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Why is a classification system used for periodontal and peri-implant diseases?
It provides a framework to study these diseases in an organized manner.
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Why must classification systems for diseases be updated regularly?
As scientific knowledge and understanding of disease cause and pathogenesis increase, classification systems must be aligned and updated.
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Which of the following is categorized under 'Peri-Implant Diseases and Conditions' in the 2017 classification?
Periodontitis
Mucogingival Deformities
Peri-Implantitis
Necrotizing Periodontal Diseases
Which of the following is categorized under 'Peri-Implant Diseases and Conditions' in the 2017 classification?
Periodontitis
Mucogingival Deformities
Peri-Implantitis
Necrotizing Periodontal Diseases
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Which category of conditions includes 'Systemic diseases or conditions affecting the periodontal supporting tissues'?
Peri-Implant Diseases
Periodontitis
Other Conditions Affecting the Periodontium
Periodontal Health
Which category of conditions includes 'Systemic diseases or conditions affecting the periodontal supporting tissues'?
Peri-Implant Diseases
Periodontitis
Other Conditions Affecting the Periodontium
Periodontal Health
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What are the two major divisions under 'Periodontal Diseases and Conditions'?
Peri-Implant Health; Peri-Implantitis
Periodontitis; Other Conditions Affecting the Periodontium
Gingivitis; Necrotizing Periodontal Diseases
Periodontal Health, Gingival Diseases and Conditions; Periodontitis
What are the two major divisions under 'Periodontal Diseases and Conditions'?
Peri-Implant Health; Peri-Implantitis
Periodontitis; Other Conditions Affecting the Periodontium
Gingivitis; Necrotizing Periodontal Diseases
Periodontal Health, Gingival Diseases and Conditions; Periodontitis
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What is the primary aetiological factor of gingivitis?
The presence of microbial biofilm.
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Which of the following is considered a systemic modifying risk factor for dental plaque-induced gingivitis?
Prominent restoration margins
Hyperglycemia
Dental plaque biofilm retention
Oral dryness
Which of the following is considered a systemic modifying risk factor for dental plaque-induced gingivitis?
Prominent restoration margins
Hyperglycemia
Dental plaque biofilm retention
Oral dryness
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List the three patient categories for dental biofilm induced gingivitis.
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Define biofilm-induced gingivitis in terms of physiological response.
It is an inflammatory response of the gingival tissues resulting from bacterial biofilm accumulation near and below the gingival margin.
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Which of the following is categorized as a predisposing local risk factor for dental plaque-induced gingivitis?
Puberty
Smoking
Hyperglycemia
Oral dryness
Which of the following is categorized as a predisposing local risk factor for dental plaque-induced gingivitis?
Puberty
Smoking
Hyperglycemia
Oral dryness
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What broad body reaction occurs in response to trauma or bacterial infection?
An inflammatory response.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What are the primary clinical characteristics of gingivitis?
ここでカードを閲覧するか、 sign up to study with spaced repetition.
Why is the control of gingivitis essential for the prevention of tooth loss?
Gingival inflammation is a key risk factor for the onset of periodontitis, a condition that causes attachment loss and eventually leads to tooth loss.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
How is gingivitis typically diagnosed?
It is a purely clinical diagnosis based on professional assessment, as there are no standard microbiological or molecular tests performed during routine clinical examinations.
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What is the distinction between a symptom and a sign in the context of gingivitis?
A symptom is a subjective experience reported by the patient, while a sign is objective evidence observable by others.
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List common symptoms reported by patients with gingivitis.
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What are the clinical signs of gingivitis that a clinician would observe?
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Is gingivitis typically a painful condition?
No, it is usually painless despite being an inflammatory disease.
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Why are radiographs not used to diagnose gingivitis?
Gingivitis is limited to the gingival soft tissues and does not cause attachment loss or alveolar bone loss.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What are the clinical signs and symptoms of gingivitis?
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What is the clinical case definition of a patient with an intact periodontium?
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What is the Bleeding on Probing (BOP) score threshold for localized gingivitis in an intact periodontium?
\(≤ 10\)%
\(≥ 50\)%
\(> 30\)%
\(≥ 10\)%, \(≤ 30\)%
What is the Bleeding on Probing (BOP) score threshold for localized gingivitis in an intact periodontium?
\(≤ 10\)%
\(≥ 50\)%
\(> 30\)%
\(≥ 10\)%, \(≤ 30\)%
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What is the Bleeding on Probing (BOP) score threshold for generalized gingivitis in an intact periodontium?
\(≥ 10\)%, \(≤ 30\)%
\(> 30\)%
\(≤ 10\)%
\(> 50\)%
What is the Bleeding on Probing (BOP) score threshold for generalized gingivitis in an intact periodontium?
\(≥ 10\)%, \(≤ 30\)%
\(> 30\)%
\(≤ 10\)%
\(> 50\)%
ここでカードを閲覧するか、 sign up to study with spaced repetition.
Can a patient with a reduced periodontium exhibit gingival recession without having periodontitis?
Yes, for example, due to the effects of orthodontic treatment.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What Bleeding on Probing (BOP) percentage defines localized gingivitis in a reduced periodontium?
\(10\% \le \text{BOP} \le 30\%\)
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What Bleeding on Probing (BOP) percentage defines generalized gingivitis in a reduced periodontium?
\(\text{BOP} > 30\%\)
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What is the only objective measure available to assess the extent of gingival inflammation?
Bleeding on Probing (BOP)
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What components should be included when writing a diagnostic statement for gingivitis?
ここでカードを閲覧するか、 sign up to study with spaced repetition.
Why is the severity of gingivitis no longer formally defined in clinical practice?
It relies on highly variable clinical signs like colour and swelling, and lacks objective clinical criteria.
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What is the probing depth criterion for a diagnosis of gingivitis in a reduced periodontium?
Probing depth of \(\le 3 \text{ mm}\)
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What are the clinical signs of moderate gingivitis?
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What are the clinical signs of severe gingivitis?
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How does the bacterial composition of biofilm change as it matures and gingivitis develops?
It shifts from relatively simple communities dominated by gram-positive cocci and rods to increasingly complex communities, trending from aerobic to anaerobic and gram-negative bacteria.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What is the result of removing bacterial biofilm in the context of gingival inflammation?
Removal of bacterial biofilm leads to the resolution of gingival inflammation.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
How do oral hygiene practices influence the plaque index?
Stopping oral hygiene practices causes the plaque index to increase, while continuing or restarting practices causes the plaque index to decrease.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What characterizes early bacterial biofilm in a healthy state?
It consists of relatively simple bacterial communities dominated by gram-positive cocci and rods.
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Which Gram-negative bacterial genera are positively correlated with the development of gingivitis?
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What structure acts as a biological seal at the site of the gingival epithelium?
The junctional epithelium.
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What is the typical timeframe for changes in microvascular structures within gingival tissue after exposure to biofilm?
Within 24-48 hours.
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Which of the following is a factor that can give dental biofilm a competitive advantage over host defenses?
Increased saliva production
Open proximal contact
Healthy junctional epithelium
Frequent tooth brushing
Which of the following is a factor that can give dental biofilm a competitive advantage over host defenses?
Increased saliva production
Open proximal contact
Healthy junctional epithelium
Frequent tooth brushing
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Which immune cells are present even in clinically healthy gingiva?
PMNs and lymphocytes.
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Upon entering the sulcus opening, what specific immune components do microorganisms first encounter?
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What is the consequence of allowing supragingival biofilm to accumulate without disruption?
It irritates the sulcular epithelial cells.
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List the metabolites produced by the bacteria of supragingival biofilm.
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How does the immune system respond to LPS present in the sulcus region?
It recognizes LPS as an antigen and initiates an inflammatory response.
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Which inflammatory mediators are released by sulcular and junctional epithelial cells in response to biofilm products?
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In reaction to cytokines, what substances do gingival tissues produce?
Neuropeptides and histamine.
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What is the function of histamine in the local vascular reaction?
It causes local capillaries to open up.
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How does histamine release by mast cells assist in the immune response?
It widens capillaries and slows blood flow, which allows PMNs to get closer to the vessel wall.
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What are the two pathways by which bacterial metabolites trigger PMN recruitment?
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What is the function of the adhesion molecule ELAM-1 expressed on the surface of endothelial cells?
It causes PMNs (polymorphonuclear leukocytes) to roll along the endothelium.
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Which specific receptor interaction facilitates stable contact between PMNs and the endothelium?
The interaction between the leukocyte adhesion receptor integrin beta 2 and the endothelial integrin ICAM-1.
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Through what process do PMNs leave blood vessels after contacting the endothelium?
Amoeboid diapedesis.
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Which chemical factors form the gradient that guides PMN migration towards the sulcus?
Chemotactic factors including FMLP and IL-8.
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Which cells release chemotactic factors such as FMLP and IL-8 in response to biofilm?
Junctional epithelial cells.
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What components support PMNs in the sulcus to assist in the phagocytosis of bacteria and their products?
Complement and antibodies.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
What is the primary immune response to increased biofilm accumulation in clinically healthy-looking gingiva?
A constant PMN (polymorphonuclear leukocyte) reaction.
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What condition occurs when dental biofilm continues to grow beyond the initial accumulation phase?
The first histological signs of gingivitis.
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What triggers the increased recruitment and migration of PMNs through the junctional epithelium?
The accumulation of bacterial metabolites.
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How do PMNs interact with dental biofilm to protect gingival tissues?
PMNs form a dense palisade layer over the biofilm, engulfing bacteria to separate them from the gingival sulcus.
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What happens when the PMN barrier is overwhelmed by continuous biofilm growth?
The inflammatory response intensifies, leading to the increased release of inflammatory substances by tissues and PMNs.
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What physiological processes are regulated by pro-inflammatory cytokines?
They regulate cell proliferation, cell growth, cell activation, inflammation, immunity, and repair.
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What is the typical volume percentage of the free gingiva occupied by an infiltrate in early gingivitis?
It occupies about 10-15% of the volume of the free gingiva.
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What is the cellular composition of the infiltrate in an early gingivitis lesion?
It consists of 75% T-cells, activated macrophages, and a few plasma cells.
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What vascular changes cause the redness observed in the gingival margin during early gingivitis?
The redness is caused by an increase in both the size and the number of vascular units due to the opening of previously inactive capillary beds.
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What causes the influx of plasma proteins, such as acute phase reactants and complement, into the connective tissue?
The influx is caused by an increase in vascular permeability.
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What is the effect of PMN-related micro abscesses on the gingival sulcus?
They cause the sulcus to begin to deepen.
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Why do the basal cells of the junctional epithelium proliferate in early gingivitis?
They proliferate as an attempt by the body to enhance the mechanical barrier against biofilm bacteria and their products.
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What enzyme is responsible for breaking down collagen fibers within a lesion?
MMP (Matrix Metalloproteinase)
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How long of undisturbed biofilm accumulation is required for an established lesion to develop in adults?
2-4 weeks
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What occurs to the bacterial population as a biofilm grows and matures in the periodontal tissues?
There is a shift from gram-positive to more gram-negative bacteria.
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What function does the PMN wall perform in an established lesion?
It acts to separate the biofilm from the periodontal tissues.
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Which cells coordinate the inflammatory response in the infiltrate by releasing cytokines?
Activated T cells
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What is the result of B cell differentiation in the inflammatory infiltrate?
They turn into plasma cells and produce immunoglobulin gamma antibodies and cytokines.
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What characterizes tissue homeostasis in healthy periodontal tissue?
A balance between the synthesis and resorption of the extracellular matrix and collagen.
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Which mediators help fine-tune the balance of tissue homeostasis?
Cytokines, growth factors, prostaglandin E2, MMP, and TIMP
Only PMNs and lymphocytes
Only biofilm and gram-negative bacteria
Only growth factors and vitamins
Which mediators help fine-tune the balance of tissue homeostasis?
Cytokines, growth factors, prostaglandin E2, MMP, and TIMP
Only PMNs and lymphocytes
Only biofilm and gram-negative bacteria
Only growth factors and vitamins
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What substance do macrophages release during gingivitis that leads to the destruction of collagen and the extracellular matrix?
MMP (Matrix metalloproteinases)
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How do macrophages alter fibroblast activity during gingivitis?
They stimulate fibroblasts to secrete destructive mediators like MMP instead of producing collagen.
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Why does a pseudopocket form during gingivitis?
The sulcus deepens because the junctional epithelium (JE) cells attempt to move away from the bacteria.
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Why is the gingival pocket formation during early gingivitis called a 'pseudopocket'?
Because the base of the junctional epithelium (JE) still covers the cemento-enamel junction (CEJ).
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What type of bacteria thrive in the subgingival region after the formation of a pseudopocket?
Anaerobic bacteria
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What defines the transition from longstanding gingivitis to destructive periodontitis?
Changes in the pathogenic potential of the biofilm, shifts in the host immune response, and the presence of risk factors.
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What is the full term for the abbreviation \(LPS\) as used in immune signaling?
Lipopolysaccharide
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What does the abbreviation \(TIMP\) represent in the context of biological mediators?
Tissue inhibitors of MMP
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What clinical signs are associated with the proliferation of blood vessels and vasodilation during gingival inflammation?
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What is a 'pseudopocket' in the context of periodontal assessment?
A pocket measurement of up to 4mm caused by gingival swelling rather than true attachment loss.
A pocket resulting from the complete destruction of collagen fibers inserted into the cementum.
A clinical sign indicating the loss of all stippling and retractability in healthy periodontium.
A deep pocket formed exclusively by bacterial biofilm accumulation under the CEJ.
What is a 'pseudopocket' in the context of periodontal assessment?
A pocket measurement of up to 4mm caused by gingival swelling rather than true attachment loss.
A pocket resulting from the complete destruction of collagen fibers inserted into the cementum.
A clinical sign indicating the loss of all stippling and retractability in healthy periodontium.
A deep pocket formed exclusively by bacterial biofilm accumulation under the CEJ.
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What physiological change occurs in the JE (junctional epithelium) within the first 4 days after removal of bacterial biofilm?
Repair of the junctional epithelium (JE) and a reduction in the number of polymorphonuclear leukocytes (PMNs) in the sulcus tissue.
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What clinical improvements are typically reported by a patient 4 days after biofilm removal?
The mouth feels fresher, often with a reduction in bad taste or breath.
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Approximately how long after biofilm removal does a reduction in vascular permeability and chronic inflammatory infiltrate typically occur?
21-28 days
1-2 days
4 days
7-14 days
Approximately how long after biofilm removal does a reduction in vascular permeability and chronic inflammatory infiltrate typically occur?
21-28 days
1-2 days
4 days
7-14 days
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What happens to gingival tissues during the healing process as fibroblast numbers and collagen increase?
Tissues become firmer and more resistant to probing.
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What is the typical clinical sign of healing after 7-14 days?
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What histopathological changes occur at 4+ days of healing?
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Are tissue alterations in gingivitis reversible?
Yes, all tissue alterations that occur during gingivitis are completely reversible once the dental biofilm is removed.
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What characterizes periodontitis regarding attachment loss?
Once attachment loss occurs, it is irreversible.
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What is considered the key risk factor for the onset of periodontitis?
Any inflammation in response to biofilm accumulation.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
Why is the control of gingival inflammation essential?
It is absolutely essential for the primary prevention of periodontitis.
ここでカードを閲覧するか、 sign up to study with spaced repetition.
Why is a classification system used for periodontal and peri-implant diseases?
It provides a framework to study these diseases in an organized manner.
Why must classification systems for diseases be updated regularly?
As scientific knowledge and understanding of disease cause and pathogenesis increase, classification systems must be aligned and updated.
Which of the following is categorized under 'Peri-Implant Diseases and Conditions' in the 2017 classification?
Periodontitis
Mucogingival Deformities
Peri-Implantitis
Necrotizing Periodontal Diseases
Which category of conditions includes 'Systemic diseases or conditions affecting the periodontal supporting tissues'?
Peri-Implant Diseases
Periodontitis
Other Conditions Affecting the Periodontium
Periodontal Health
What are the two major divisions under 'Periodontal Diseases and Conditions'?
Peri-Implant Health; Peri-Implantitis
Periodontitis; Other Conditions Affecting the Periodontium
Gingivitis; Necrotizing Periodontal Diseases
Periodontal Health, Gingival Diseases and Conditions; Periodontitis
What is the primary aetiological factor of gingivitis?
The presence of microbial biofilm.
Which of the following is considered a systemic modifying risk factor for dental plaque-induced gingivitis?
Prominent restoration margins
Hyperglycemia
Dental plaque biofilm retention
Oral dryness
List the three patient categories for dental biofilm induced gingivitis.
Define biofilm-induced gingivitis in terms of physiological response.
It is an inflammatory response of the gingival tissues resulting from bacterial biofilm accumulation near and below the gingival margin.
Which of the following is categorized as a predisposing local risk factor for dental plaque-induced gingivitis?
Puberty
Smoking
Hyperglycemia
Oral dryness
What broad body reaction occurs in response to trauma or bacterial infection?
An inflammatory response.
What are the primary clinical characteristics of gingivitis?
Why is the control of gingivitis essential for the prevention of tooth loss?
Gingival inflammation is a key risk factor for the onset of periodontitis, a condition that causes attachment loss and eventually leads to tooth loss.
How is gingivitis typically diagnosed?
It is a purely clinical diagnosis based on professional assessment, as there are no standard microbiological or molecular tests performed during routine clinical examinations.
What is the distinction between a symptom and a sign in the context of gingivitis?
A symptom is a subjective experience reported by the patient, while a sign is objective evidence observable by others.
List common symptoms reported by patients with gingivitis.
What are the clinical signs of gingivitis that a clinician would observe?
Is gingivitis typically a painful condition?
No, it is usually painless despite being an inflammatory disease.
Why are radiographs not used to diagnose gingivitis?
Gingivitis is limited to the gingival soft tissues and does not cause attachment loss or alveolar bone loss.
What are the clinical signs and symptoms of gingivitis?
What is the clinical case definition of a patient with an intact periodontium?
What is the Bleeding on Probing (BOP) score threshold for localized gingivitis in an intact periodontium?
\(≤ 10\)%
\(≥ 50\)%
\(> 30\)%
\(≥ 10\)%, \(≤ 30\)%
What is the Bleeding on Probing (BOP) score threshold for generalized gingivitis in an intact periodontium?
\(≥ 10\)%, \(≤ 30\)%
\(> 30\)%
\(≤ 10\)%
\(> 50\)%
Can a patient with a reduced periodontium exhibit gingival recession without having periodontitis?
Yes, for example, due to the effects of orthodontic treatment.
What Bleeding on Probing (BOP) percentage defines localized gingivitis in a reduced periodontium?
\(10\% \le \text{BOP} \le 30\%\)
What Bleeding on Probing (BOP) percentage defines generalized gingivitis in a reduced periodontium?
\(\text{BOP} > 30\%\)
What is the only objective measure available to assess the extent of gingival inflammation?
Bleeding on Probing (BOP)
What components should be included when writing a diagnostic statement for gingivitis?
Why is the severity of gingivitis no longer formally defined in clinical practice?
It relies on highly variable clinical signs like colour and swelling, and lacks objective clinical criteria.
What is the probing depth criterion for a diagnosis of gingivitis in a reduced periodontium?
Probing depth of \(\le 3 \text{ mm}\)
What are the clinical signs of moderate gingivitis?
What are the clinical signs of severe gingivitis?
How does the bacterial composition of biofilm change as it matures and gingivitis develops?
It shifts from relatively simple communities dominated by gram-positive cocci and rods to increasingly complex communities, trending from aerobic to anaerobic and gram-negative bacteria.
What is the result of removing bacterial biofilm in the context of gingival inflammation?
Removal of bacterial biofilm leads to the resolution of gingival inflammation.
How do oral hygiene practices influence the plaque index?
Stopping oral hygiene practices causes the plaque index to increase, while continuing or restarting practices causes the plaque index to decrease.
What characterizes early bacterial biofilm in a healthy state?
It consists of relatively simple bacterial communities dominated by gram-positive cocci and rods.
Which Gram-negative bacterial genera are positively correlated with the development of gingivitis?
What structure acts as a biological seal at the site of the gingival epithelium?
The junctional epithelium.
What is the typical timeframe for changes in microvascular structures within gingival tissue after exposure to biofilm?
Within 24-48 hours.
Which of the following is a factor that can give dental biofilm a competitive advantage over host defenses?
Increased saliva production
Open proximal contact
Healthy junctional epithelium
Frequent tooth brushing
Which immune cells are present even in clinically healthy gingiva?
PMNs and lymphocytes.
Upon entering the sulcus opening, what specific immune components do microorganisms first encounter?
What is the consequence of allowing supragingival biofilm to accumulate without disruption?
It irritates the sulcular epithelial cells.
List the metabolites produced by the bacteria of supragingival biofilm.
How does the immune system respond to LPS present in the sulcus region?
It recognizes LPS as an antigen and initiates an inflammatory response.
Which inflammatory mediators are released by sulcular and junctional epithelial cells in response to biofilm products?
In reaction to cytokines, what substances do gingival tissues produce?
Neuropeptides and histamine.
What is the function of histamine in the local vascular reaction?
It causes local capillaries to open up.
How does histamine release by mast cells assist in the immune response?
It widens capillaries and slows blood flow, which allows PMNs to get closer to the vessel wall.
What are the two pathways by which bacterial metabolites trigger PMN recruitment?
What is the function of the adhesion molecule ELAM-1 expressed on the surface of endothelial cells?
It causes PMNs (polymorphonuclear leukocytes) to roll along the endothelium.
Which specific receptor interaction facilitates stable contact between PMNs and the endothelium?
The interaction between the leukocyte adhesion receptor integrin beta 2 and the endothelial integrin ICAM-1.
Through what process do PMNs leave blood vessels after contacting the endothelium?
Amoeboid diapedesis.
Which chemical factors form the gradient that guides PMN migration towards the sulcus?
Chemotactic factors including FMLP and IL-8.
Which cells release chemotactic factors such as FMLP and IL-8 in response to biofilm?
Junctional epithelial cells.
What components support PMNs in the sulcus to assist in the phagocytosis of bacteria and their products?
Complement and antibodies.
What is the primary immune response to increased biofilm accumulation in clinically healthy-looking gingiva?
A constant PMN (polymorphonuclear leukocyte) reaction.
What condition occurs when dental biofilm continues to grow beyond the initial accumulation phase?
The first histological signs of gingivitis.
What triggers the increased recruitment and migration of PMNs through the junctional epithelium?
The accumulation of bacterial metabolites.
How do PMNs interact with dental biofilm to protect gingival tissues?
PMNs form a dense palisade layer over the biofilm, engulfing bacteria to separate them from the gingival sulcus.
What happens when the PMN barrier is overwhelmed by continuous biofilm growth?
The inflammatory response intensifies, leading to the increased release of inflammatory substances by tissues and PMNs.
What physiological processes are regulated by pro-inflammatory cytokines?
They regulate cell proliferation, cell growth, cell activation, inflammation, immunity, and repair.
What is the typical volume percentage of the free gingiva occupied by an infiltrate in early gingivitis?
It occupies about 10-15% of the volume of the free gingiva.
What is the cellular composition of the infiltrate in an early gingivitis lesion?
It consists of 75% T-cells, activated macrophages, and a few plasma cells.
What vascular changes cause the redness observed in the gingival margin during early gingivitis?
The redness is caused by an increase in both the size and the number of vascular units due to the opening of previously inactive capillary beds.
What causes the influx of plasma proteins, such as acute phase reactants and complement, into the connective tissue?
The influx is caused by an increase in vascular permeability.
What is the effect of PMN-related micro abscesses on the gingival sulcus?
They cause the sulcus to begin to deepen.
Why do the basal cells of the junctional epithelium proliferate in early gingivitis?
They proliferate as an attempt by the body to enhance the mechanical barrier against biofilm bacteria and their products.
What enzyme is responsible for breaking down collagen fibers within a lesion?
MMP (Matrix Metalloproteinase)
How long of undisturbed biofilm accumulation is required for an established lesion to develop in adults?
2-4 weeks
What occurs to the bacterial population as a biofilm grows and matures in the periodontal tissues?
There is a shift from gram-positive to more gram-negative bacteria.
What function does the PMN wall perform in an established lesion?
It acts to separate the biofilm from the periodontal tissues.
Which cells coordinate the inflammatory response in the infiltrate by releasing cytokines?
Activated T cells
What is the result of B cell differentiation in the inflammatory infiltrate?
They turn into plasma cells and produce immunoglobulin gamma antibodies and cytokines.
What characterizes tissue homeostasis in healthy periodontal tissue?
A balance between the synthesis and resorption of the extracellular matrix and collagen.
Which mediators help fine-tune the balance of tissue homeostasis?
Cytokines, growth factors, prostaglandin E2, MMP, and TIMP
Only PMNs and lymphocytes
Only biofilm and gram-negative bacteria
Only growth factors and vitamins
What substance do macrophages release during gingivitis that leads to the destruction of collagen and the extracellular matrix?
MMP (Matrix metalloproteinases)
How do macrophages alter fibroblast activity during gingivitis?
They stimulate fibroblasts to secrete destructive mediators like MMP instead of producing collagen.
Why does a pseudopocket form during gingivitis?
The sulcus deepens because the junctional epithelium (JE) cells attempt to move away from the bacteria.
Why is the gingival pocket formation during early gingivitis called a 'pseudopocket'?
Because the base of the junctional epithelium (JE) still covers the cemento-enamel junction (CEJ).
What type of bacteria thrive in the subgingival region after the formation of a pseudopocket?
Anaerobic bacteria
What defines the transition from longstanding gingivitis to destructive periodontitis?
Changes in the pathogenic potential of the biofilm, shifts in the host immune response, and the presence of risk factors.
What is the full term for the abbreviation \(LPS\) as used in immune signaling?
Lipopolysaccharide
What does the abbreviation \(TIMP\) represent in the context of biological mediators?
Tissue inhibitors of MMP
What clinical signs are associated with the proliferation of blood vessels and vasodilation during gingival inflammation?
What is a 'pseudopocket' in the context of periodontal assessment?
A pocket measurement of up to 4mm caused by gingival swelling rather than true attachment loss.
A pocket resulting from the complete destruction of collagen fibers inserted into the cementum.
A clinical sign indicating the loss of all stippling and retractability in healthy periodontium.
A deep pocket formed exclusively by bacterial biofilm accumulation under the CEJ.
What physiological change occurs in the JE (junctional epithelium) within the first 4 days after removal of bacterial biofilm?
Repair of the junctional epithelium (JE) and a reduction in the number of polymorphonuclear leukocytes (PMNs) in the sulcus tissue.
What clinical improvements are typically reported by a patient 4 days after biofilm removal?
The mouth feels fresher, often with a reduction in bad taste or breath.
Approximately how long after biofilm removal does a reduction in vascular permeability and chronic inflammatory infiltrate typically occur?
21-28 days
1-2 days
4 days
7-14 days
What happens to gingival tissues during the healing process as fibroblast numbers and collagen increase?
Tissues become firmer and more resistant to probing.
What is the typical clinical sign of healing after 7-14 days?
What histopathological changes occur at 4+ days of healing?
Are tissue alterations in gingivitis reversible?
Yes, all tissue alterations that occur during gingivitis are completely reversible once the dental biofilm is removed.
What characterizes periodontitis regarding attachment loss?
Once attachment loss occurs, it is irreversible.
What is considered the key risk factor for the onset of periodontitis?
Any inflammation in response to biofilm accumulation.
Why is the control of gingival inflammation essential?
It is absolutely essential for the primary prevention of periodontitis.
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