DH 390: Exam #2

Describe the health stage

• Firm and resilient tissue, minimal sulcus depth

• Coral pink

• Variations in color may depend on race

• Evidence of previous disease may be present

Describe gingivitis

• Inflammation of the gingiva

• Clinically: change in color, gingival form, position, surface appearance, presence of bleeding/exudate

Describe early stage of periodontitis

• Progression of gingival inflammation into deeper periodontal structures and alveolar bone crest

• Slight bone loss

• Slight loss of CT attachment + alveolar bone

Describe moderate stage of periodontal disease

• More advanced stage of previous condition

• Increased destruction of periodontal structures

• Noticeable bone loss, support, and increase in mobility

• Furcation involvement 

Describe advanced stage of periodontal disease

• Major loss of alveolar bone support

• increased tooth mobility

• Furcation involvement

What are the three subcategories that periodontal health, gingival diseases, and conditions are divided into?

• Periodontal health and gingival health

• Gingivitis: dental biofilm-induced

• Gingival diseases: nondental biofilm-induced

Describe periodontal health and gingival health subcategoy

• Clinical gingival health on an intact periodontium

• Clinical gingival health on a reduced periodontium

  • Stable periodontitis patient

  • Non-periodontitis patient

Describe gingivitis - dental biofilm induced subcategory

• Associated with DENTAL BIOFILM alone

• Mediated by systemic or local risk factors

• Drug-influenced gingival enlargement 

Describe gingival diseases - nondental biofilm induced subcategoy

• Genetic/developmental disorders

• Specific infections

• Inflammatory and immune conditions

• Reactive processes

• Neoplasms

• Endocrine, nutritional, and metabolic diseases

• Traumatic lesions

• Gingival pigmentation

What are the three forms that periodontitis is divided into?

• Necrotizing periodontal diseases

• Periodontitis

• Periodontitis as a manifestation of systemic disease

What are the other five categories that periodontitis is subdivided into?

• Systemic diseases or conditions affecting the periodontal supporting tissues

• Periodontal abscesses and endodontic periodontal lesions

• Mucogingival deformities and conditions

• Traumatic occlusal forces

• Tooth and prosthesis related factors

Describe mucogingival deformities and conditions around teeth

• Gingival pheotype

• Gingival/soft tissue recession

• Lack of gingiva

• Decreases vestibular depth

• Aberrant frenum/muscle position

• Gingival excess

• Abnormal color

• Condition of the exposed root surface

What are the subdivisions of Peri-implant Diseases and Conditions?

• Peri-implant health

• Peri-implant mucositis

• Peri-implantitis

• Peri-implant soft and hard tissue deficiencies

What are characteristics of periodontal health?

• Absence of:

  • Bleeding on probing

  • Erythema

  • Edema

  • Attachment loss

  • Bone loss

• Gingival tissue = uniform pink color

• Gingival margin tightly encircles tooth’s cervical region (contour)

What is intact periodontium?

• No loss of periodontal tissue

• No signs of inflammation

• No loss in bone level

What is reduced periodontium?

Preexisting loss of periodontal tissue but not currently undergoing loss of CT/alveolar bone

Describe periodontial health on reduced periodontium in non-periodontitis patient?

• No inflammation

• Recession

• No bone loss

Features of dental biofilm-induced gingivitis

• Most common form of periodontal disease

• Does NOT directly cause tooth loss, must be managed as active disease

• Inflammatory response of gingival tissues by periodontal pathogens

• Prevalent in all age groups

Describe tissue contour in gingivitis

• Edema causes enlargement of gingival tissues

• EX: Bulbous papilla

Describe the tissue contour in this image?

Blunted papilla

Describe the tissue contour in this image?

Cratered papilla

Describe the tissue contour in this image?

Rolled - thickened gingival margin

What is the tissue consistency in gingivitis?

• Inflamed free gingiva loses firm consistency

• Tissue spongy with light pressure

• Compressed air readily deflects gingival margin and papillae away from neck of tooth

• Can appear smooth and very shiny

• Almost has “stretched” appearance

• May lose gingival 

What is the position margin of gingivitis

• More coronal

• B/c tissue swelling and enlargement

What is presence of bleeding like in gingivitis?

• Occurs with gentle probing before color changes

• Epithelial lining of sulcus becomes ulcerated and blood vessels engorge

• Heavier bleeding as inflammation increases

Where can distribution of inflammation affect?

• Only interdental papilla (papillary gingivitis)

• Gingival margin and papilla (marginal gingivitis0

• Gingival margin, papilla, and attached gingiva (diffuse gingivitis)

What are the subcategories of dental biofilm induced gingivitis?

• Dental biofilm induced gingivitis on intact periodontium

• Dental biofilm induced gingivitis on reduced periodontium in non-periodontitis patient

• Gingival inflammation on reduced periodontium in a successfully treated stable periodontitis patient

What are the treatment objectives for dental biofilm induced gingivitis on reduced periodontium in a non periodontitis patient?

• Remove etiologic factors

• Reinforce oral hygiene

• Avoid further loss of periodontal tissues

• Minimize risk of gingivitis converting into periodontitis

What are some potential modifying factors of biofilm-induced gingivitis?

• Systemic condiitons

• Oral factors enhancing plaque biofilm accumulation

• Drug influenced gingival enlargements

Describe systemic conditions as modifying factors?

• Sex and steroid hormones

  • Puberty

  • Menstrual cycle

  • Pregnancy

  • Oral contraceptives

Describe gingivitis associated with puberty?

• TEMPORARY increase in gingival inflammation b/c of increased steroid hormone levels

• Exaggerated response to little plaque biofilm

Describe gingivitis associated with menstrual cycle?

• Only MODEST observable inflammatory changes during ovulation

• Few women extremely sensitive to hormonal changes in gingiva

• No clinically evident inflammatory changes in gingiva in most women

Describe gingivitis associated with pregnancy?

• Increased hormones = more gingival crevicular fluid flow

• High inflammation w/ little plaque biofilm

• Can spontaneously resolve postpartum

• Pregnancy associated pyogenic granuloma 

What is hyperglycemia?

• Presence of abnormally high concentration of glucose in circulating blood

• Occurs with DM

• Inflammation exacerbated by high blood glucose levels

Describe gingivitis associated with leukemia?

• Bleeding and tissue enlargement

• Gingival tissues appear swollen, spongy, red

• Tissues = friable = bleed with slight provocation

• You do not need biofilm to have gingivitis for pts w/ leukemia

Describe gingivitis associated with smoking?

• Gingival fibrosis = abnormal amount of fibrous tissue

• Smokers have fewer clinical signs

Describe gingivitis associated with malnutrition>

• Not fully understood

• Similar to biofilm-induced gingivitis

• Vitamin C important for:

  • Collagen and fibrous tissue for normal intercellular matrices

  • Structural integrity of capillary walls

  • Deficiency = scurvy, delayed healing

What are some oral factors that enhance plaque biofilm accumulation?

• Prominent subgingival restoration margins

  • Increase plaque accumulation

• Hyposalivation can cause:

  • Progressive caries, taste disorders, halitosis, inflammation

  • Worsen gingival inflammation

What medications cause gingival enlargements?

• Anticonvulsants (Phenytoin/dilantin, methsuximide, divalproex sodium)

• Calcium channel blockers (Amlodipine, nifedipine, verapamil)

• Immunosuppressants (Cyclosporine)

• Enlargements occur within 3 months of use

Characteristics of drug influenced gingival enlargements?

• More in younger age groups

• Tissues in anterior sextants most commonly affected

• Irregular pattern of enlargement

• Increased flow of crevicular fluid from sulcus

• BOP with no attachment loss

What is hereditary gingival fibromatosis?

• Rare benign oral condition involving slow, progressive enlargement of maxillary and mandibular attached gingiva

• Causes: specific bacterium not typically found

• Oral ulcerations, chancres, mucous patches

Describe hypersensitivity reactions: intraoral allergic reactions

• Often caused by flavoring agents

• Most common in pts with allergic conditions

• Diffuse fiery red gingivitis

• May have ulcerations

What is erythema multiforme?

• Uncommon acute inflammatory disorder

• Causes large symmetrical erythematous papules resembling target in circular pattern

• Cause: unknown

What is oral lichen planus?

• Purplish, itchy, flat-topped bumps on skin

• Lacy white patches, sometimes w/ painful sores in mouth

• Usually chronic

• Increases risk for oral cancer

• 6 clinical manifestations

  • Papular, reticular, plaque type, erythematous, ulcerative, bulbous lesions

What are some signs and symptoms of periodontitis?

• Accumulation of plaque biofilm and calculus

• Erythema, edema

• Gingival bleeding

• Suppuration (pus)

• Periodontal pockets

• CAL, mobility

• Pain

• Odor

What is loss of attachment characterized by?

• Apical migration of junctional epithelium

• Destruction of gingival and periodontal ligament fibers

• Loss of alveolar bone support around tooth

What are some contributing factors of periodontitis?

• Environmental - smoking

• Systemic - diabetes, HIV

• Genetic

• Local intra oral factors such as tooth crowding and or overhanging restorative margin

What are some symptoms of periodontitis?

• Usually painless

• Gingival bleeding while brushing

• Spaced between teeth

• Mobility

• Food impaction, sensitive to temp, dull pain radiating into jaw

Onset of periodontitis?

• Dental biofilm induced gingivitis:

  • Always precedes onset of periodontitis

  • May remain stable for years

  • Manifests days or weeks after biofilm accumulation

• Can occur ANY AGE, most common in adults

Localized vs. Generalized periodontitis: LESS than 30% of teeth exhibit attachment loss and or bone loss?

Localized periodontitis

Localized vs. Generalized periodontitis: 30% or MORE of teeth exhibit attachment loss and or bone loss

Generalized periodontitis

What are the types of progressions of periodontal disease?

• Continuous disease

• Random burst

• Asynchronous burst

Describe recurrent form of periodontitis?

• Return of destructive periodontitis that had been previously arrested by conventional therapy

• Risk for anyone with history of periodontitis

• Recurrence common

Describe refractory form of periodontitis?

• PTs that do not respond well despite treatment

  • Receiving appropriate perio therapy

  • Practicing self care

  • Following recall schedule

• Etiology unknown

Treatment for refractory form of periodontitis?

• PT education and behavior modification

• Periodontal instrumentation

• Use of systemic and or local antibiotics

• Removal of hopeless teeth

• Correction of restorations that cause plaque retention

• Surgical therapy

• Strict adherence to perio maintenance regimen

Describe the structure of bacterial cell envelope

• Complex multilayered structure

• Protects microorganism from unpredictable and inhospitable external environment

• Gram staining

  • Classifies bacteria based on structure

  • Gram positive or gram negative

What is gram staining?

• Depends on permeability of strain through cell envelope when viewed under light/microscope

• Gram positive: purple

• Gram negative: pink

What is biofilm?

• Complex, dynamic microbial community embedded within matrix adhered to living or nonliving surface

• May be responsible for 65% of diseases

Describe timeline for biofilm formation

• Minutes

  • Free floating microbes attach to surface

• 2-4 hours

  • Form strongly attached microcolonies

• 6-12 hours

  • Produce initial ECM

• 2-4 days

  • Biofilm evolves into fully mature biofilm

How does mature biofilm protect bacteria?

• Blocking

  • Preventing large molecules from penetrating matrix

• Mutual protection

• Hibernation (quiescence)

  • Laying dormant until conditions become more favorable

Define oral biofilm

• Polymicrobial

• 3D community embedded in protective matrix

• Consists of microbial metabolic products and or host components

What does commensal bacteria contribute to the oral cavity?

• Normal flora in mouth

• Prevent colonization by opportunistic pathogenic bacteria

• Symbiotic relationship w/ host

  • Host nutrition, maintain robust immune system, provide cover for mucous membranes

  • Host provides nutrients, stable environment for survival

What is dysbiosis?

• Microbial imbalance on or inside body

• Occurs when oral biofilm not disrupted frequently

• Leads to gingival inflammation (initial dysbiosis or incipient dysbiosis)

What is established dysbiosis?

• Symbiotic host = microbe becomes pathogenic

• Triggers inappropriate, excessive host response = irreversible periodontal tissue damage

Model of Host-microbe interactions

Why is physical removal of dental plaque biofilms important?

• Breaks up biofilm = forces bacteria to start over

• Periodontal instrumentation needed for subgingival plaque

TRUE OR FALSE: Biofilm bacteria is resistant to antibiotics and antimicrobial agents

TRUE

Describe transmission of biofilm bacteria

• Transmissible via DIRECT or INDIRECT contact

• Most common route: vertical transmission

  • Sharing saliva between caregiver + child

• Less common route: horizontal transmission

  • Same generation kissing

TRUE OR FALSE: Periodontal pathogens are transmissible, but periodontal disease is not an infectious disease

TRUE

What are the 5 stages of biofilm formation?

• Initial attachment

• Permanent attachment

• Maturation I

• Maturation II

• Dispersion

Describe stage 1: initial attachment

• Acquired salivary pellicle immediately forms over clean tooth surface

• Free-floating microbes attach using fimbriae

• Initial attachment dynamic and reversible

Describe stage 2: permanent attachment

• Attained by microbes that can weather hydrodynamic forces and maintain steadfast grip on tooth surface

• Microbes begin producing substances that attract other free floating bacteria to community

• Process = coaggregation 

Describe stage 3: Maturation phase I - Self protective matrix formation

• Attached bacteria secrete extracellular protective matrix = protects against host immune defenses

• Consists of: proteins, glycolipids, bacterial DNA

Describe stage 4: Maturation Phase II - Mushroom shaped microcolonies

• Microcolony formation

  • Combination of cell division and recruitment

  • Microbes cluster, form mushroom shaped microcolonies = exchange and share nutrients + genetic info

  • Diverse population

• Internal organization of mature biofilm

  • Layers of microbes

  • Fluid channels form = penetrate ECM = direct fluids around biofilm

  • Cell to cell communication using chemical signals

  • Quorum sensing = bacteria communicates by releasing small proteins

Describe stage 5: Dispersion - Escape from the matrix

• Essential stage of biofilm life cycle

• Dispersal enables:

  • Spread

  • Colonize new tooth surfaces

Describe sequence of bacterial colonization

• Early bacterial colonizers = release chemical signals = indicate conditions favorable for joining biofilm

• Favorable conditions necessary for microbes to join

• Mature biofilm collection of multiple microbial species 

What are the bacterial attachment zones?

• Tooth surface

• Epithelial lining of periodontal pocket

• 😄 HI

What are some more specific bacterial attachment zones?

• Tooth associated plaque biofilms

  • Attached to tooth surface = invade dentinal tubules

• Tissue associated plaque biofilms

  • Adhere to epithelium = invade gingival tissue

• Unattached bacteria

  • Free floating = not part of biofilm

What are the 5 hypotheses that explain role in periodontal disease?

• Nonspecific plaque 

• Specific plaque

• Ecological plaque

• Microbial homeostasis-host response 

• Keystone pathogen-host response

What is the nonspecific plaque hypothesis?

• Accumulation of plaque biofilm at gingival margin = gingival inflammation + tissue destruction

• Limitations:

  • Too simple, superficial

  • Fails to explain why most gingivitis never become periodontitis

What is the specific plaque/microbial shift hypothesis?

• Oral microbiota shifts from primarily beneficial to primarily pathogenic as periodontitis develops

• Increase in specific pathogens causes periodontitis

• Bacteria change from mainly gram+ aerobic community to gram- anaerobes

• Socranksy:

  • Assigned colors for each microbes

  • Orange + red = periodontal disease

  • Yellow, blue, green and purple = gingival HEALTH

What is the current perspective of ecological plaque hypothesis?

• Accumulation of nonspecific bacteria triggers host inflammatory response, altering local environment

• Environment becomes more conducive to growth of pathogenic bacteria

• Support for hypothesis:

  • Sites with BOP + deeper probing depths strongly associated with higher GCF flow = alters microbial ecology = favors pathogens

What is microbial homeostasis-host response hypothesis?

• Plaque biofilms cause initial inflammatory response = gingivitis

• But pathogenic bacteria is NOT direct cause of tissue destruction in periodontitis 

• Pathogenic biofilm community → triggers uncontrolled host response → damage to periodontal tissues

What is the keystone pathogen-host response hypothesis?

• Specific bacterial species is key in creating shift from symbiotic microbes to dysbiotic microbes

• Dysbiotic biofilm community triggers uncontrolled host response = damage to periodontal tissues

Difference of immune status of periodontal tissue between healthy vs. diseased patients?

• Healthy tissue: mild subclinical inflammation

• Diseased tissue: disordered severe inflammation

• Shift from beneficial pathogenic community = triggers potent host inflammatory response = contributes to tissue destruction + alveolar bone loss

Describe heathy gingiva structure

• Few mainly G+ aerobic bacteria

• Normal junctional epithelium

• A few PMNs (WBCs) with very little crevicular exudate

• Connective tissue WNL

• Alveolar bone WNL

Describe early gingivitis structure

• Build up of G+ aerobic bacteria

• Alteration of junctional epithelium

• Vasculitis, increase in crevicular fluid outflow, increase PMNs, inflammatory cell migration

• Attention fibroblasts, collagen changes

• Attention bone WNL

Describe progressing or Est. Gingivitis structure

• Build up of G+ AND G- anaerobic bacteria

• JE migrates both laterally + apically

• Acute inflammatory alterations, further increase of crevicular fluid flow, increase in PMNs, formation of wall PMNs

• Severe fibroblast damage, further collagen loss with exudate

• Alveolar bone WNL

Describe periodontitis structure

• Mostly G- anaerobic bacteria, subepithelial

• Further migration of JE, ulcerations, and true pocket formation

• Acute inflammatory alterations with gingivitis, massive PMN migration, expansion of inflammatory cells

• Further collagen loss and fibrosis in surrounding CT

• Resorption of alveolar bone loss, attachment loss

Define immune system

• A network of biological systems that protects an organism from diseases

• Detects and response to pathogens, viruses, cancer, and foreign objects 

• Distinguishes from organism’s own healthy tissue

What are the two major subsystems of the immune system?

• Innate immune system

• Adaptive immune system

What is the function of the innate immune system?

Provides a preconfigured response to broad groups of situations and stimuli

What is the function of the adaptive immune system?

Provides a tailored response to each stimulus by recognizing molecules it has previously encountered

When does innate immunity develop?

Present at birth

Is innate immunity antigen specific or nonspecific?

• NON SPECIFIC

• Exposure results in NO immunologic memory

TRUE OR FALSE: Innate immunity is always present

• TRUE

• Responds quickly to infection

• Programmed to respond to many pathogens

What are the cells of innate immunity?

• Neutrophils

• Monocytes

• Macrophages

• Eosinophils

• Basophils

• Mast cells

• NKT lymphocytes

• NOTE: Physical barriers such as skin and mucosal membranes help protect

When does adaptive immunity develop?

• Develops throughout life after initial exposure to antigen

• Learns how to counterattack pathogen

Is adaptive immunity antigen specific or non specific?

• ANTIGEN SPECIFIC

• Repeated exposure = immunologic memory

TRUE OR FALSE: Adaptive immunity is alway present

• FALSE

• Responds slowly the 1st time