Perio Final part 1

• (1) PDL
• (2) cementum
• (3) alveolar bone

• 1. gingiva
• 2. PDL
• 3. cementum
• 4. alveolar bone

• 1. gingiva (free, interdental, and attached)
• 2. hard palate

• surrounds the neck of the tooth; smooth, firm surface
• KERATINIZED

• space between the tooth and gingiva
• contains GCF

• not moveable tissue
• pigmentation
• stippling
• KERATINIZED

• extension of the free gingiva
• anterior=pyramidal
• posterior=flat

• posterior teeth
• concavity apical to the contact area
• NONKERATINIZED

• pink
• firm
• stippled
• knife-like margins
• interdental papilla

• bathes the gingival crevice subgingivally
• originates from blood vessels; both protective and destructive
• increased GCF=increased inflammation

• Advantages: rapid and inexpensive; technique insensitive; good for screening purposes; in-office use
• Disadvantages: cannot identify specific bacteria; need sufficient amount of enzymes

• circular
• dentogingival
• dentoperiosteal
• alveologingival
• transseptal

• encircles tooth within free gingiva
• supports and contour of the free gingiva

• from base of sulcus, flares coronally into the free gingiva, laterally into the attached gingivam and apically into the periosteum
• support of the gingiva

• from cementum apically over the alveolar crest into periosteum
• anchors tooth to bone

• from periosteum of the alveolar crestal bone coronally into the connective tissue
• attached gingiva to alveolar bone

• from cementum of one tooth interproximally to the cementum of the adjacent tooth
• keeps teeth in alignmnent and protects the interproximal bone from inflammatory infiltrate

paired with hemidesmosomes; epithelial attachment- attachment between junctional epithelium and the tooth surface

outer electron-lucent (lighter) zone

inner electron-dense (darker) zone

• alveolar crest
• hoizontal
• oblique
• apical
• interradicular

• from cementum, apically into alveolar crest
• resists lateral movement of tooth to keep in socket
• first fiber to be formed after tooth eruption

• from cementum, right angles into bone
• opposes lateral forces
• second fiber to be formed as soon as there is tooth-to-tooth contact

• middle third of the root apical to horizontal fibers
• from cementum and runs coronally and diagnoally into bone
• absorbs occlusal forces
• the most abundant and thus the principal attachment of the tooth

• from cementum of the apex, spreads apically and laterally into bone
• resists tipping
• one of the last to form

• from the crest of the interradicular septum to cementum in the furcation area
• resists foces of luxation and tipping
• lost when bone is destroy in the fucation area in disease

• a layer of mineralized tissue covering the root of the tooth and is composed of collagen, ground substance, cells and calcium and phosphate in the form of hydroxyapatite
• Primary function: attach the principal fibers to the root surface

• formed before tooth eruption; found in the coronal 2/3 of the root; approx. .1mm thick
• CEJ is the thinnest area

• apical 1/3 of the rooth and furcation
• 5mm thick
• formed faster than acellular cementum

• alveolar bone proper: directly supports the tooth
• 1. cribiform plate: hard compact bone that lines the tooth socket
• 2. bundle bone
• 3. lamina dura
• supporting bone: compact bone
• 1. compact cortical plates>dense: covers the alveolar process
• 2. spongy cancellous trabecular bone> between plates

number of individuals having disease at a given time

rate of new cases occuring within a certain period of time

degree of periodontal disease involvement> nild/moderate/severe

number or percentage of disease teeth per person> localized or generalized

• characteristics that have been shown directly cause perio disease> not causal but put the person at risk
• used to predict the occurrence of diseae

• behavioral and socioeconomic characteristics that are associated with periodontal disease but are not considered cause of disease
• i.e.-aging, is considered risk indicator for perio diseae but does not cause disease

• poor oral hygiene
• tobacco
• genetics
• age
• stress
• history of perio
• systemic disease
• male
• immunocompromised
• race
• dental care
• interleukin-1 production

• a complete assessment of all tooth surfaces, but will not pick up differences in plaque quantity
• done in private practice
• ideal = <10%

good for research purposes but qualitative changes can be measured, but it is somewhat subjective and limited to the cervical portion of the tooth

measures severity and extent; measures past disease activity rather than currrent or future

• measures inflammation, pocket formation, and loss of function
• measures both periodontitis and gingivitis in the same index

• measures periodontal pockets, calculus, and gingival bleeding
• developed by World Health Organization (WHO)
• measures severity of periodontal conditions and treatment needs
• simple, but only selected teeth are measured

• measures periodontal pockets, calculus, bleeding and defective resortations
• for general practice
• evaluates patients treatment needs
• records periodontal status of patient in private practice

• dental plaque exists as a biofilm>primary risk factor for periodontal disease
• can only be removed by toothbrushing, or scaling and root planning
• extracellular matrix: protects the bacteria from external sources such as antibiotics/antimicrobials

• aerobic
• nonmotile
• gram-positive

• P. gingivalis
• T. forythensis
• P. intermedia
• Eikenella corrodens

• P. intermedia
• A. actinomycetemcomitans (A.A)

• Capnocytophage species
• A. actinomycetemcomitans (A.A)

• Streptococcus sanguis
• Streptococcus mitis
• Veillonella species
• Actinomyces naeslundii
• Actinomyces viscosus

• P. gingivalis
• T. forythensis
• T. denticola

• appears 1-2 days
• gram+
• clonal expansion lateral, perpendicular to tooth
• thin continuous band at gingival margin with clear zone

• appears 2-4 days
• Gram+ rods
• Gram- species
• Anaerobes become to occupy interstices
• Zone obliterated: Marginal back thicker

• 4-7 days
• Gram+rods and Palisades OBLITERATED
• Difficult to distinguish rows
• plaque extends coronally; thickens
• PMNs increase in crevice

• 7-11 days
• Clinical: inflammation at subclinical level; PMNs, enlargement at gingiva
• Histological: Bacteria migrates subgingival; move toward chemottractants; others piggyback apically by coaggregation

• Growth, accumulation and pathogenicity are strongly influenced by supragingival biofilm
• edema causes gingival enlargment and alters the anatomic relationship btwn the tooth surface and the gingival margin and allows the bacteria to invade the subgingival dental plaque on the root surface or adjacent to the epithelial tissue in the sulcus.

• anerobic
• gram-negative
• motile
• asacchrolytic

• tooth associated
• tissue associated
• unattached subgingival plaques

• densely packed strongly adherent to tooth surface (biofilm)
• Gram+ rods, cocci, filmentous bacteria
• Facultative aerobic or facultative anaerobes
• less virulent (limited ability to cause disease)
• REMOVED BY SCALING AND ROOT PLANNING

• Loosely packed, loosely adherent to soft tissue wall
• Gram-, motile, anaerobic
• spirochetes, "bottle brush types"
• more virulent
• cannot be removed by scaling and root planning
• SURGICALLY REMOVED

• Free swimming in pocket (NOT a biofilm)
• Gram-, motile, anaerobic
• Spirochetes and others
• More virulent
• REMOVED BY FLUSHING

• A.A
• P. gingivalis
• spirochetes

• Lipooligosaccharide (LOS) is found in the cementum of untreated periodontally involved root surfaces.
• found on the cell wall of Gram- bacteria
• can initiate inflammation
• cuase soft tissue destruction
• stimulate bone resorption

is a toxin released by some bacteria such as A.A that can cause damage to the host by kiling PMNs

is a cytotoxic agent released from the cell wall upon death of Gram- bacteria

• Cause-antigen such as bacteria in dental plaque
• Involved-PMNs, mononuclear cells (macrophages)
• Mediators-Vasoactive amine (histamine/bradykinin)
• immediate onset
• last several days
• healing occurs if inflammation is resolved

• Cause-unresolved acute inflammation; cont. presence of antigens
• Involved- monocytes, macrophages, lymphocytes, plasma cells
• Mediators-cytokines, growth factors, reactive oxygen species, hydrolytic enzymes
• delayed onset
• last a long time (months or years)
• Tissue destruction

• first line of defense
• hallmark of acute inflammation
• one the first defensive cells to be recruited to inflammation site
• enter gingival crevice and JE

• monocytes change into MACROPHAGES
• migrate from the blood vessel into the inflammed CT by chemotaxis and a few cont. into the gingival crevice
• kills bacteria by phagocytosis
• secretes prostaglandins and cytokines

• process of engulfing and digesting foreign bacteria
• process is more effective if opsonins are present

antibodies or complement that bind to the surface of the bacteria, coating the bacteria so they are easier to be id by the PMNs and to be "swallowed"

• 20-30 plasma proteins that migrate form blood vessels inot gingival tissues and cervicular area during inflammation
• destroys invaders/antigens and signals to other immune system cells that an attack is occuring
• generates chemotactic factors, which attract PMNs, Macrophages, and other leukocytes

• 1. Classical pathway: antibodies bind to antigens
• 2. Alternative pathwayL endotoxins activate the sytem

• B lymphocytes
• Antibodies
• Macrophages
• Cytokines
• T-lymphocytes: T-Killer: directly invovled, T-helper: help plasma cells

• Humoral : B-cells
• Cellular: T-cells

• the major cells in the immune system are WBCs (lymphocytes)
• Lymphocytes predonminate in the gingival CT
• the role of the immune system is to "patrol" the body, id pathogens, or damagaed tissue and eliminating them

• most effective against bacteria such as those found in periodontitis
• B-cells originate in the bone marrow and migrate and deposit in the blood and various lymphatic tissues

• immune response activated
• macrophages carry antigenic substances to lymph nodes
• in lymph nodes macrophages present antigens to B-cells
• B-cells transform to plasma cells and memory cells
• antibodies are formulated by plasma cells
• memory cells are inactivated ready to respond if antigen appears
• plasma cells secrete antiobodies into the blood stream
• immunoglobulins are produced
• macrophages phagocytize and digest the debris and stimulate repair
• plasma cells disappear into GCF while memory cells continue circulating
• Prostaglandins are potent stimulators of osteoclast activity responsible for bone resorption

• T-cell mediated. T-cells undergo maturation in the THYMUS
• "watch" tissues
• T-cells are also called killer T-cells because they can directly kill viruses, cancer cells, parasites, and certain bacteria by boring holes in them
• Helper T-cells- CD4 receptor: secrete cytokines that activate phagocytic cells to destroy target antigens
• Cytotoxic T-cells- CD8 receptor

• macrophages presents antigen to T-cell and are now stimulated to produce more T-cells
• T-cells kill other cells when they are recognized as foreign or have antigen attached
• AIDS is a manifestation of what happens when T-cells are destroyed