Pathology Flashcards
List and describe 10 eukaryotic cell components
Eukaryotic cell structure (10 points):
- Nucleus (contains genetic material)
- Nucleolus (synthesis of RNA/assembly of ribosome)
- Cell membrane (lipid bilayer with proteins and sugars)
- Cytoplasm (80% water, suspends organelles)
- Mitochondria (double membrane, supplies ATP for cell)
- Golgi apparatus (processes and packages proteins into vesicles)
- Smooth ER (lipid synthesis and metabolism)
- Rough ER (studded with ribosomes, protein metabolism)
- Ribosome (site of protein synthesis)
- Lysosome (contains enzymes, breakdown of waste products of cell).
List 6 types of cell
Types of cell:
“BBGGNM”
- Bone
- Blood (erythrocytes, leukocytes, lymphocytes)
- Gland
- Gamete.
- Nerve
- Muscle (voluntary striated; involuntary smooth; cardiac)
List and describe 3 shapes of cell
Shapes of cell:
- Squamous
- simple squamous e.g. capillary epithelium
- stratified squamous e.g. skin
- keratinized e.g. masticatory surfaces
- non-keratinized (or parakeratinized) e.g. lips, buccal surface
- Cuboidal
- simple cuboidal e.g. ovary surface
- Columnar
- simple columnar e.g. digestive tract
- pseudocolumnar e.g. respiratory tract.
Categorize different types of cell by their ability to divide and differentiate (3 main categories)
Tissue homeostasis – different types of cell have different abilities to divide and differentiate:
- Labile cells – constantly renewed e.g. stratified squamous epithelium of skin
- Stable cells – usually quiescent but can be stimulated to divide e.g. hepatocytes
- Permanent cells – incapable of regeneration in post-natal life e.g. neurons, cardiac myocytes.
What is the difference between hyperplasia and hypertrophy?
Cell growth:
- Hyperplasia (cell proliferation) – increase in number of cells
- Hypertrophy – increase in size of cells.
Recall each phase the eukaryotic cell cycle (4 phases)
Cell cycle: M → G1 → S → G2
G0 phase: cells are quiescent outside of cell cycle
Outline the 7 stages of mitosis (M phase of cell cycle)
Stages of mitosis (7 points):
“I _P_ush _P_oor _M_idgets _A_round _T_esco _C_arparks”
- Interphase
- Prophase
- Prometaphase
- Metaphase
- Anaphase
- Teleophase
- Cyctokinesis
Describe reversible and irreversible injury in cells under physiological stresses and pathological stimuli
Physiological stresses and patholigical stimuli pathway
List the causes of cell injury (10 points)
“THE MAGNIFIC” injury
The extra “E” is not included in the photo, however, take this as an extra injury: endocrine.
List the 4 main cell injury mechanisms
Cell injury mechanisms (4 points):
- Loss of energy (ATP/O2 depletion)
- Oxygen and oxygen-derived free radicals
- Loss of calcium homeostasis
- Defects in plasma membrane
Describe the mechanism of cell injury due to loss of energy (ATP/O2)
Loss of energy (ATP/O2):
- Mitochondria susceptible to injury from ischaemia, oxidants, free radicals, cations, weak acids
- Mitochondria damage leads to leakage of pro-apoptic proteins, reduced ATP
Describe the mechanism of cell injury due to oxygen and oxygen-derived free radicals
Oxygen and oxygen-derived free radicals:
- Free radicals chemically unstable (unpaired valence electrons) so prone to reacting with other stable molecules
- Causes chain reaction (autocatalytic)
- Cellular injury caused by:
- Lipid peroxidation causing cell membrane damage
- Protein fragmentation
- Reacts with thymine causing DNA mutations
Describe the mechanism of cell injury due to loss of calcium homeostasis
Loss of calcium homeostasis:
- Normally extracellular Ca2+ > intracellular Ca2+
- Ca2+ gradient maintained by membrane ATPase pumps
- Increase in cytoplasm Ca2+:
- Activation of intracellular enzymes
- Ca2+ is pro-aptotic
Describe the changes in cell morphology following reversible cell injury
Reversible cell injury:
- Light microscopic changes – cell swelling, fat accumulation
- Ultrastructural changes – cell membrane alterations, mitochondrial swelling, RER swelling and ribosomal detachment.
Describing the changes in cell morphology following irreversible cell injury
Irreversible cell injury:
- Light microscopic changes: loss of RNA, cytoplasmic vacuolisation, chromatin clumping
- Ultrastructural changes: membrane disruption, mitochondrial amorphous densities, nuclear changes (pyknosis – shrinkage; karyorrhexis – fragmentation; karyolysis – fading).
Define necrosis and describe the 5 distinct patterns of necrosis
Necrosis – pathological early cell death:
- Unregulated; initiated by extrinsic factors (e.g. infection, trauma).
- Separate distinctive morphological patterns (5 points):
- Coagulative
- Liquefactive
- Gangrenous
- Caseous
- Fat.
Describe coagulative necrosis
Coagulative necrosis:
- Most commonly caused by ischaemia (e.g. myocardial infarction)
- Basic tissue architecture stays the same due to denatured lysosomal enzymes, so no degradation
- Necrotic cells ultimately removed by inflammatory cells
- Dead cells replaced by regeneration (or scar tissue in the case of cardiac infarction).
Describe liquefactive necrosis
Liquefactive necrosis:
- Most commonly caused by brain tissue infarcts
- Enzymatic break down of tissue which leads to loss of tissue architecture (viscous liquid mass)
- Puss due to leukocyte accumulation.
Describe gangrenous necrosis
Gangrenous necrosis:
- Most commonly caused by disrupted blood supply to extremities (e.g. toes)
- Dry gangrene (no bacterial superinfection; mainly coagulative necrosis)
- Wet gangrene (bacterial superinfection; mainly liquefactive necrosis)
- Advanced and macroscopically obvious presentation.
Describe caseous necrosis
Caseous necrosis:
- Most commonly caused by mycobacterium and fungal infections
- Macroscopically “cheesy”
- Microscopically amorphous granular debris surround by inflammatory cells (i.e. granuloma)
- Tissue architecture unrecognizable (due to combination of coagulative and liquefactive necrosis).
Describe fat necrosis
Fat necrosis:
- Most commonly found in adipose tissue (especially of pancreas in pancreatitis)
- Occurs following hydrolytic action of lipases
- Fatty acids released are mopped up by free calcium – saponification reaction (soap).
Define and describe the triggers and mechanisms of apoptosis
Apoptosis – programmed cell death (“cell suicide”):
- Controlled; triggered by intrinsic or extrinsic pathway; active process (requires ATP)
- Physiological – embryonic development, hormone-dependent involution of organs
- Pathological – controlled cell death in tumours; controlled cell death of virally infected cells
- Excessive apoptosis results in atrophy; insufficient apoptosis leads to hyperplasia.
Differentiate between necrosis and apoptosis; stimuli, cell morphology, biochemical mechanism and tissue reaction (6 points each)
Define acute inflammation
Acute inflammation is an essential defence mechanism in response to tissue injury e.g. traumas:
- Mechanical
- Thermal
- Radiation
- Chemical
- Infection
- Ischaemia
- Immunological
- Foreign body
List the 5 cardinal signs of acute inflammation
Macroscopic features – cardinal signs of acute inflammation (5 points):
- Rubor
- Tumor
- Calor
- Dolor
- Functio laesa.
List the keys stages (3 points) and key components (3 points) of acute inflammation
Acute inflammation:
- 3 key stages of acute inflammation:
- vasodilatation
- increased vascular permeability
- migration of leukocytes.
- 3 key components of acute inflammatory process:
- vascular component
- cellular component
- chemical mediator component
Describe the vascular changes in acute inflammation (7 points)
Vascular changes in acute inflammation (7 points):
- Initial rapid & transient arteriolar vasoconstriction
- Activation of clotting cascade
- Resultant fibrin plug traps platelets
- Platelets activation causes release of inflammatory mediators (e.g. histamine, 5-HT, LKTs, PGs)
- Arteriolar smooth muscle relaxation → increased blood flow
- Increased vessel permeability → leak of exudate
- Increased oncotic pressure in interstitial tissue draws H20.
Describe the cellular changes in acute inflammation (6 points)
Cellular changes in acute inflammation (6 points):
“MRADCP”
- Margination – as blood flow slows (vascular changes) leukocytes move to lie against endothelium
- Rolling – GLPs on leukocytes (salyl-Lewis X) bind on and off to endothelial selectins (E- and P-selectins)
- Adhesion – firm adhesion of leukocytes (not on and off) occurs via integrin molecules (LFA-1) on leukocytes bind to corresponding Ig ligands (ICAM-1 and ICAM-2) on endothelium
- Diapedesis – adherent leukocytes transmigrate through endothelium into interstitial space of tissues
- Chemotaxis – migrated leukocytes move along gradient of chemotactic factors* toward site of injury
- Phagocytosis – opsonized bacteria are engulfed by neutrophils and macrophages to create a phagosome; phagosome fuses with lysosome and engulfed particles are digested and exocytosed.
*Initially neutrophils (initial 24 hr) followed by macrophages (after 48 hr) migrate to area of injury
List the plasma and cellular chemical mediators of acute inflammation
Chemical mediators of acute inflammation
- Plasma chemical mediators:
- Complement system (membrane attack complex); kinin system (bradykinin vasodilatation); coagulation system (clot formation); fibrinolytic system (clot breakdown)
- Cellular chemical mediators:
- Vasoactive amines (leukocytes – histamine, 5-HT; endothelium – NO)
- Lysosomal enzymes
- Arachidonic acid derivatives (COX pathway – PG, LKT)
- Cytokines (TNF, IL-1, IL-6, Chemokines, IL-17)
- Free radicals
List the diagnostic outcomes of acute inflammation (4 points)
Diagnostic outcomes of acute inflammation (4 points):
“SCAR”
- Scaring and fibrosis
- Chronic inflammation
- Abscess and pus formation
- Resolution
List the key systemic effects of acute inflammation (3 points)
Key systemic effects of acute inflammation:
- Fever (endogenous pyrogens: IL-1 – prostaglandins in hypothalamus; TNF-α)
- Leukocytosis – IL-1 and TNF-α produce an accelerated release of leukocytes from bone marrow
- Acute phase response:
- Decreased appetite
- Altered sleep patterns
- Changes in plasma concentrations of CRP, fibrinogen, serum amyloid A
List 3 key features of chronic inflammation
Key features of chronic inflammation (3 points):
- Ongoing tissue destruction (hence “chronic”)
- Infiltration of tissues by mononuclear inflammatory cells
- Evidence of healing.
List 3 main causes of chronic inflammation
Main causes of chronic inflammation (3 points):
- Non-specific (underlying injurious agent persists, inadequate blood supply, failure to drain)
- Autoimmune (production of antibodies against self – antibody complexes, necrosis)
- Granulomatous (organized collection of macrophages; offending agent walled off in pus-filled cavity).
Define granuloma and describe its formation
Organized collection of macrophages during inflammation.
Granulomas form when the immune system attempts to wall off foreign substances which it is unable to eliminate, e.g. infection organisms (TB), foreign objects, keratin and suture fragments.
Define periapical granuloma (6 points)
Localized mass of chronically inflamed granulation tissue that forms at the opening of the pulp canal, generally at the apex of a nonvital tooth root.
Most cases of periapical granuloma are completely asymptomatic and are discovered incidentally on radiograph → well-circumscribed radiolucency
Describe periapical (i.e. radicular) cyst (7 points)
Describe periapical cyst (radicular cyst):
- True cyst (unlike periapical granuloma)
- A true cyst is an abnormal, closed, epithelium-lined cavity in the body
- There is a proliferation of the epithelial rests of Malassez
- As the cells in the core of the mass become increasingly separated from the source of nutrition in the connective tissue, they undergo necrosis centrally, forming a cavity that is lined by epithelium and filled with fluid.
- Most periapical (radicular) cysts are asymptomatic and discovered on radiographic examination (similar to periapical granuloma)
- It is not possible to differentiate reliably a periapical granuloma from a periapical (radicular) cyst on the basis of the radiographic appearance alone
- Lateral periapical (radicular) cyst may be used to describe this inflammatory cyst when it occurs laterally (e.g. due to laterally positioned foramen of root apex)
List 7 diseases with associated chronic inflammation
Diseases associated with chronic inflammation (non-exhaustive list):
- Atherosclerosis
- Allergy
- Asthma
- Transplant rejection
- Vasculitis
- Inflammatory bowel disease
- Sarcoidosis
List the macroscopic features of chronic inflammation (5 points)
Macroscopic features of chronic inflammation (5 points):
- Chronic ulcer
- Chronic abscess
- Thickening of hollow viscus wall
- Granuloma
- Fibrosis.
Recall the microscopic features of chronic inflammation
List the predominant cell types present in different chronic inflammatory infiltrates
Cellular response to chronic inflammation – predominant cell in the inflammatory infiltrate varies according to cause of inflammation
Cell type:
- Neutrophils – common bacteria
- Lymphocytes – viral and autoimmune disease
- Plasma cells – spirochaetal disease (e.g. syphilis)
- Macrophages – fungal infections (e.g. TB), typhoid fever
- Eosinophils – parasites, allergy (e.g. allergic asthma), gut inflammation.
List the key cytokines found in chronic inflammation (3 points)
Key cytokines found in chronic inflammation:
- IL-12
- IFN-γ
- IL-17
Describe the basic diagnostic indicators for inflammation, including systemic inflammatory response syndrome (SIRS)
History and examination:
- Pyrexia
- Leukocytosis
- ESR
- Acute phase proteins – ESR, fibrinogen
- Cardinal signs.
Systemic inflammatory response syndrome (SIRS):
- Excessive reaction of acute phase response
- Defined by 2 or more of the following:
- Tachycardia >90 bpm
- Respiratory rate >20 breaths/min
- Temperature >38°C or <36°C
- WCC >12 or <4 x 109/L.
Can lead to multi-organ failure due to changes in vascular endothelium
List and describe the 3 basic layers of the skin
Skin basic structure (3 layers):
- Epidermis (avascular, keratinized, stratified squamous epithelium)
- Dermis (bloods vessels, nerves, glands)
- Hypodermis (i.e. subcutaneous tissue, vascularized, fatty, connective tissue).
List the histologic strata of the epidermis (5 points)
Epidermis (5 distinct strata from superficial to deep):
- Stratum corneum – most superficial stratum; cornified to protect from abrasion and microbes
- Stratum lucidum – contains eleidin, a transparent (i.e. lucid) protein derived from keratohyalin
- Stratum granulosum – grainy layer due to keratin and keratohyalin
- Stratum spinosum – spiny in appearance due to protruding cell processes connected via desmosomes
- Stratum basale – deepest stratum; single base layer of cuboidal cells; contains melanin.
List the key types of wounds (7 points)
Types of wounds (7 key points):
“CLAPHIP”
- Contusion
- Laceration
- Abrasion
- Puncture
- Haematoma.
- Incision
- Penetration
List the types of surgical wound (4 points)
Types of surgical wound (4 points):
- Clean – no inflammation, no break in sterile technique, respiratory, GI and GU tracts not entered
- Clean-contaminated – controlled incision through respiratory, GI or GU tracts, contamination present
- Contaminated – break in sterile technique; spillage from GI tract; acute, non-purulent inflammation
- Dirty – viscera perforated, acute inflammation with pus, e.g. perforated bowel (faecal contamination).
Outline the progression of burn wounds
Burn wound progression:
Superficial → Superficial-partial → Deep-partial → Full thickness (3rd degree) → (4th degree)
Describe the different types of wound healing, including:
- Primary
- Secondary
- Tertiary (Delayed Primary)
List the phases of wound healing (4 points)
Phases of wound healing (4 points):
- Haemostasis
- Inflammation
- Proliferation
- Maturation and remodelling.
Describe the haemostasis phase of wound healing
Following immediate tissue injury, the phases of wound healing begin.
Phase 1 Haemostasis phase (0–15 min):
- Immediate vasoconstriction
- Activated platelets aggregate at site of endothelial injury
- Initiation of clotting cascade
- Fibrin matrix stabilized wound by forming a mesh.
Describe the inflammation phase of wound healing
Following the haemostasis phase of wound healing
Phase 2 Inflammation phase (hours–days):
- Vasodilatation and increased vascular permeability
- Migration of neutrophils and macrophages
- Phagocytosis of debris
- Influx of fibroblasts (important in next phase; produce extracellular matrix and collagen type III)
- Release of cytokines and platelet-derived growth factors.
Describe the proliferation phase of wound healing
Following the inflammation phase of wound healing
Phase 3 Proliferation phase (days–months):
- Formation of granulation tissue (presence of growth factor proliferates cells recruited earlier)
- Angiogenesis (development of vascular endothelial cells)
- Epithelialisation (epithelial cells at edge of wound proliferate and bridge across wound)
- Wound contraction (development of myofibroblasts; act like muscle to contract wound).
Describe the maturation and remodeling phase of wound healing
Following the proliferation phase of wound healing
Phase 4
Maturation and remodelling phase (weeks–months):
- Stage lasts for months (takes longer if wound in site of movement, e.g. elbow)
- Scar becomes less vascular (red to pale)
- Tensile strength increases as collagen is modified (type III collagen replaced with type I collagen; multiple molecules orient to form fibrils – cross-linkage of fibrils aided by vitamin C.
Describe the 2 main types of abnormal wound healing
Hypertrophic scar:
- Excess collagen but scar does not extend beyond edges of original wound
- Should have sutured.
Keloid scar:
- Overgrowth of granulation tissue (more common in Afro-Caribbean ethnicities)
- Scar extends beyond edges of original wound (tumour-like).
List the local factors that can affect wound healing (4 points)
Local factors that can affect wound healing:
- Oxygenation
- Infection
- Foreign body
- Venous sufficiency.
List the systemic factors that can affect wound healing (11 points)
Systemic factors that can affect wound healing:
- Age
- Sex hormones (females heal better than males)
- Stress
- Ischaemia
- Disease (jaundice, diabetes etc)
- Obesity
- Medications
- Alcoholism
- Smoking
- Immunocompromise
- Nutrition.
List the main bone cell types (4 points)
Main bone cell types:
- Osteogenic cell (stem cell)
- Osteoblast (matrix-synthesizing – bone growth)
- Osteocyte (mature bone cell – maintains bone matrix)
- Osteoclast (matrix-breakdown – bone resorption).
Recall the types of bone fracture (8 points)
Describe primary and secondary fracture healing
Fracture healing
Primary:
- Requires rigid fixation – bring two ends of fracture together (surgeons)
- Requires absolute stability of fracture
- Haversian remodelling
Secondary:
- Does not require rigid fixation (natural way)
- Response from periosteum and surrounding soft tissue
List the phases of fracture healing (4 points)
Phases of fracture healing (4 points):
“Haematoma Starts Healing Bone”
- Haematoma formation
- Soft callus formation
- Hard callus formation
- Bone remodelling (Haversian)
Describe phase 1 of fracture healing
Phase 1 – Inflammation (involves haematoma formation)
Haematoma formation:
- Rupture of blood vessels in medullary cavity
- Blood fills gap and spills into surrounding tissues forming a haematoma
- Formation of fibrin mesh; seals off fracture site; influx of inflammatory cells
- Cytokines activate osteoprogenitor cells to fibroblasts and chondroblasts
Describe phase 2 of fracture healing
Phase 2 – Soft callus formation:
- Haematoma replaced by soft callus (after 1–2 weeks)
- Granulation tissue provides matrix for woven bone to be deposited by osteoblasts
- Still damageable by shear forces
- Axial traction and pressure promote matrix formation
Describe phase 3 of fracture healing
Phase 3 – Hard callus formation:
- Mineralization of soft callus to form hard callus
- Organized parallel to long axis of bone
- Fracture strength increases (allows weight bearing)
- 6-week healing time
Describe phase 4 of fracture healing
Phase 4 – Bone remodelling:
- Hard callus replaced with lamellar bone via Haversian remodelling
- Occurs over months months–years
- Internal architecture dependant on Wolff’s law
Define Wolff’s law
Internal architecture of any bone alters in response to loads placed on it
Mechanotransduction:
- Osteocytes send signals via molecules or direct contact when load sensed
- Osteoprogenitor cells differentiate on load conditions
List the 4 AO principals of fracture management
The 4 AO principals:
- Fracture reduction to restore anatomical relationships
- Fracture fixation to provide absolute or relative stability as the “personality” of fracture, patient and injury requires
- Preservation of blood supply to soft tissues and bone
- Early and safe mobilization of the injured part and the patient as a whole
Recall the 4 key structural components of the periodontium
Periodontium structure – only exists when teeth are present.
Consists of 4 key structural components:
- Gingiva (gingival epithelium – ectodermal origin)
- Cementum (ectomesenchymal origin)
- Periodontal ligament (attaches cementum to alveola bone; ectomesenchymal origin)
- Alveolar bone (mesodermal origin)
List the 5 periodontal investing structures
Recall the investing structures surrounding the gingival sulcus
Describe the structure and function of the oral epithelium (7 points)
Oral epithelium (OE):
- Extends from the mucogingival junction to the free gingival margin (“keratinised gingiva” in diagram).
- Orthokeratinized, stratified, squamous epithelium
- Surface cells lose nuclei and are packed with protein keratin:
- Protection – impermeable physical barrier to oral bacteria
- Protection – provides resistance against masticatory forces
- Surface cells lose nuclei and are packed with protein keratin:
- The basal aspect of the OE is folded into rete ridges to increase surface area of contact between the OE and the underlying connective tissue
- It is continuous with the sulcular epithelium at the free gingival margin.
List the structure and function of the sulcular epithelium (4 points)
Sulcular epithelium (SE):
- That epithelium which lines the gingival sulcus
- The cells of the sulcular epithelium are keratinized but still contain a nucleus → parakeratinized
- The SE faces the tooth, but it not attached to it
- Apically bound to the tooth (i.e. in the direction of the root apex) by the junctional epithelium.
List the structure and function of the junctional epithelium (9 points)
Junctional epithelium (JE):
- The junctional epithelium forms a specialized attachment to the tooth:
- Hemidesmosomal layer within the JE cells
- Basal lamina produced by epithelial cells
- The JE is non-keratinized and has a very fast turnover of cells (2–6 days compared to ~1 month for OE)
- The most apical part of the JE lies at the cemento-enamel junction in health
- The coronal aspect of the JE is the widest part of the JE (2–3 mm, ~20–30 cells thick coronally)
- The JE tapers downwards (apically) until it is only one cell in width at the apical aspect
- The JE is permeable with wide intercellular spaces through which cells and substances can migrate (e.g. bacterial toxins or host defence cells)
- Apical migration of the JE from its healthy position onto the root cementum indicates a loss of periodontal attachment and progression to the disease state periodontitis.
Summarize the key aspects of the junctional epithelium
Junctional epithelium (key summary):
- Attachment to tooth
- Barrier
- Rapid turnover (2-6 days)
- Antimicrobial defence
- GCF flow
List the structure and function of the interdental papilla (4 points)
Interdental papilla:
- Interdental papilla occupies the space between adjacent teeth
- Prevents impaction of food and debris between closely adjacent teeth
- When view from the coronal aspect there is an indentation called the col.
- The col forms a concave curve from the labial aspect to the lingual aspect of the interdental papilla
Define gingival (periodontal) fibres (7 points)
Gingival (periodontal) fibres:
Gingival connective tissue (i.e. lamina propria) is made up of collagen fibre bundles called gingival fibres (5 different types), around which lie ground substance, fibroblasts, blood and lymph vessels, and neural tissues.
Recall the 5 principal gingival fibres
Define periodontal ligament (PDL)
Periodontal ligament (PDL):
Periodontal ligament forms the attachment of the cementum (bone-like substance) to the alveolar bone, hence it is referred to as a ligament (tissue that connects bone to bone).
Describe the key components of the periodontal ligament (5 points)
Key components of PDL:
-
Highly vascularized connective tissue (grouped into 5 different types based on their position)
- Not be confused with the gingival fibres which attach the tooth to the gingival tissue, rather than the tooth to the alveolar bone.
- Within the ligament are mechanoreceptors that provide sensory (e.g. proprioception) input for jaw reflexes
- Cells of the PDL are involved in the formation and remodelling of the alveolar bone and cementum
- “Rests of Mallassez” are remnants of the epithelial root sheath responsible for the root development
- The PDL acts to dissipate the masticatory forces to the supporting alveolar bone → physiologic mobility
List the 5 groups of periodontal ligament (PDL) fibres
Groups of PDL fibres (5 points):
- Alveolar crest fibres
- Horizontal fibres
- Interradicular fibres (between two roots of the same tooth)
- Oblique fibres
- Apical fibres
List the 5 functions of the periodontal ligament (PDL)
Function of the periodontal ligament (5 points):
“Strong Periodontal Fibres Support Nashers”
- Supportive – PDL forms a functional system to secure teeth in alveola bone but allows some mobility
- Protective – PDL is highly neurovascular and can therefore respond to protect itself from injury
- Formative – mesenchymal stem cells to form osteoblasts, osteoclasts, cementocytes, cementoclasts
- Sensory – proprioceptive reflex protects teeth in case of overload (inhibits muscles of mastication)
- Nutritive – PDL is highly vascular with rich nutrient supply to cells of ligament and surrounding tissues
List the 2 types of cementum
Two types of cementum:
- Cellular
- Acellular
List the strucutre and function of cellular cementum (5 points)
Cellular cementum:
- Cellular cementum lies over the acellular cementum
- Found near the apex of the root
- It contains cells called cementocytes which lie in the lacunae (gaps) of the cellular cementum
- Cellular cementum layer is thicker in the apical region of the root (0.2–1 mm thick)
- The cementum is continuously replaced as it ages, and its thickness increases throughout life.
List and describe the function of acellular cementum (4 points)
Acellular cementum:
- Covers most of the root surface
- Forms on root during root formation and tooth eruption – tightly bound to underlying dentine
- Fibres inserted from the terminal end of the periodontal ligament are embedded within the cementum and are known as Sharpey’s fibres – insert at close intervals in acellular cementum
- At the other terminal end of the periodontal ligament, the PDL fibres are partially mineralized within the periosteum of the alveolar bones.
List 4 functions of the alveolar bone
Function of the alveolar bone:
- Alveolar bone forms and protects the sockets for the teeth
- It gives the attachment to the periodontal ligament fibres, which are the principle fibres. These fibres which enter the bone are regarded as Sharpey’s fibres.
- It supports the tooth roots on the facial and on the palatal/lingual sides
- It helps absorb the forces placed upon the tooth by disseminating the force to underlying tissues
List the characteristic of a healthy periodontium (7 points)
Characteristics of healthy periodontium:
- Gingivae:
- Pale pink (coral pink) in lighter skinned people, and may be contain melanin pigmentation in darker skinned people
- Stippled appearance
- Scalloped (arcuate) form
- Interdental papilla fills the interdental space
- No recession, bleeding on probing (BOP), or inflammation
- Health probing depth = 1–3 mm
Define periodontal disease (3 points)
Periodontal disease:
Spectrum of diseases starting from acute gingivitis, and if left untreated, can lead to very severe periodontitis.
Describe the basic pathogensis of periodontal disease (3 points)
Basic pathogenesis of periodontal disease (3 points):
- A colourless sticky biofilm (dental plaque) forms on teeth
- If undisturbed (e.g. by tooth brushing), this biofilm matures and microbial population changes
- Certain bacterial species and their metabolic by-products then irritate the gingival tissues, causing inflammatory response.
Describe the acquired salivary pellicle (4 points)
Acquired salivary pellicle:
- Thin, acellular organic film
- Forms on any type of surface upon exposure to saliva
- Formed by selective adsorption of mostly phosphorylated salivary proteins via electrostatic attraction to hydroxyapatite
- 10–20 nm thick
List 5 key features of pulpitis
Key features of pulpitis:
- Pulpitis is caused by infection or irritation of the pulp, usually by caries
- Severe stabbing pain in a tooth, triggered by hot or cold food or starting spontaneously indicates acute irreversible pulpitis
- Pulp pain is poorly localised
- Chronic pulpitis is often symptomless
- Untreated pulpitis usually leads to death of the pulp and spread of infection to the periapical tissues
Distinguish between reversible and irreversible pulpitis
List 5 causes of pulpitis
Causes of pulpitis:
- Dental caries
- Traumatic exposure of the pulp
- Fracture of a crown or cusp
- Cracked tooth
- Thermal or chemical irritation
List 7 treatment options for pulpitis
Treatment options for pulpitis:
- If fractured or cracked, stabilise fracture and seal pulp temporarily
- Removal of caries, obtundent or steroid dressing
- Removal of caries and pulp capping
- Pulpotomy in deciduous teeth
- Endodontic treatment
- Extraction
- Analgesics are largely ineffective
List 3 characteristics of hypersensitive dentine
Hypersensitive dentine has the following characteristics:
- Dentinal tubules open to the oral cavity
- Hypersensitive dentine has eight times as many open dentinal tubules and twice the diameter of open tubules as non-sensitive dentine
- Thin, poorly calcified or breached smear layer (a deposit of salivary proteins, debris from dentifrices and/or other calcified matter that occludes dentinal tubules)
List 11 factors that contribute to dentinal hypersensitivity
Factors that contribute to dentinal hypersensitivity:
- Gingival recession
- Loss of enamel
- Toothbrush abrasion
- Erosion
- Abfraction
- Acidic foods
- Periodontal surgery
- Occlusal hyperfunction
- Cusp grinding
- Instrumentation (root planing, scaling, extrinsic stain removal)
- Cosmetic tooth whitening
Compare the characteristics of hypersensitive dentine (3 points) versus non-sensitive dentine (2 points)
Characteristics of hypersensitive versus non-sensitive dentin
Hypersensitive Dentin:
- Ends of dentinal tubules open to the oral cavity
- Tubules larger and more numerous than in nonsensitive dentin
- Smear layer is thin, poorly calcified, or breached
Nonsensitive Dentin:
- Fewer dentinal tubules at tooth surface are present than in sensitive dentin
- Either a smear layer is present or tubules are occluded by mineral compounds
Recall the hydrodynamic mechanism by which stimuli activate interdental
nerves to cause pain
Note: an open dentinal tubule channel must traverse from the exposed dentine surface to a vital pulp
