LS Flashcards
Savannah Bridge, a 32-year-old patient, came to your dental clinic with a primary complaint of mild pain and the presence of pus discharge in her upper left jaw. During the clinical examination, a noticeable swelling was observed on the palate, extending from teeth 25 to 28, crossing the midline (please refer to the accompanying image). Ms. Bridge reported a history of visiting multiple private dental clinics over the past 6 months, where she received antibiotics and pain relievers for the same persistent swelling. Her medical history did not reveal any significant health issues. Tooth 26 exhibited caries on the mesio-proximal surface and showed no signs of vitality. Surprisingly, the adjacent teeth (24, 25, 27, and 28) remained vital. Upon palpation, the swelling felt soft and fluctuant. No swelling or draining sinus tract was detected in the buccal vestibule, and there were no palpable lymph nodes. Ms. Bridge’s oral hygiene was notably poor, with significant staining and calculus buildup.
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You advised Savannah to do cone beam CT (CBCT), but she was unwilling to do it due to financial constraints. Hence, orthopantamograph was taken (please see the image below). Along with the OPG, intraoral periapical radiograph, maxillary occlusal radiograph and routine laboratory investigations were done. Radiographic examination revealed a large unilocular radiolucency with well-defined radiopaque border. Routine laboratory investigations were within normal limits. Fine needle aspiration revealed opaque, brown-coloured fluid, consisting dense infiltrate of acute inflammatory cells, predominantly polymorphonuclear leukocytes. Few isolated epithelial cells were seen, which were normal in size, shape, and appearance. Cytological picture was suggestive of an acute inflammatory lesion.
Summary of Explanation:
Correct Answer: Inflamed Radicular Cyst
Radiographic findings: Large unilocular radiolucency with a well-defined radiopaque border, typical of a radicular cyst.
Aspiration results: Opaque, brown-colored fluid with inflammatory cells supports an inflamed cyst.
Patient history: Chronic swelling unresolved by antibiotics suggests a cyst rather than an acute infection.
No systemic signs: Lack of fever or other systemic symptoms rules out spreading or glandular infections.
Why Other Options are Incorrect:
Spreading odontogenic infection: Typically shows diffuse swelling and systemic signs, which are absent here.
Localized odontogenic infection: Radiopaque border and fluid findings point to a cyst, not an abscess.
Submandibular gland infection: No signs of salivary gland involvement (e.g., tender swelling, sialadenitis).
Conclusion: Radiographic, aspirate, and clinical evidence align with the diagnosis of an inflamed radicular cyst.
Do Radicular Cysts and Periapical Abscesses Look the Same Clinically?
Radicular Cyst:
It’s like a bubble of tissue growth caused by chronic inflammation.
This happens when the body responds to long-term irritation or infection from a dead tooth (non-vital pulp).
Over time, the inflammation triggers the formation of a sac lined with tissue, which fills with fluid or semi-solid material.
It’s generally slow-growing and painless, unless it gets infected.
Periapical Abscess:
It’s a pocket of pus caused by an acute bacterial infection.
The body is fighting off the infection from the dead tooth by sending white blood cells (immune fighters) to the area.
The accumulation of dead cells, bacteria, and tissue debris creates the swelling filled with exudate (pus).
This process is fast, painful, and may lead to systemic symptoms like fever if the infection spreads.
Clinical Features of Oral Blobs (Cysts, Abscesses, and Other Lumps)
Here’s a mnemonic to help remember the clinical oral features and radiographic clues for these oral “blobs”:
“CYSTS ARE ‘SLOW’ AND ABSCESSES ‘SWEAR’”
CYSTS = SLOW (Painless, chronic, well-defined radiolucency)
S: Silent swelling (painless, slow-growing).
L: Localized (firm or fluctuant, often near teeth or unerupted teeth).
O: Other causes (e.g., inflammation or developmental anomaly).
W: Well-defined radiolucency on radiographs.
ABSCESSES = SWEAR (Painful, acute, diffuse radiolucency)
S: Severe pain (sharp, throbbing, tender to touch).
W: Warm swelling (redness, pus, or sinus tract).
E: Exudate (pus from infection like Streptococcus or Prevotella).
A: Acute onset (rapid progression).
R: Radiographically ill-defined (diffuse bone loss or periodontal ligament widening).
This mnemonic helps differentiate cysts (calm and chronic) from abscesses (angry and acute) based on their clinical and radiographic presentations.
Dental abscess may occur as a complication of infection of teeth or adjacent soft tissues. Microscopy of the taken material from an abscess is most likely to show which one of the following?
- Profuse neutrophilic polymorphonuclear leukocytes and bacteria
- Profuse neutrophilic polymorphonuclear leukocytes, bacteria and necrotic tissue debris
- Profuse plasma cells, lymphocytes and bacteria
- Profuse plasma cells, bacteria and necrotic tissue debris
- Profuse lymphocytes, bacteria and necrotic tissue debris
Question Explanation:
Correct Answer:
“Profuse neutrophilic polymorphonuclear leukocytes, bacteria, and necrotic tissue debris”
Why correct?
An abscess is a collection of pus formed in response to an infection, typically caused by bacteria.
Microscopically, pus contains neutrophils (polymorphonuclear leukocytes), which are the first line of immune cells to respond to infection.
Bacteria are the pathogens causing the abscess, and their presence is a defining feature.
Necrotic tissue debris results from the destruction of surrounding tissue by both the bacteria and the body’s immune response.
This combination is characteristic of an abscess and its microscopic findings.
Why the Other Options Are Incorrect:
“Profuse neutrophilic polymorphonuclear leukocytes and bacteria”
Why incorrect?
While this partially describes an abscess, it fails to include necrotic tissue debris, a hallmark feature caused by tissue destruction in an abscess.
An abscess is not just bacteria and immune cells—it also includes the tissue breakdown products.
“Profuse plasma cells, lymphocytes, and bacteria”
Why incorrect?
Plasma cells and lymphocytes are characteristic of chronic inflammation or immune responses, not acute infections like an abscess.
Abscesses are acute lesions dominated by neutrophils, not plasma cells or lymphocytes.
“Profuse plasma cells, bacteria, and necrotic tissue debris”
Why incorrect?
Plasma cells are indicative of a chronic immune response, such as seen in autoimmune conditions or chronic infections.
Neutrophils, not plasma cells, are the predominant immune cells in an acute abscess.
“Profuse lymphocytes, bacteria, and necrotic tissue debris”
Why incorrect?
Lymphocytes are typically associated with viral infections or chronic inflammatory conditions, not acute bacterial abscesses.
In an abscess, neutrophils are the dominant immune cells, not lymphocytes.
Summary:
**The correct answer includes all the components characteristic of an acute abscess: neutrophils, bacteria, and necrotic tissue debris. The other options are incorrect because they either omit essential components (e.g., necrotic debris) or involve the wrong type of immune cells for an acute bacterial infection.
**
- What is the main role of dentin matrix proteins?
Correct Answer
Enhancing nucleation of hydroxyapatite
You Answered
Dentinal strength
Enhancing growth phase of hydroxyapatite crystals
Dentinal flexibility
Explanation:
Correct Answer:
“Enhancing nucleation of hydroxyapatite”
Why correct?
Dentin matrix proteins, particularly dentin phosphoprotein (DPP) and dentin sialoprotein (DSP), play a crucial role in the mineralization of dentin.
These proteins promote nucleation of hydroxyapatite crystals, the key mineral component of dentin, which gives dentin its hardness and structure.
The process of hydroxyapatite nucleation is essential for forming the mineralized dentin matrix.
Why “Dentinal Strength” is Incorrect:
While hydroxyapatite contributes to the overall strength of dentin, the primary role of dentin matrix proteins is in the nucleation and mineralization process, not directly in providing strength.
Strength is a secondary result of mineralization, which is initiated by these proteins.
Why the Other Options Are Incorrect:
“Enhancing growth phase of hydroxyapatite crystals”:
This is related to the later stages of crystal growth. Dentin matrix proteins are primarily involved in the initiation (nucleation) phase of hydroxyapatite formation.
“Dentinal Flexibility”:
Flexibility in dentin comes from the collagen matrix, not from the dentin matrix proteins responsible for hydroxyapatite nucleation.
Summary:
The main role of dentin matrix proteins is to enhance the nucleation of hydroxyapatite, which is essential for the mineralization process. While they indirectly contribute to dentinal strength, their primary function is initiating mineral deposition, making “Enhancing nucleation of hydroxyapatite” the correct answer.
Scenario 3
- In individuals with ectodermal dysplasia, what dental feature is commonly observed?
Calcified dental pulp and thick dentin layer
Correct Answer
Hypodontia and delayed tooth eruption
You Answered
Enamel hypoplasia and conical teeth
Amelogenesis imperfecta with mottled enamel
Explanation:
Correct Answer:
“Hypodontia and delayed tooth eruption”
Why correct?
Ectodermal dysplasia affects the development of tissues derived from the ectoderm, including teeth.
A hallmark feature in affected individuals is hypodontia (missing teeth) and delayed tooth eruption, which are characteristic findings due to abnormal tooth development.
Teeth that do form are often reduced in number and erupt later than normal.
Why “Enamel Hypoplasia and Conical Teeth” is Incorrect:
While conical teeth may occur in ectodermal dysplasia, enamel hypoplasia (thin or poorly formed enamel) is not the primary dental feature associated with this condition.
The main dental issues in ectodermal dysplasia are the reduced number of teeth (hypodontia) and delayed eruption, not necessarily defects in enamel thickness.
Why the Other Options Are Incorrect:
“Calcified dental pulp and thick dentin layer”:
This is seen in other conditions, like dentinogenesis imperfecta, but not ectodermal dysplasia.
“Amelogenesis imperfecta with mottled enamel”:
This describes a genetic condition affecting enamel formation but is unrelated to ectodermal dysplasia, which primarily impacts the number and timing of tooth eruption rather than enamel quality.
Lay Term Summary:
Ectodermal dysplasia causes missing teeth (hypodontia) and delays when teeth come through (eruption). While teeth may look conical, the main problem is fewer teeth and slower development.
Explanation:
Correct Answer:
“Protrusion”
Why correct?
The medial and lateral pterygoid muscles, when contracting symmetrically, work together to protrude the mandible (move it forward).
The lateral pterygoid muscle is the primary muscle responsible for mandible protrusion, while the medial pterygoid assists in stabilizing this movement. Together, they generate forward movement of the jaw.
Why “Elevation” is Incorrect:
Elevation (closing the jaw) is primarily the function of the masseter, temporalis, and medial pterygoid muscles. The lateral pterygoid does not contribute to elevation and is instead associated with forward and lateral movements.
Why the Other Options Are Incorrect:
“Depression”:
Depression (opening the jaw) is primarily caused by the lateral pterygoid in conjunction with gravity and the digastric and suprahyoid muscles. Symmetric contraction of the medial pterygoid does not contribute to this action.
“Lateral Excursion”:
Lateral excursion (side-to-side jaw movement) involves asymmetric contraction of the lateral and medial pterygoids, not symmetric contraction.
“Protrusion” (repeated in the list but already correctly answered):
This is correct and the reason given above.
“Elevation” tmj muscles
Elevation (closing the jaw) is primarily the function of the masseter, temporalis, and medial pterygoid muscles. The lateral pterygoid does not contribute to elevation and is instead associated with forward and lateral movements.
depression tmj muscles
“Lateral Excursion” tmj muscles
Lateral excursion (side-to-side jaw movement) involves asymmetric contraction of the lateral and medial pterygoids, not symmetric contraction.
James Little, a 45-year-old male, presents at dental clinic with a concern about a white patch inside his mouth. He reports that the patch has been present for the past few weeks and has gradually increased in size (please see the image below). He mentions occasional discomfort while eating and speaking, particularly when the patch rubs against his tongue. Upon intraoral examination, a well-defined white plaque-like lesion is observed on the right buccal mucosa. The lesion appears slightly elevated, with a pebbly or granular surface texture. The surrounding mucosa appears normal. The patient reports that he has tried to scrape off the lesion, but it has remained persistent. During the medical history review, it is noted that James has a history of hypertension and type 2 diabetes, which is being managed with medication. He also mentions occasional use of inhaled corticosteroids for his seasonal allergies. His oral hygiene practices seem adequate, but he occasionally uses over-the-counter mouthwashes. James reports that he’s been a smoker for 25 years, and on average he smokes a pack per week.
White, interlacing lines (striae of Wickham) on the buccal mucosa are a characteristic clinical feature of:
Explanation:
Correct Answer:
“Lichen planus”
Why correct?
The presence of white, interlacing lines (striae of Wickham) is a hallmark feature of lichen planus, a chronic inflammatory condition affecting the mucosa.
The lesion described is well-defined, with a granular or pebbly surface, and cannot be scraped off, which aligns with lichen planus.
Lichen planus is often bilateral, painless (unless erosive), and associated with discomfort when rubbed or irritated.
Why “Leukoplakia” is Incorrect:
Leukoplakia refers to a white patch that cannot be scraped off and has no specific clinical appearance (it’s a diagnosis of exclusion).
Unlike lichen planus, leukoplakia lacks the characteristic striae of Wickham and is typically smooth or homogenous in texture.
Leukoplakia often has risk factors such as smoking or irritation (not necessarily autoimmune/inflammatory like lichen planus).
Why the Other Options Are Incorrect:
“Lupus erythematosus”:
Oral lesions in lupus erythematosus are typically red (erythematous), often with central ulceration, and not characterized by interlacing white lines.
They may involve multiple areas of the mucosa but lack the specific striae seen in lichen planus.
“Carcinoma in situ”:
This describes a pre-malignant or early malignant lesion, which often presents as irregular, red/white patches or ulcerated areas with poorly defined borders.
It does not show the interlacing white lines typical of lichen planus.
Key Takeaway:
The striae of Wickham (white, interlacing lines) are specific to lichen planus, making it the correct answer. Other conditions like leukoplakia or carcinoma lack these defining features and present differently.
Scenario 8
- Taste buds of the posterior 1/3 of the tongue are innervated by which nerve?
VII cranial nerve
X cranial nerve
XI cranial nerve
IX cranial nerve
IX cranial nerve
Scenario 10
- On further clinical investigation, Mrs. Gold’s saliva pH value was 6.9 (normal range 6.8-7.8) however her stimulated saliva was 3 mL at 5 minutes. In regard to saliva formation, during the primary secretion, which of the following is correct?
During the primary secretion stage saliva is isotonic
During the primary secretion stage, saliva is hypotonic
Normal stimulated salivary flow is 0.3-0.8 mL/min
During the secondary secretion stage, saliva is isotonic
Simplified Explanation:
The correct answer is “During the primary secretion stage, saliva is isotonic” because when saliva is first made by the salivary glands (primary secretion), it has the same salt concentration as blood (isotonic). Later, as it travels through the salivary ducts, salts are removed, and it becomes less salty (hypotonic).
Why the Other Choices Are Wrong:
“During the primary secretion stage, saliva is hypotonic”:
At the start, saliva is not less salty (hypotonic)—it’s isotonic, like blood. Salts are removed later in the ducts.
“Normal stimulated salivary flow is 0.3-0.8 mL/min”:
This describes saliva flow when the glands are resting (unstimulated). Stimulated flow (e.g., chewing gum) is much higher—around 1-3 mL/min.
“During the secondary secretion stage, saliva is isotonic”:
Saliva becomes hypotonic (less salty) in the ducts during the secondary stage, not isotonic.
Key Takeaway:
At the start (primary secretion), saliva is similar to blood in saltiness (isotonic). It only becomes less salty (hypotonic) after the glands process it in the ducts.
- Before leaving your office, Mrs. Gold complained about a sudden headache. She asks you if you could give her some painkillers for her headache. Which of the following you should not give to Mrs. Gold?
Ibuprofen
COX-2 selective NSAID
Panadol Osteo
Paracetamol
Correct Answer:
“COX-2 selective NSAID” (You Should Not Give)
Why COX-2 selective NSAIDs are NOT suitable for Mrs. Gold:
COX-2 inhibitors (like celecoxib) are designed for chronic inflammatory conditions like arthritis, not acute pain like a headache.
They carry a higher cardiovascular risk, particularly in patients with hypertension (Mrs. Gold has a history of hypertension), making them unsuitable for her.
Why the Other Options Are Correct Choices for a Headache:
Ibuprofen:
Why suitable?
Ibuprofen is a commonly used non-selective NSAID that effectively relieves acute pain like headaches.
It has a better safety profile than COX-2 inhibitors when used short-term, even in patients with hypertension, as long as it is taken at the correct dose.
Panadol Osteo:
Why suitable?
Panadol Osteo is a paracetamol-based extended-release formulation, which is safe and effective for mild to moderate pain, including headaches.
It has minimal side effects and no cardiovascular risks, making it suitable for someone like Mrs. Gold with hypertension.
Paracetamol:
Why suitable?
Paracetamol is a first-line treatment for headaches due to its excellent safety profile.
It doesn’t impact blood pressure or have cardiovascular risks, making it ideal for patients with underlying conditions like hypertension.
Key Takeaway:
Ibuprofen, Panadol Osteo, and Paracetamol are all safe and effective options for treating a headache in a patient like Mrs. Gold.
COX-2 selective NSAIDs should be avoided due to their higher cardiovascular risk, especially in someone with hypertension.
Which of the following statements is most correct with regard to acute suppurative osteomyelitis?
a)Acute suppurative osteomyelitis of the jaws rarely causes trismus
b)Acute suppurative osteomyelitis is always associated with bone necrosis
c)Acute dental abscesses often result in acute suppurative osteomyelitis
d)Acute suppurative osteomyelitis is usually associated with actinomycosis infection
e)There is never bone necrosis in the acute disease, while bone necrosis is always seen in chronic osteomyelitis
The correct answer is B because acute suppurative osteomyelitis is always associated with bone necrosis due to the infection damaging the bone tissue.
C is incorrect because, while acute dental abscesses can lead to osteomyelitis, they do not always result in it. Therefore, it doesn’t accurately capture the relationship compared to the certainty of necrosis in acute osteomyelitis.
The correct answer is (b) Acute suppurative osteomyelitis is always associated with bone necrosis because acute suppurative osteomyelitis involves a severe, rapid infection of the bone that leads to bone necrosis (bone death) due to the loss of blood supply. The infection spreads quickly and causes parts of the bone tissue to die as a result.
Using a biblical analogy, think of this process like a vineyard in which the grapevines need constant nourishment from the soil. If the roots are cut off from the soil and water, they wither and die. Similarly, in acute suppurative osteomyelitis, the infection is so intense that it “cuts off” the bone from its nourishing blood supply, leading to bone death.
Here’s why the other options aren’t correct:
(a) Acute suppurative osteomyelitis of the jaws rarely causes trismus: Trismus (difficulty opening the mouth) can occur with jaw infections, but it’s not the primary or distinguishing feature of acute suppurative osteomyelitis. It’s more like a side effect and not a defining trait.
(c) Acute dental abscesses often result in acute suppurative osteomyelitis: While abscesses can spread infection, not all dental abscesses lead to osteomyelitis. It’s like saying a small brushfire will always become a forest fire—it can happen, but it’s not a certainty.
(d) Acute suppurative osteomyelitis is usually associated with actinomycosis infection: Actinomycosis is a specific type of infection that doesn’t commonly cause acute osteomyelitis. It’s more like saying a rare kind of pest is always present in the vineyard, which isn’t the case.
(e) There is never bone necrosis in the acute disease, while bone necrosis is always seen in chronic osteomyelitis: This is incorrect because bone necrosis can occur in the acute phase of osteomyelitis as well. When the infection is severe, bone tissue can die quickly, like the vineyard vines withering due to sudden drought or damage to their roots.
In summary, option (b) is correct because bone necrosis is a direct result of the intense infection in acute suppurative osteomyelitis, much like how a vineyard cut off from its source of nourishment withers and dies rapidly. This characteristic of bone death is a defining feature of acute suppurative osteomyelitis.
Mr. Kumar mentioned that his saliva production has increased but he hasn’t had any problems with swallowing. Regarding salivary secretion and swallowing, which is correct:
a)Breathing is not possible during swallowing
b)Efficient swallowing can occur without formation of food bolus
c)Swallowing is a purely voluntary activity.
d)Swallowing is an automatic activity in the pharyngeal and oesophageal stages
a)Breathing is not possible during swallowing
d)Swallowing is an automatic activity in the pharyngeal and oesophageal stages
Which of the following is a common genetic cause of dentinogenesis imperfecta?
a)Down syndrome
b)Marfan syndrome
c)Ehlers-Danlos syndrome
d)Mutations in dentin genes such as DSPP or COL1A1
The correct answer is D because dentinogenesis imperfecta, a condition affecting tooth development, is primarily caused by mutations in specific genes like DSPP or COL1A1 that are directly involved in making dentin (the layer beneath the enamel of teeth).
The correct answer is (d) Mutations in dentin genes such as DSPP or COL1A1 because dentinogenesis imperfecta is specifically caused by genetic mutations in these dentin-related genes, DSPP and COL1A1, which are directly responsible for the proper formation and strength of dentin, the hard tissue underneath tooth enamel.
To explain this with a biblical analogy:
Imagine the genes DSPP and COL1A1 as the master builders of a temple’s foundation. They oversee how each stone (or part of the dentin) is laid, ensuring the temple (tooth) is strong and stable. When these genes function as they should, the “temple” of our teeth is built on a solid foundation, ready to withstand daily wear.
However, if there’s a mutation (a change in these builder’s instructions), the foundation doesn’t form correctly. This faulty foundation causes the dentin to be weaker and more prone to breakage and discoloration, leading to dentinogenesis imperfecta.
Here’s why the other options don’t fit as causes of dentinogenesis imperfecta:
(a) Down syndrome: Down syndrome affects many aspects of development but doesn’t directly alter the specific “builders” responsible for dentin formation. It’s like a general condition that may influence many parts of the body, but it doesn’t specifically disrupt the master builders DSPP or COL1A1.
(b) Marfan syndrome: Marfan syndrome affects connective tissues, like ligaments and blood vessels, but it doesn’t interfere with the particular building blocks of dentin. It’s like having an issue with the ropes and beams that hold the temple’s ceiling in place but not the foundational stones of the walls.
(c) Ehlers-Danlos syndrome: This syndrome also affects connective tissues, causing flexibility and elasticity issues. While it can affect collagen in the body, it doesn’t specifically cause dentinogenesis imperfecta, as it doesn’t disrupt DSPP or COL1A1, the critical genes for dentin structure.
In summary, (d) is correct because dentinogenesis imperfecta occurs specifically due to mutations in genes that directly oversee dentin formation. This genetic change weakens the “temple foundation,” making teeth more fragile, just as the mislaid stones in a foundation would compromise the strength of a building.
A (Down syndrome), B (Marfan syndrome), and C (Ehlers-Danlos syndrome) are all genetic conditions, but they do not specifically cause dentinogenesis imperfecta. Instead, they have their own distinct features and symptoms that do not directly impact tooth formation in the same way.
