NEET MDS Synopsis
Bias in Public Health Dentistry
Public Health DentistryHere are some common types of bias encountered in public health dentistry,
along with their implications:
1. Selection Bias
Description: This occurs when the individuals included in a
study are not representative of the larger population. This can happen due to
non-random sampling methods or when certain groups are more likely to be
included than others.
Implications:
If a study on dental care access only includes patients from a specific
clinic, the results may not be generalizable to the broader community.
Selection bias can lead to over- or underestimation of the prevalence of
dental diseases or the effectiveness of interventions.
2. Information Bias
Description: This type of bias arises from inaccuracies in
the data collected, whether through measurement errors, misclassification, or
recall bias.
Implications:
Recall Bias: Patients may not accurately remember their
dental history or behaviors, leading to incorrect data. For example,
individuals may underestimate their sugar intake when reporting dietary
habits.
Misclassification: If dental conditions are
misdiagnosed or misreported, it can skew the results of a study assessing
the effectiveness of a treatment.
3. Observer Bias
Description: This occurs when the researcher’s expectations
or knowledge influence the data collection or interpretation process.
Implications:
If a dentist conducting a study on a new treatment is aware of which
patients received the treatment versus a placebo, their assessment of
outcomes may be biased.
Observer bias can lead to inflated estimates of treatment effectiveness
or misinterpretation of results.
4. Confounding Bias
Description: Confounding occurs when an outside variable is
associated with both the exposure and the outcome, leading to a false
association between them.
Implications:
For example, if a study finds that individuals with poor oral hygiene
have higher rates of cardiovascular disease, it may be confounded by
lifestyle factors such as smoking or diet, which are related to both oral
health and cardiovascular health.
Failing to control for confounding variables can lead to misleading
conclusions about the relationship between dental practices and health
outcomes.
5. Publication Bias
Description: This bias occurs when studies with positive or
significant results are more likely to be published than those with negative or
inconclusive results.
Implications:
If only studies showing the effectiveness of a new dental intervention
are published, the overall understanding of its efficacy may be skewed.
Publication bias can lead to an overestimation of the benefits of
certain treatments or interventions in the literature.
6. Survivorship Bias
Description: This bias occurs when only those who have
"survived" a particular process are considered, ignoring those who did not.
Implications:
In dental research, if a study only includes patients who completed a
treatment program, it may overlook those who dropped out due to adverse
effects or lack of effectiveness, leading to an overly positive assessment
of the treatment.
7. Attrition Bias
Description: This occurs when participants drop out of a
study over time, and the reasons for their dropout are related to the treatment
or outcome.
Implications:
If patients with poor outcomes are more likely to drop out of a study
evaluating a dental intervention, the final results may show a more
favorable outcome than is truly the case.
Addressing Bias in Public Health Dentistry
To minimize bias in public health dentistry research, several strategies can
be employed:
Random Sampling: Use random sampling methods to ensure
that the sample is representative of the population.
Blinding: Implement blinding techniques to reduce
observer bias, where researchers and participants are unaware of group
assignments.
Standardized Data Collection: Use standardized
protocols for data collection to minimize information bias.
Statistical Control: Employ statistical methods to
control for confounding variables in the analysis.
Transparency in Reporting: Encourage the publication of
all research findings, regardless of the results, to combat publication
bias.
Adrenocortical Hyperfunction
General Pathology
Adrenocortical Hyperfunction (Hyperadrenalism)
Hypercortisolism (Cushing Syndrome) is caused by any condition that produces an elevation in glucocorticoid levels. The causes of this syndrome are
A. Exogenous through administration of exogenous glucocorticoids; the most common causeB. Endogenous
1. Hypothalamic-pituitary diseases causing hypersecretion of ACTH (Cushing disease)
2. Adrenocortical hyperplasia or neoplasia
3. Ectopic ACTH secretion by nonendocrine neoplasms (paraneoplastic)
Pathological features
- The main lesions of Cushing syndrome are found in the pituitary and adrenal glands.
- The most common change in the pituitary, results from high levels of endogenous or exogenous glucocorticoids, is termed Crooke hyaline change. In this condition, the normal granular, basophilic cytoplasm of the ACTH-producing cells in the anterior pituitary is replaced by homogeneous, lightly basophilic material. This is due to accumulation of intermediate keratin filaments in the cytoplasm.
- There is one of four changes in the adrenal glands, which depends on the cause.
1. Cortical atrophy
2. Diffuse hyperplasia
3. Nodular hyperplasia
4. Adenoma, rarely a carcinoma
1. In patients in whom the syndrome results from exogenous glucocorticoids, suppression of endogenous ACTH results in bilateral cortical atrophy, due to a lack of stimulation of the cortex by ACTH. In cases of endogenous hypercortisolism, in contrast, the adrenals either are hyperplastic or contain a cortical neoplasm.
2. In Diffuse hyperplasia the adrenal cortex is diffusely thickened and yellow, as a result of an increase in the size and number of lipid-rich cells in the zonae fasciculata and reticularis.
3. Nodular hyperplasia, which takes the form of bilateral, up to 2.0-cm, yellow nodules scattered throughout the cortex.
4. Primary adrenocortical neoplasms causing Cushing syndrome may be benign or malignant. The adrenocortical adenomas are yellow tumors surrounded by capsules, and most weigh < 30 gm .
Osteomyelitis
General Pathology
Osteomyelitis
This refers to inflammation of the bone and related marrow cavity almost always due to infection. Osteomyelitis can be acute or a chronic. The most common etiologic agents are pyogenic bacteria and Mycobacterium tuberculosis.
Pyogenic Osteomyelitis
The offending organisms reach the bone by one of three routes:
1. Hematogenous dissemination (most common)
2. Extension from a nearby infection (in adjacent joint or soft tissue)
3. Traumatic implantation of bacteria (as after compound fractures or orthopedic procedures). Staphylococcus aureus is the most frequent cause. Mixed bacterial infections, including anaerobes, are responsible for osteomyelitis complicating bone trauma. In as many as 50% of cases, no organisms can be isolated.
Pathologic features
• The offending bacteria proliferate & induce an acute inflammatory reaction.
• Entrapped bone undergoes early necrosis; the dead bone is called sequestrum.
• The inflammation with its bacteria can permeate the Haversian systems to reach the periosteum. In children, the periosteum is loosely attached to the cortex; therefore, sizable subperiosteal abscesses can form and extend for long distances along the bone surface.
• Lifting of the periosteum further impairs the blood supply to the affected region, and both suppurative and ischemic injury can cause segmental bone necrosis.
• Rupture of the periosteum can lead to an abscess in the surrounding soft tissue and eventually the formation of cutaneous draining sinus. Sometimes the sequestrum crumbles and passes through the sinus tract.
• In infants (uncommonly in adults), epiphyseal infection can spread into the adjoining joint to produce suppurative arthritis, sometimes with extensive destruction of the articular cartilage and permanent disability.
• After the first week of infection chronic inflammatory cells become more numerous. Leukocyte cytokine release stimulates osteoclastic bone resorption, fibrous tissue ingrowth, and bone formation in the periphery, this occurs as a shell of living tissue (involucrum) around a segment of dead bone. Viable organisms can persist in the sequestrum for years after the original infection.
Chronicity may develop when there is delay in diagnosis, extensive bone necrosis, and improper management.
Complications of chronic osteomyelitis include
1. A source of acute exacerbations
2. Pathologic fracture
3. Secondary amyloidosis
4. Endocarditis
5. Development of squamous cell carcinoma in the sinus tract (rarely osteosarcoma).
Tuberculous Osteomyelitis
Bone infection complicates up to 3% of those with pulmonary tuberculosis. Young adults or children are usually affected. The organisms usually reach the bone hematogenously. The long bones and vertebrae are favored sites. The lesions are often solitary (multifocal in AIDS patients). The infection often spreads from the initial site of bacterial deposition (the synovium of the vertebrae, hip, knee, ankle, elbow, wrist, etc) into the adjacent epiphysis, where it causes typical granulomatous inflammation with caseous necrosis and extensive
bone destruction. Tuberculosis of the vertebral bodies (Pott disease), is an important form of osteomyelitis.
Infection at this site causes vertebral deformity and collapse, with secondary neurologic deficits. Extension of the infection to the adjacent soft tissues with the development of psoas muscle abscesses is fairly common in Pott disease. Advanced cases are associated with cutaneous sinuses, which cause secondary bacterial infections. Diagnosis is established by synovial fluid direct examination, culture or PCR
Bone Healing: Primary vs. Secondary Intention
Oral and Maxillofacial SurgeryBone Healing: Primary vs. Secondary Intention
Bone healing is a complex biological process that can occur through different
mechanisms, primarily classified into primary healing and secondary
healing (or healing by secondary intention). Understanding these
processes is crucial for effective management of fractures and optimizing
recovery.
Secondary Healing (Callus Formation)
Secondary healing is characterized by the
formation of a callus, which is a temporary fibrous tissue that bridges the
gap between fractured bone fragments. This process is often referred to as
healing by secondary intention.
Mechanism:
When a fracture occurs, the body initiates a healing response that
involves inflammation, followed by the formation of a soft callus
(cartilaginous tissue) and then a hard callus (bony tissue).
The callus serves as a scaffold for new bone formation and provides
stability to the fracture site.
This type of healing typically occurs when the fractured fragments
are approximated but not rigidly fixed, allowing for some movement at
the fracture site.
Closed Reduction: In cases where closed reduction is
used, the fragments are aligned but may not be held in a completely stable
position. This allows for the formation of a callus as the body heals.
Primary Healing (Direct Bone Union)
Primary healing occurs when the fractured
bone fragments are compressed against each other and held in place by rigid
fixation, such as with bone plates and screws. This method prevents the
formation of a callus and allows for direct bone union.
Mechanism:
In primary healing, the fragments are in close contact, allowing for
the migration of osteocytes and the direct remodeling of bone without
the intermediate formation of a callus.
This process is facilitated by rigid fixation, which stabilizes the
fracture and minimizes movement at the fracture site.
The healing occurs through a process known as Haversian
remodeling, where the bone is remodeled along lines of stress,
restoring its structural integrity.
Indications for Primary Healing:
Primary healing is typically indicated in cases of:
Fractures that are surgically stabilized with internal fixation
devices (e.g., plates, screws).
Fractures that require precise alignment and stabilization to
ensure optimal healing and function.
Urinary tract infection
General Pathology
Urinary tract infection
Most often caused by gram-negative, rod-shaped bacteria that are normal residents of the enteric tract, especially Escherichia coli.
Clinical manifestations:
frequent urination, dysuria, pyuria (increased PMNs), hematuria, and bacteriuria.
May lead to infection of the urinary bladder (cystitis) or kidney (pyelonephritis).
The External Ear
AnatomyThe External Ear
The auricle (L. auris, ear) is the visible, shell-like part of the external ear.
It consists of a single elastic cartilage that is covered on both surfaces with thin, hairy skin.
The external ear contains hairs, sweat glands, and sebaceous glands.
The cartilage is irregularly ridged and hollowed, which gives the auricle its shell-like form.
It also shapes the orifice of the external acoustic meatus.
The Ear Lobule
The ear lobule (earlobe) consists of fibrous tissue, fat and blood vessels that are covered with skin.
The arteries are derived mainly from the posterior auricular artery and the superficial temporal artery.
The skin of the auricle is supplied by the great auricular and auriculotemporal nerves.
The great auricular nerve supplies the superior surface and the lateral surface inferior to the external acoustic meatus with nerve fibres from C2.
The auriculotemporal nerve supplies the skin of the auricle superior to the external acoustic meatus.
The External Acoustic Meatus
This passage extends from the concha (L. shell) of the auricle to the tympanic membrane (L. tympanum, tambourine). It is about 2.5 cm long in adults.
The lateral 1/3 of the S-shaped canal is cartilaginous, whereas its medial 2/3 is bony.
The lateral third of the meatus is lined with the skin of the auricle and contains hair follicles, sebaceous glands, and ceruminous glands.
The latter glands produce cerumen (L. cera, wax).
The medial two-thirds of the meatus is lined with very thin skin that is continuous with the external layer of the tympanic membrane.
The lateral end of the meatus is the widest part. It has the diameter about that of a pencil.
The meatus becomes narrow at its medial end, about 4 mm from the tympanic membrane.
The constricted bony part is called the isthmus.
Innervation of the external acoustic meatus is derived from three cranial nerves:
The auricular branch of the auriculotemporal nerve (derived from the mandibular, CN V3).
The facial nerve (CN VII) by the branches from the tympanic plexus.
The auricular branch of the vagus nerve (CN X).
The Tympanic Membrane
This is a thin, semi-transparent, oval membrane at the medial end of the external acoustic meatus.
It forms a partition between the external and middle ears.
The tympanic membrane is a thin fibrous membrane, that is covered with very thin skin externally and mucous membrane internally.
The tympanic membrane shows a concavity toward the meatus with a central depression, the umbo, which is formed by the end of the handle of the malleus.
From the umbo, a bright area referred to as the cone of light, radiates anteroinferiorly.
The external surface of the tympanic membrane is supplied by the auriculotemporal nerve.
Some innervation is supplied by a small auricular branch of the vagus nerve (CN X); this nerve may also contain some glossopharyngeal and facial nerve fibres.
Porosity defects in Dental casting
Prosthodontics
Porosity
Porosity refers to the presence of voids or spaces within a solid material. In
the context of prosthodontics, it specifically pertains to the presence of small
cavities or air bubbles within a cast metal alloy. These defects can vary in
size, distribution, and number, and are generally undesirable because they
compromise the integrity and mechanical properties of the cast restoration.
Causes of Porosity Defects
Porosity in castings can arise from several factors, including:
1. Incomplete Burnout of the Investment Material: If the wax pattern used to
create the mold is not completely removed by the investment material during the
burnout process, gases can become trapped and leave pores as the metal cools and
solidifies.
2. Trapped Air Bubbles: Air can become trapped in the investment mold during the
mixing and pouring of the casting material. If not properly eliminated, these
air bubbles can lead to porosity when the metal is cast.
3. Rapid Cooling: If the metal cools too quickly, the solidification process may
not be complete, leaving small pockets of unsolidified metal that shrink and
form pores as they solidify.
4. Contamination: The presence of contaminants in the metal alloy or investment
material can also lead to porosity. These contaminants can react with the metal,
forming gases that become trapped and create pores.
5. Insufficient Investment Compaction: If the investment material is not packed
tightly around the wax pattern, small air spaces may remain, which can become
pores when the metal is cast.
6. Gas Formation During Casting: Certain reactions between the metal alloy and
the investment material or other substances in the casting environment can
produce gases that become trapped in the metal.
7. Metal-Mold Interactions: Sometimes, the metal can react with the mold
material, resulting in gas formation or the entrapment of mold material within
the metal, which then appears as porosity.
8. Incorrect Spruing and Casting Design: Poorly designed sprues can lead to
turbulent metal flow, causing air entrapment and subsequent porosity.
Additionally, a complex casting design may result in areas where metal cannot
flow properly, leading to incomplete filling of the mold and the formation of
pores.
Consequences of Porosity Defects
The presence of porosity in a cast restoration can have several negative
consequences:
1. Reduced Strength: The pores within the metal act as stress concentrators,
weakening the material and making it more prone to fracture or breakage under
functional loads.
2. Poor Fit: The pores can prevent the metal from fitting snugly against the
prepared tooth, leading to a poor marginal fit and potential for recurrent decay
or gum irritation.
3. Reduced Biocompatibility: The roughened surfaces and irregularities created
by porosity can harbor plaque and bacteria, which can lead to peri-implant or
periodontal disease.
4. Aesthetic Issues: In visible areas, porosity can be unsightly, affecting the
overall appearance of the restoration.
5. Shortened Service Life: Prosthodontic restorations with porosity defects are
more likely to fail prematurely, requiring earlier replacement.
6. Difficulty in Polishing and Finishing: The presence of porosity makes it
challenging to achieve a smooth, polished finish, which can affect the comfort
and longevity of the restoration.
Prevention and Management of Porosity
To minimize porosity defects in prosthodontic castings, the following steps can
be taken:
1. Proper Investment Technique: Carefully follow the manufacturer's instructions
for mixing and investing the wax pattern to ensure complete burnout and minimize
trapped air bubbles.
2. Slow and Controlled Cooling: Allowing the metal to cool slowly and uniformly
can help to reduce the formation of pores by allowing gases to escape more
easily.
3. Pre-casting De-gassing: Some techniques involve degassing the investment mold
before casting to remove any trapped gases.
4. Cleanliness: Ensure that the metal alloy and investment materials are free
from contaminants.
5. Correct Casting Procedure: Use proper casting techniques to reduce turbulence
and ensure a smooth flow of metal into the mold.
6. Appropriate Casting Design: Design the restoration with proper spruing and a
simple, well-thought-out pattern to allow for even metal flow and minimize
trapped air.
7. Proper Casting Conditions: Control the casting environment to reduce the
likelihood of gas formation during the casting process.
8. Inspection and Quality Control: Carefully inspect the cast restoration for
porosity under magnification and radiographs before it is delivered to the
patient.
9. Repair or Replacement: When porosity defects are detected, they may be
repairable through techniques such as metal condensation, spot welding, or
adding metal with a pin connector. However, in some cases, the restoration may
need to be recast to ensure optimal quality.
Seborrheic dermatitis
General Pathology
Seborrheic dermatitis is a scaly dermatitis on the scalp (dandruff) and face.
- due to Pitysporium species
- can be seen in AIDS as an opportunistic infection