Tooth Structure, Enamel, Dentin, Periodontium, Oral Mucosa, Salivary Glands, and Oral Microbiome (Video Notes Review)

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A comprehensive set of practice flashcards covering enamel, dentin, cementum, alveolar bone, periodontal ligament, oral mucosa, salivary glands, tongue and taste, oral microbiome, and related pathology as described in the lecture notes.

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90 Terms

1
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What is the enamel and where is it located on the tooth?

Enamel is the outermost mineralized tissue of the tooth crown, overlying dentin.

2
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What is the color of enamel and what is underneath it?

Enamel is translucent yellow to white; dentin underneath is yellow.

3
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What is the enamel thickness range mentioned in the notes?

2.5 mm to a few micrometers.

4
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What is the mineral/organic/water composition of enamel?

Enamel is 96% inorganic (hydroxyapatite), 1% organic (enamel proteins like amelogenin), and 3% water; no collagen.

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What is the main organic enamel protein?

Amelogenin.

6
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Which enzymes degrade amelogenin during enamel formation?

MMP20 (matrix metalloproteinase 20; neutral) and KLK4 (kallikrein-related peptidase 4; acidic).

7
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What happens if KLK4 or MMP20 are defective?

Amelogenesis imperfecta (hypomineralization of enamel).

8
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Does enamel contain collagen?

No—enamel contains no collagen.

9
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How does enamel protein content change during development?

Protein content decreases dramatically from secretory to maturation stage (66% to about 1%). Amelogenin becomes almost undetectable in mature enamel.

10
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What is enamel space and why is enamel often lost in preparations?

Enamel space is empty; during sectioning, demineralization/decalcification can cause enamel to be lost and become nearly invisible.

11
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What are the two enamel microstructures?

Enamel rods and interrod enamel; rods and interrods are perpendicular to each other.

12
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Where do interrod enamel and rod enamel originate?

Interrod enamel is secreted from the proximal portion; rod enamel is from the distal portion.

13
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What is the diameter of an enamel rod?

5–8 μm.

14
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What is Tomes’ process?

The process by which a single ameloblast produces a single enamel rod.

15
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During tooth development, which tissues arise from epithelial vs mesenchymal components?

Epithelial: enamel; Mesenchymal: dentin, pulp, cementum, bone.

16
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What are the primary sites of epithelial-mesenchymal interaction during amelogenesis?

Enamel organ interacts with dental papilla (IEE to ameloblasts; dental papilla to odontoblasts) with enamel and dentin formation coordinated.

17
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What tissues arise from the dental follicle?

Cementum, periodontal ligament (PDL), and alveolar bone.

18
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What are the tooth germ components and their cells?

Enamel organ; inner enamel epithelium (IEE) differentiates into ameloblasts to make enamel; dental papilla differentiates into dentin/pulp.

19
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List the bell-stage tooth formation states in order.

Morphogenetic stage; Histodifferentiation stage; Initial Secretory stage; Secretory stage; End of Secretory stage; Transition stage; Maturation stage.

20
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What marks the secretory stage of amelogenesis?

Growth of enamel matrix, with Tome’s process producing enamel matrix (initially interrod enamel).

21
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What occurs at the end of the secretory stage?

Loss of Tome’s process and transition to maturation stage.

22
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What characterizes the maturation stage of enamel formation?

Ruffle-ended ameloblasts remove enamel proteins and water; acidic conditions with acid production; KLK4 is active; maturation ends with mineralization of enamel.

23
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Which enamel proteins are dominant and what is their role (the KNOW CHART)?

Amelogenin (90%) promotes enamel layer growth and crystal formation during the secretory stage; non-amelogenin (10%) includes MMP-20/enamelysis (degrades enamel protein at neutral pH) and KLK4 (degrades enamel protein at acidic pH during maturation).

24
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What is the Bonus Question topic related to enamel proteins?

Enamel matrix derivative from pig tooth germs used for periodontal tissue regeneration; drawbacks include animal-derived material, crude proteins, and incomplete understanding of mechanisms.

25
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What are enamel tuft and lamellae?

Enamel tufts project from the dentin-enamel junction into enamel; enamel lamellae extend from the DEJ through enamel.

26
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What are enamel spindles?

Odontoblast processes that are found within enamel (split between enamel and dentin).

27
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Why should decalcified histology sections not be used to observe enamel structures?

Because demineralization removes enamel, making observations unreliable.

28
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What genes are implicated in amelogenesis imperfecta and what are their inheritance patterns?

AMELX (X-linked; typically milder in females, severe in males with AMELY involvement), ENAM, AMBN, MMP20, KLK4; defects cause hypomineralized or hypoplastic enamel.

29
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What are the three types of dentinogenesis imperfecta described?

Type 1: associated with osteogenesis imperfecta (COL1A1/COL1A2 mutations; pulp chamber not visible). Type 2: not associated with bone phenotypes. Type 3: rare; enlarged pulp chambers; shell teeth.

30
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What is predentin?

Unmineralized dentin matrix deposited first, later mineralized to become dentin.

31
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What is dentin’s composition compared to enamel and bone?

Dentin is 65–70% inorganic (calcium phosphate/hydroxyapatite), 5–10% type I collagen, and 15–20% water; more mineralized than bone but less than enamel.

32
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What are the major and non-collagenous dentin matrix proteins?

Major: type I collagen; non-collagenous: DSPP family (DSPP, DPP, DSP). These proteins are also found in bone.

33
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What are the two dentin mineralization patterns and where do they occur?

Globular dentin (mantle/crown dentin, more rapid formation) and linear dentin (circumpulpal/root dentin, slower formation).

34
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What is mantle dentin and what fibers does it contain?

Initial dentin layer with von Korff fibers (type III collagen); perpendicular to DEJ; less mineralized; first dentin formed.

35
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What is Tome’s fiber?

Extension of the odontoblast process into dentin.

36
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Describe the dentin tubule system and its functional significance.

Dentinal tubules traverse dentin from DEJ to the mineralization front; contain odontoblast processes; important for nutrient diffusion and dentin sensitivity; tubules widen near pulp and narrow near DEJ.

37
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What are peritubular and intertubular dentin?

Peritubular dentin is highly mineralized around tubules; intertubular dentin lies between tubules.

38
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What are the three mechanisms proposed for dentin sensitivity?

Nerve endings in dentinal tubules; odontoblasts as receptors; hydrodynamic fluid movement within tubules.

39
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What zones constitute dental pulp?

Odontoblastic zone, cell-free zone of Weil, cell-rich zone, and pulp core (major vessels and nerves).

40
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What are the main cell types in dental pulp?

Odontoblasts, fibroblasts, endothelial cells, neurons, immune cells (macrophages, dendritic cells, T and B lymphocytes, neutrophils).

41
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What are pulp stones (denticles)?

Discrete calcified masses within pulp; not necessarily connected to dentin but can be with secondary or tertiary dentin.

42
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What are age-related changes in pulp?

Decreased pulp volume, decreased cell numbers, increased collagen, dystrophic calcification, reduced tubule diameter (sclerosis).

43
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What is cementum and what are its key features?

Mineralized connective tissue covering root dentin; avascular and aneural; predominantly type I collagen.

44
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What cells are involved in cementogenesis and cementum remodeling?

Cementoblasts (form cementum), cementoclasts (resorb cementum), cementocytes (regulate formation/resorption).

45
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Describe the three cementum types and their main features.

1) Acellular, extrinsic fibrous (AEFC/Primary cementum): forms slowly, covers cervical 2/3, anchors via Sharpey’s fibers, no embedded cells. 2) Cellular, intrinsic fibrous (CIFC/Secondary cementum): forms faster in apical/interradicular regions; cementoblasts become embedded as cementocytes; cementoid layer present; intrinsic fibers exist. 3) Acellular Afibrillar cementum: no collagen fibers, highly mineralized ground substance, deposited over CEJ; function not clearly defined.

46
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What are the cementoenamel junction (CEJ) types and their prevalence?

Overlaps enamel (60%, most common); edge-to-edge (30%); gap (10%), which exposes dentin and causes root sensitivity.

47
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What is the alveolar bone proper and lamina dura?

Thin layer of compact bone lining the tooth socket; also called bundle bone/lamina dura.

48
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How is the alveolar bone structured besides the bone proper?

Cortical plates (buccal/labial and palatal/lingual) and trabecular (cancellous) bone between cortical plates and bone proper; the alveolar crest is 1–2 mm below CEJ.

49
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What is the periodontal ligament (PDL) and its function?

Soft, specialized connective tissue between cementum and alveolar bone proper; suspends the tooth, nourishes cementum, maintains width, and provides sensory input (proprioception) and vascular supply for bone and cementum maintenance.

50
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Name the main PDL cell type and its function.

Fibroblasts are the most abundant; they drive high protein turnover and remodeling; they help maintain PDL integrity.

51
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Which protein in PDL helps prevent ankylosis?

MSX2 (muscle segment homeobox 2).

52
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What are the innervation types in the PDL?

Sensory (nociception and mechanoreception) and autonomic (vasomotor); most fibers are myelinated for pain, with Ruffini-like endings; autonomic fibers are unmyelinated/adrenergic.

53
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List the principal PDL fiber groups and their functions.

Alveolar crest (prevents extrusion; resists lateral movement); Horizontal (resists horizontal and tipping forces); Oblique (largest; resists vertical and intrusive forces); Apical (resists vertical forces); Interradicular (between roots; resists vertical and lateral forces).

54
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List the gingival fiber groups and their functions.

Trans-septal (interdental, connect cementum of adjacent teeth); Dento-gingival (cervical cementum to gingiva); Alveolo-gingival (alveolar crest to gingiva); Circular (around tooth neck); Dento-periosteal (cementum to periosteum of alveolar bone).

55
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What are common clinical periodontal conditions mentioned?

Hypercementosis (thickened cementum at apex/interradicular areas); Cementicle (small cementum masses); Cementoblastoma (benign cementum-like mass on root apex); Hypophosphatasia (reduced alkaline phosphatase, reduced cementum formation).

56
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What is oral mucosa composed of?

Oral mucosa = epithelium + connective tissue (lamina propria) with optional submucosa; functions include protection, sensation, secretion, and limited absorption.

57
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What type of epithelium comprises the oral mucosa and what is parakeratinization?

Stratified squamous epithelium; can be keratinized or non-keratinized; parakeratinization is normal in oral mucosa (not normal in skin).

58
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What are the layers of keratinized oral epithelium (four layers)?

Stratum corneum (outermost), Stratum granulosum, Stratum spinosum, Stratum basale (basal layer is the only layer with cell division in normal state).

59
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What structures are found in the basement membrane and how do epithelial cells attach?

Basement membrane consists of lamina lucida, lamina densa, and lamina fibroreticularis; attachment via hemidesmosomes and integrins (α6 and β4); BP180 (collagen XVII) and BP230 (plectin) are bullous pemphigoid antigens.

60
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What is the lamina propria and its two layers?

Connective tissue supporting the epithelium; papillary layer with interdigitating papillae and a reticular layer deeper in the tissue.

61
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Name cell types found in the lamina propria and their roles.

Fibroblasts (matrix synthesis/turnover), macrophages (phagocytosis/immune signaling), mast cells (histamine/heparin), plasma cells and lymphocytes (immune response), melanocytes (pigmentation).

62
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What are the major differences between keratinized and non-keratinized oral epithelium?

Keratinized epithelium has four layers (basale, spinosum, granulosum, corneum) and a protective keratinized surface; non-keratinized lacks the corneum and has a more permeable surface suited for moisture and absorption.

63
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What are the main components involved in oral mucosa pigmentation and sensation?

Melanocytes in the basal layer (melanin production); Langerhans cells in suprabasal layer (antigen trapping); Merkel cells in basal layer (tactile sensation).

64
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What is the tongue divided into and what papillae exist on the dorsal surface?

Dorsal tongue is keratinized; four papillae types: Filiform (most abundant, no taste buds), Fungiform (taste buds present), Circumvallate (large, many taste buds), Foliate (taste buds on sides). von Ebner’s glands (serous) drain into the furrows of circumvallate papillae.

65
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What is the taste bud structure and the cell types in a taste bud?

Taste buds contain 50–150 taste receptor cells (TRCs); cell types: gustatory cells (receptors), sustentacular cells (support), basal cells (divide to form other types); apical ends have microvilli in a taste pore.

66
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Where are taste buds most commonly located and which papillae contain them?

Taste buds are located in circumvallate, foliate, and fungiform papillae, with filiform papillae lacking taste buds.

67
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What is the dentogingival junction and what is distinctive about junctional epithelium (JE)?

Region between gingiva and tooth; JE is 12–18 cell layers thick, has fewer tonofilaments and desmosomes, and can migrate to the surface but does not fully keratinize; JE regenerates readily from adjacent epithelium.

68
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What is the organization of the oral mucosa compared to skin?

Oral mucosa is non-keratinized in many areas and lacks hair and sweat glands; mucosa is moist and has a thinner epithelium than skin; skin is the largest organ and has a keratinized epidermis with appendages.

69
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What are major salivary glands and their secretions?

Parotid (serous; Stensen’s duct); Submandibular (mixed, mostly serous); Sublingual (mixed, mostly mucous); minor glands (hard/soft palate, tongue, lips; von Ebner’s glands are serous on the tongue).

70
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Describe the acini types in salivary glands and the presence of myoepithelial cells.

Serous acini: pyramidal cells around a central lumen; mucous acini: tubular with a flat nucleus; some mucous acini have serous demilunes; myoepithelial cells may surround serous/mucous portions to aid secretion.

71
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Outline the salivary duct system from acini to excretory ducts.

Intercalated ducts (smallest; collect initial secretions); Striated ducts (columnar with basal striations due to mitochondria); Excretory intralobular ducts; Interlobular and Interlobar ducts (larger ducts) that drain into the oral cavity.

72
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What stimulates saliva secretion at the cellular level?

Secretory granules in acinar cells fuse with the apical membrane via exocytosis; sympathetic (norepinephrine) triggers exocytosis of protein-rich components; parasympathetic signals drive fluid secretion via acetylcholine.

73
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What are the main functions of saliva?

Lubrication, protection, buffering (bicarbonate), clearance, remineralization (Ca2+, PO4-), antimicrobial activity (IgA, lactoferrin, lysozyme, peroxidases, histatins, statherin, PRPs, cystatins), taste and digestion (amylase) and pellicle formation.

74
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Name key salivary proteins and their roles.

Mucins (lubrication and protection); IgA (immune protection); Lactoferrin (iron sequestration); Lysozyme (cell wall lysis); Peroxidases (antimicrobial); Histatins (antifungal); Statherin (inhibits mineral precipitation); Proline-rich proteins (PRPs) – pellicle formation and mineralization regulation; Cystatins (protease inhibition).

75
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What is xerostomia and its causes?

Subjective oral dryness; true salivary hypofunction can be due to medications, Sjögren’s syndrome, or radiation therapy.

76
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What factors influence salivary flow and composition?

Hydration, posture, smoking, medications, radiation, stimulation, age, systemic disease, nutrition; flow rate affects pH and buffering capacity.

77
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Describe saliva production and flow rates in unstimulated and stimulated states.

Unstimulated flow ~0.32 ml/min; stimulated flow ~1.7 ml/min (typical values); major glands contribute variably (parotid ~5–30% unstimulated; 50–65% stimulated; submandibular and sublingual provide the remainder).

78
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What is the oral microbiome and how does it relate to health and disease?

A community of microorganisms in the mouth; about 10x more bacteria than human cells; balance is essential for health; dysbiosis can contribute to caries, periodontitis, halitosis, and systemic effects.

79
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What is the Human Oral Microbiome Database (HOMD) and its significance?

HOMD catalogs oral prokaryotes; includes about 775 species; 57% named, 13% unnamed but cultivated, ~301 uncultivated; a resource for oral microbiology.

80
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What is the difference between resident and transient oral flora?

Resident flora are stable, co-evolved with the host; transient flora are acquired after birth and can change with environment and health status.

81
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Name a few key perio-pathogenic organisms associated with the red complex.

Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola.

82
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What is the ecological plaque hypothesis and Keystone Pathogen hypothesis?

Ecological plaque hypothesis: disease results from ecological shifts in the biofilm due to stress; Keystone Pathogen hypothesis: certain low-abundance pathogens can disproportionately drive inflammation and disease.

83
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What is the difference between non-specific and specific plaque hypotheses?

Non-specific plaque hypothesis (NSPH) suggests disease from overgrowth of all bacteria in plaque; Specific plaque hypothesis (SPH) implicates particular bacteria (e.g., mutans streptococci) as culprits.

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What is the Updated NSPH (U-NSPH)?

Indigenous flora can be present in health or disease; virulence depends on context and case; not all pathogens are exclusively disease-causing.

85
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What is the Keystone Pathogen concept in periodontitis?

Certain pathogens can disproportionately influence the disease process even if not the most abundant; they can trigger inflammation and alter the microbial community.

86
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How does plaque formation begin and what is the role of the acquired pellicle?

Plaque formation begins with the acquired pellicle, a protein-based layer on surfaces; early colonizers attach to pellicle; late colonizers attach via early colonizers; surface appendages (fibrin, etc.) aid attachment.

87
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What is ANUG trench mouth and which bacteria are involved?

Acute necrotizing ulcerative gingivitis; associated with anaerobic, spirochete-rich infection; often involves Fusobacterium spp. and spirochetes; associated with poor oral hygiene and stress.

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How does gingivitis differ from periodontitis?

Gingivitis is inflammation of the gingiva and is reversible; periodontitis involves destruction of supporting tissues and potential tooth loss due to chronic inflammation.

89
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What is the reported link between periodontal disease and Alzheimer's disease in the notes?

Periodontal pathogens and inflammation may travel to the brain and contribute to Alzheimer's pathology, including amyloid-beta and tau protein accumulation.

90
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What is ethereal to the FAST platform and EC16 in periodontitis research?

FAST platform and EC16 oral rinse have been studied; EC16 reduces P. gingivalis growth, bone loss, and proinflammatory Th17/Treg ratio in mouse models of periodontitis, suggesting anti-inflammatory effects.