Periodontology Flashcards
What are the tissues of the Peridontium?
PDL, Gingiva, Cementum, and Alveolar bone.
What are the functions of the PDL?
Made of fiber bundles and cells.
Tooth anchorage, transmits occlusal forces to the bone and resists impact of these forces, supplies nutrients to periodontal structures, sensory functions include touch, pressure and pain, shock absorber for the teeth, nerves and blood vessels.
Where do the PDL fibers attach to?
Tooth’s cementum
Sharpey’s fibers
Fiber bundles that are attached ad embedded in cementum and bone.
Transseptal Fibers
“interdental ligament”, interproximally, hold teeth in interproximal contact with each other. Horizontal
Alveolar crest fibers
Located apical to the junctional epithelium. Resists tilting and horizontal forces.
Oblique fibers
Most numerous type of fiber, resists “intrusive” or “vertical” masticatory forces. Prevents the tooth from being “jammed” into the bony socket. Diagonal
Horizontal fibers
resist horizontal and tilting forces. Horizontal running.
Apical Fibers
Prevents the tooth from being lifted out of the bony socket. Resists “extrusive forces”. Extend from apical area of tooth to base of tooth socket.
Interradicular fibers
Found only in multi-rooted teeth, located in tooth furcations, and stabilizes tooth root.
Most common cell of PDL, important in collagen synthesis, and fiber production. “Primary cell of the PDL”
Fibroblasts
Production of bone
Osteoblasts
Resorption (break down) of bone
Osteoclasts
Production of cementum
Cementoblasts
Resorption of cementum
Cementoclasts
Signs of a healthy gingiva
Firm, light pink, fills interproximal spaces, knife-edged, gingival margin on enamel, 1-3 mm gingival sulcus
Signs of unhealthy gingiva
Spongy, swollen, red, bleeds upon probing, bulbous, festooned, recession, hyperplastic, deep pockets or probing depths.
Reversible inflammation of the gingiva, directly related to plaque accumulation, results from ulceration at the base of the sulcus.
Gingivitis
What is most gingivitis termed?
Chronic plaque-associated gingivitis
Signs of acute gingivitis?
Develops rapidly, obvious inflammation, may be painful, neutrophil is the most prevalent cell.
Signs of chronic gingivitis
Develops slowly, may appear normal, not usually painful.
Where is cyanosis of the gingiva often found?
Bluish, highly vascular and often found around crowns
What is pallor gingiva associated with?
Lighter than normal, associated with anemia, leukemia, and fibrotic tissue.
This gingiva is stippled and this one is not.
Attached gingiva is stippled and marginal gingiva is not
What is edematous?
Glossy appearance due to increased fluid. Edema is the result of vasodilation of the peripheral circulation
Increase in cellular and fibrous components, may present with pallor.
Fibrotic
How is stillmans cleft indicated?
By vertical loss of tissue, caused by improper flossing, bulbous, and blunted
Inner tube-like swelling at gingival margin, due to inflammation and an increased cell number.
Festoon
Caused by age, plaque, iatrogenic, tooth malposition, Occlusion, Frenum pull, trauma, inadequate attachment, improper flossing technique.
Recession
Drugs that increase the risk of gingival enlargement
Phenytoin (Dilantin)
Nifedipine (procardia)
Cyclosporin
Other causes of gingival enlargement.
Mouthbreathing, periodontal inflammation, genetic/hereditary factors, systemic conditions like leukemia and hormonal imbalance.
Gingival enlargement due to an increase in cell numbers.
Hyperplasia
Gingival enlargement fit to an increase in cell size
Hypertrophy
Oval-shaped root exposure apical to the CEJ, alveolar bone loss and root exposure.
Dehiscence
Window-like opening in the bone covering the roof of a tooth and bordered by alveolar bone on the coronal aspect of the tooth.
Fenestration
Major etiology factor in the initiation and progression of inflammatory periodontal diseases, known as biofilm which is bacteria forming on tooth surfaces.
Dental Plaque
How is Plaque formed?
Glycoproteins from saliva are absorbed to the tooth surface, forming the acquired pellicle.
Bacteria then adhere to the acquired pellicle
Bacteria multiply to form colonies on the tooth, creating a biofilm
As Plaque grows, bacteria detach from the biofilm and become “planktonic” bacteria (free)
Later, calculus forms from the mineralized Plaque biofilm
Cocci
Round/spherical-shaped bacteria found in early Plaque formation.
Bacilli
Rod-shaped bacteria, most common type found in periodontal disease.
Spirochetes
Spiral-shaped bacteria, often associated with NUG/NUP.
Aerobic
Require oxygen to grow, NOT found in periodontal pockets
Anaerobic
Grow in the absence of oxygen, found in periodontal pockets and gingival sulcus.
Faculative anaerobic
Can grow in presence of oxygen or absence of oxygen.
Streptococcus: s. Mitis, s. Oralis, s. Sanguis, and s. Mutans are all gram positive bacteria.
Early “healthy” Plaque, able to attach to the acquired pellicle.
Actinomyces: a. Viscous is an example of a gram positive rod and?
Early colonizer in Plaque formation
Most common/most important periodontal pathogen, is an anaerobic gram negative rod shaped bacteria.
Porphyromonas Gingivalis (P. Gingivalis)
This is a spirochete
Treponema denticola (t. Denticola)
Pathogen in adult periodontitis
Tannerella forsythia
Plays a critical role in biofilm formation, anaerobic gram negative rod shaped bacteria
Fusobacterium nucleatum
Associated with periodontal disease, gram negative facultative anaerobes associated with inflammation during pregnancy
Campylobacter rectus ( C. Rectus)
Associated with periodontal disease, gram negative anaerobe most often associated with inflammation during pregnancy
Prevotella intermedia
Gram negative rod-shaped bacteria associated with aggressive periodontal disease
Aggregatibacter actinomycetemcomitans
Bacterial species associated with NUG/NUP
T. Denticola, P. Intermedia, P. Gingivalis, and fusobacterium
What are the Plaque-retentive zones?
Pits and fissures, irregular tooth surfaces and interproximal areas
What makes up the bulk of the Plaque biofilm and functions to hold the bacteria together, allow for exchange of nutrients and removal of waste products.
Extra cellular matrix
Pellicle formation is derived from salivary glycoproteins
Sticky matrix that allows for bacterial attachment to the tooth
Attachment begins with gram positive cocci
As Plaque matures, more facultative anaerobic bacteria are present.
Supragingival
Accumulates after supragingival Plaque
More motile bacteria, gram negative anaerobic than supragingival Plaque
Free-floating or loosely adherent Plaque in the pocket/sulcus
Subgingival
Densely interconnected
Contains non-motile bacteria
May mineralize and become calculus
Adherent
Also known as planktonic Plaque
Mostly motile rods and spirochetes
Increase during acute infection/inflammation
Non-adherent
What oral hygiene aid is most suited for removal of loose or non-adherent Plaque?
Oral irrigator
What do poorly fitted crowns cause?
Marginal inflammation, overhangs, food impaction, often caused by open contacts between teeth.
What often contributes to tissue destruction?
Bacterial products such as endotoxins, collagenase, protease, hyaluronidase, and exotoxins.
Associated with gram negative bacteria, stimulate osteoclasts, and inhibits fibroblasts and May harm neutrophils (PMNs)
Endotoxins
Directly breaks down connective tissues
Collagenase
Directly breaks down tissues
Protease
Breaks down the extra cellular matrix, allowing bacteria to detach “spreading factor”.
Hyaluronidase
Bacterial waste products that cause direct tissue injury, examples: hydrogen sulfite, uric acid and fatty acids
Exotoxins
Inflammation of the periodontal tissues, and loss of CT attachment to the tooth, characterized by the apical (downward) migration of the JE, the rat of destruction varies due to the virulence of bacteria and the host response.
Periodontitis
How is periodontitis documented?
By CAL over time
Measures from the CEJ to the base of the pocket, best indicator of damage to the periodontium, means disease progression.
CAL
How is CAL measured?
Measure the pocket depth first
Measure how much recession is present
Add two numbers together
What is the best instrument to detect a Furcation?
Nabers probe
What is the attached gingiva connected to?
Tooth cementum and the periosteum of the alveolar bone
What is NOT calculated for palatial surfaces?
Width of attached gingiva
Signs of healthy periodontium.
Intact, distinct RO lamina dura should be present.
PDL space should be visible and uniform width.
Crest of alveolar bone should be 1-2 mm apical to the CEJ.
Signs of disease/periodontitis
Loss of bone in Furcation areas
Bone loss vertical or horizontal
Best evaluated on bitewing radiographs
Lamina dura becomes less distinct
Tooth mobility
Class 1: slight, up to 1 mm horizontally (facial-lingual)
Class 2: moderate, 1-2 mm horizontal (facial-lingual)
Class 3: severe, >2 mm horizontal/vertical (depressable in the socket)
How do you check for mobility?
Two instruments with hard handles
Occur ABOVE (coronal to) the alveolar crest of bone.
Suprabony pockets
Base of pocket is BELOW (apical to) the alveolar crest and treated with regenerative procedures.
Infrabony pockets
What does increased pocket/probing depth occur from?
Coronal movement of the gingival margin, “pseudopockets” due to inflammation and swelling, deepening of the sulcus/pocket due to loss of attachment to tooth, apical margination of the JE
This DOES NOT cause periodontal disease.
Occlusal Trauma
Excessive force on a tooth with normal bone support
Primary occlusal trauma
Result of forces applied to a tooth that has previously experienced bone or attachment loss.
Secondary occlusal trauma
What may result from excessive occlusal forces on a tooth that has bone/attachment loss previously?
Rapid bone loss/pocket formation
Signs/symptoms of occlusal trauma.
Sensitivity Wear facets Tooth migration Increased mobility Widening of PDL space on radiograph
Associated with dental Plaque (bacteria) only, but may be modified by systemic factors, nutrition and meds
Plaque-induced gingival disease
Associated with viruses, fungus, genetic or systemic conditions. May also result from trauma or foreign body reactions. Gingival inflammation may be caused by open contacts and subgingival margins of restorations.
Non-Plaque induced gingival disease
Examples of non-Plaque induced gingival disease.
Primary Herpes Recurrent herpes (cold sores, fever blisters) Aphthous ulcers (canker sores)
What is chronic periodontitis classified as?
Localized or generalized
What is aggressive periodontitis classified as and associated with?
Localized or generalized and associated with aggregatibacter actinomycetemcomitans(Aa)
Periodontitis as a manifestation of systemic diseases
Examples include acquired neutropenia and leukemia
A lack deficiency of neutrophils (polymorphonuclear leukocytes)
Neutropenia
Periodontitis associated with genetic disorders
Familial and cyclic neutropenia Down syndrome (but no increased risk for caries) Papillon-LaFevre syndrome (severe periodontal destruction, premature tooth loss, hyperkeratosis of palms of hands and soles of feet) Chediak-Higashi syndrome (inherited dx of of immune and nervous systems, impairment of neutrophils, and aggressive periodontitis associated with this)
Necrotizing Ulcerative Periodontitis
Loss of clinical attachment and bone
Necrotizing ulcerative gingivitis
Affects gingiva only
(treponema denticola), prevotella intermedia, porphyromonas Gingivalis And fusobacterium
Remember-associated with spirochetes
What’s the drug of choice for necrotizing periodontal diseases?
Tetracycline, because it concentrates in gingival crevicular fluid
What are the clinical findings of necrotizing periodontal diseases?
“Punched out” papillae, pseudomembrane, fetid bad odor, pain and severe inflammation
Results from injury to or infection of the surface gingival tissue.
Gingival Abscess
Results when infection spreads deep into pocket, and drainage is blocked, may develop after periodontal debridement.
Periodontal abscess
Develops in inflamed dental follicular tissue, overlying the crown of a partially erupted tooth (most often mandibular third molars), often does NOT show up on a radiograph.
Pericoronal abscess
Infection of the tooth pulp, secondary to deep dental caries, diagnosis often requires a periapical radiograph.
Periapical Abscess
Localized tooth-related factors that may increase the risk of developing Plaque-induced gingivitis and periodontitis, or exacerbate these conditions:
Gingival recession, lack of attached gingiva, frenum position and “pull”, enlarged/excessive gingiva, and occlusal trauma.
2-4 days, no clinical changes, vasodilation of small capillaries, increased flow of gingival fluid.
Stage I, Initial lesion
4-7 days, clinical signs of gingivitis appear, collagen destruction, bleeding occurs due to ulcerated sulcular lining, PMNs found in sulcus.
Stage II, Early lesion or gingivitis
2-3 weeks, capillary proliferation (overgrowth) causes erythema, gingival enlargement may increase probing depths
Stage III, established lesion
3 weeks + to years, transition from gingivitis to periodontitis, irreversible, JE detaches from root surface and migrates apically, osteoclasts And bone loss.
Stage IV, Advanced lesion
Events occurring as periodontal disease progresses?
Increased probing depths, increased attachment loss and increased bone resorption
Transient (temporary) vasoconstriction first,
Then vasodilation
Excess of blood in the vessels in the tissues
Hyperemia
Movement of WBCs to the periphery of vessel walls
Margination
WBCs line the wall of the vessel
Pavementing
Process by which neutrophils squeeze between endothelial cells in the vessel wall
Diapidesis
Cells move into the tissues from the blood vessel
Emigration
Movement of cells to the site of inflammation
Chemotaxis
Significant to development and progression of disease, most prevalent in acute inflammation, may active in the periodontal pocket, and main function is phagocytosis
Neutrophils
Increased risk of periodontal disease, xerostomia and increased caries risk, candidiasis, and delayed wound healing
Diabetes mellitus
Vitamin C deficiency, it is necessary for collagen production and wound healing
Scurvy
Protein deficiency, proteins are necessary for a healthy periodontium
Kwashiorkor
Erythroblastic anemia, cyclic neutropenia, radiation therapy and acute mono grid leukemia can all affect periodontal tissues
Blood cell dyscrasias
Prevotella intermedia and campylobacter rectus, meds, puberty, menstruation, and menopause can all affect periodontal tissues
Hormonal effects: pregnancy gingivitis
Are at an increased risk of developing periodontal disease due to vasoconstriction, NOT at an increased risk of developing caries, have deeper pockets and more bone loss, may develop “black hairy tongue”.
Smokers
Cancer patients may present with?
Xerostomia, mucositis, dysgeusia (loss of taste or altered taste), increased risk of fungal and viral infections.
Patients who are HIV + may present with?
Linear gingival erythema (band of redness of the marginal gingiva), NUP (necrosis of gingiva and alveolar bone), Aphthous ulcers, Kaposi’s sarcoma (malignancy of vessels, presents as a blue/purple macule)
Objectives of periodontal therapy?
Identify the disease, control inflammation and deal with defects resulting from the disease.
Goals of periodontal surgery?
Allow easier cleaning for the patient, replace lost tissue, and gain new attachment
What happens after periodontal therapy?
Re-evaluation appointment 4-6 weeks after therapy is necessary to determine effectiveness and the first factor to assess at this appointment is the degree of inflammation of the tissues.
Factors that affect the prognosis after treatment?
Tooth mobility, endosperm tic status, depth and width of pockets, the more bony walls present the better the prognosis, a 3 wall defect has a better prognosis than all wall defect.
Treatment of periodontal disease?
SRP, antimicrobials/antibiotics, gingivectomy, Osseous surgery, periodontal dressings, and regenerative procedures.
Most common surgical procedure to reduce pocket depths, removes soft tissue only, and treatment for gingival hyperplasia and pseudopockets.
Gingivectomy
Requires gingival flap (incision), bone recontoured (osteoplasty), bone removed (osteoectomy), sutures are required.
Osseous surgery
Rarely used, used for protection, comfort and to maintain tissue contour. “White patches” can occur after dressing is removed which are composed of dead cells and tissue debris, and DO NOT prevent Plaque build up.
Periodontal Dressings
Uses barrier membrane to block migration of epithelial cells, Osseous and soft tissue grafts are examples of regenerative procedures, main reason is to treat infrabony defects.
Guided Tissue Regeneration
What does tissue repair generally involve?
Fibrous repair through the formation of granulation tissue.
Initial tissue formed in the CT after injury, is an immature tissue with many capillaries (neovascularization) and fibroblasts.
Granulation tissue
What are the four stages of fibrous repair?
Blood clotting, wound cleansing, tissue rebuilding and wound remodeling.
Is composed of fibrin, fibronectin, and platelets. It fills the wound serving as a scaffolding for PMNs and macrophages.
Blood clotting
Macrophages invest debris and degrade the clot, PMNs attack bacteria, new capillaries and fibroblasts move in debris is removed.
Wound cleansing
Fibroblasts synthesize/deposit fibronectin, collagen and proteoglycans. Granulation tissue is formed, and is highly cellular and vascular.
Tissue rebuilding
Granulation tissue is eventually remodeled into a scar composed of dense collagen interspersed with cells and blood vessels.
Wound remodeling
When is arachidonic acid produced and why is it metabolized?
Produced when there is a tissue injury and metabolized to produced inflammatory mediators.
Cause swelling, pain and inflammation. Inhibited by NSAIDs and aspirin.
Prostaglandins
Cause bronchoconstriction, cellular infiltration, cytokines release and inflammation. Derived from leukocytes especially mast cells and inhibited by asthma drugs such as singular.
Leukotrienes
