma cell gingivitis 5. 
Nonspecific conditioned enlargement (pyogenic
granuloma) 
B. Systemic diseases causing gingival enlargement 1. 
Leukemia 2. Granulomatous diseases (e.g., Wegener’s
granulomatosis, sarcoidosis)
IV. Neoplastic enlargement (gingival tumors) 
A. Benign tumors 
B. Malignant tumors
V. False enlargement Using the criteria of location and 
distribution, gingival enlargement is designated as 
follows: 
• Localized: Limited to the gingiva adjacent to a single 
tooth or group of teeth. 
• Generalized: Involving the gingiva throughout the 
mouth. 
• Marginal: Confined to the marginal gingiva. 
• Papillary: Confined to the interdental papilla. 
• Diffuse: Involving the marginal and attached gingivae 
and papillae. 
• Discrete: An isolated sessile or pedunculated, tumorlike 
enlargement. 
Infecciones 
gingivales 
agudas
NECROTIZING ULCERATIVE GINGIVITIS (NUG) 
PRIMARY HERPETIC GINGIVOSTOMATITIS
PERICORONITIS
Necrotizing ulcerative gingivitis (NUG) is a microbial disease of the gingiva in the context of 
an impaired host response. It is characterized by the death and sloughing of gingival tissue 
and presents with characteristic signs and symptoms.
Clinical Features
NUG can cause tissue destruction involving the periodontal attachment apparatus, 
especially in patients with long-standing disease or severe immunosuppression
When bone loss occurs, the condition is called necrotizing ulcerative periodontitis 
(NUP)
NUG is characterized by sudden onset, sometimes after an episode of debilitating 
disease or acute respiratory tract infection. A change in living habits, protracted 
work without adequate rest, poor nutrition, tobacco use, and psychologic stress 
are frequent features of the patient’s history
Clinical Features
Characteristic lesions are punched-out, craterlike depressions at the crest of the interdental papillae, 
subsequently extending to the marginal gingiva and rarely to the attached gingiva and oral mucosa. 
The surface of the gingival craters is covered by a gray, pseudomembranous slough, demarcated from the 
remainder of the gingival mucosa by a pronounced linear erythema
In some cases, the lesions are denuded of the surface pseudomembrane, exposing the gingival margin, which 
is red, shiny, and hemorrhagic
NUG can occur in otherwise disease-free mouths or can be superimposed on chronic gingivitis or periodontal 
pockets
Etiology
Role of Bacteria. Plaut in 1894 and Vincent in 1896 postulated that NUG is caused by specific 
bacteria: fusiform bacillus and a spirochetal organism.
The constant flora is composed of Prevotella intermedia, in addition to Fusobacterium, 
Treponema, and Selenomonas species. The variable flora consists of a heterogeneous array 
of bacterial types.
Treatment with metronidazole results in a significant reduction of Treponema species, 
Prevotella intermedia, and Fusobacterium, with resolution of the clinical symptoms
PRIMARY HERPETIC GINGIVOSTOMATITIS
is an infection of the oral cavity caused by the herpes simplex virus type 1 (HSV-1)
It occurs most often in infants and children younger than 6 years of age, but it is also seen in 
adolescents and adults. 
It occurs with equal frequency in male and female patients. 
In most persons, however, the primary infection is asymptomatic.
PRIMARY HERPETIC GINGIVOSTOMATITIS
As part of the primary infection, the virus ascends through sensory and autonomic nerves, where it persists as 
latent HSV in neuronal ganglia that innervate the site. In approximately one-third of the world’s population, 
secondary manifestations result from various stimuli such as sunlight, trauma, fever, and stress. These 
secondary manifestations include herpes labialis
Clinical Features
Oral Signs. Primary herpetic gingivostomatitis appears as a diffuse, erythematous, shiny involvement of the 
gingiva and the adjacent oral mucosa, with varying degrees of edema and gingival bleeding. In its initial 
stage, it is characterized by the presence of discrete, spherical gray vesicles, which may occur on the gingiva, 
labial and buccal mucosae, soft palate, pharynx, sublingual mucosa, and tongue
The course of the disease is limited to 7 to 10 days.
Pericoronitis
The term pericoronitis refers to inflammation of the 
gingiva in relation to the crown of an incompletely 
erupted tooth
It occurs most often in the mandibular third molar area. 
Pericoronitis may be acute, subacute, or chronic
Clinical Features
Partially erupted or impacted mandibular third molar
Overlying gingival flap (operculum)
The gingival flap is often chronically inflamed and infected and has varying degrees of 
ulceration along its inner surface
Red, swollen, suppurating lesion that is exquisitely tender, with radiating pains to the ear, 
throat, and floor of the mouth
Swelling of the cheek in the region of the angle of the jaw and lymphadenitis are common 
findings
Trismus
Complications
Pericoronal abscess
Peritonsillar abscess formation, cellulitis, and 
Ludwig’s angina are infrequent but potential
sequelae of acute pericoronitis.
Enfermedades gingivales de la 
infancia
Estudio Radiográfico
Estudio Radiográfico
	Diapositiva 1: Mecanismos de defensa de la encía
	Diapositiva 2
	Diapositiva 3: Liquido del surco 
	Diapositiva 4
	Diapositiva 5: Composition
	Diapositiva 6
	Diapositiva 7
	Diapositiva 8: Clinical Significance
	Diapositiva 9: Drugs in Gingival Crevicular Fluid 
	Diapositiva 10: SALIVA
	Diapositiva 11
	Diapositiva 12: Role in Periodontal Pathology
	Diapositiva 13: Inflamación gingival
	Diapositiva 14
	Diapositiva 15: Características Clínicas de la gingivitis
	Diapositiva 16: CHANGES IN GINGIVAL CONTOUR
	Diapositiva 17: CHANGES IN GINGIVAL CONTOUR
	Diapositiva 18: CHANGES IN GINGIVAL CONTOUR
	Diapositiva 19: COURSE AND DURATION
	Diapositiva 20
	Diapositiva21: Color Changes in the Gingiva
	Diapositiva 22: Color Changes Associated with Systemic Factors
	Diapositiva 23
	Diapositiva 24
	Diapositiva 25: Changes in Position of the Gingiva
	Diapositiva 26
	Diapositiva 27: Agrandamiento gingival
	Diapositiva 28
	Diapositiva 29
	Diapositiva 30
	Diapositiva 31
	Diapositiva 32
	Diapositiva 33: Infecciones gingivales agudas
	Diapositiva 34
	Diapositiva 35: Clinical Features
	Diapositiva 36: Clinical Features
	Diapositiva 37: Etiology
	Diapositiva 38: PRIMARY HERPETIC GINGIVOSTOMATITIS
	Diapositiva 39: PRIMARY HERPETIC GINGIVOSTOMATITIS
	Diapositiva 40: Pericoronitis
	Diapositiva 41: Clinical Features
	Diapositiva 42: Complications
	Diapositiva 43: Enfermedades gingivales de la infancia
	Diapositiva 44
	Diapositiva 45
	Diapositiva 46
	Diapositiva 47
	Diapositiva 48
	Diapositiva 49
	Diapositiva 50
	Diapositiva 51
	Diapositiva 52
	Diapositiva 53
	Diapositiva 54
	Diapositiva 55
	Diapositiva 56