Perio Exam 1 (first set of lectures)

D1 Fall

Periodontology

the specialty of dentistry that studies supporting structures of teeth as well as diseases and conditions affecting them

Periodontium

gingiva, cementum, periodontal ligament, alveolar bone

Periodontitis

inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both

effects of poor periodontal health

risk of tooth loss, heart disease, diabetes, stroke, respiratory disease, low birth weight in infants, malnutrition 

pathogenesis of periodontitis

periodontitis is a chronic disease, complex because the time frame allows for many varied individual responses

plaque as a biofilm

organized structure, individual response varies significantly due to many factors, periodontal maintenance disrupts biofilm

3 months

evidence supports complete biofilm reformation 

periodontal balance: disease

risk factors (genetics, smoking, diabetes), over production of proinflammatory or destructive mediators/ enzymes, underactivity or overactivity of host response, poor compliance/ poor plaque control, subgingival bioburden

periodontal balance: health

reduction of risk factors (quit smoking, control diabetes), expressions of host-derived anti-inflammatory or protective mediators, host modulatory therapy, resolution of inflammation, OHI/ SRP/ surgery/ antibiotics reduce bacterial challenge

periodontal assessment

medical history, dental history, intraoral radiographs, oral exam (including teeth), examination of the periodontium (PPDs)

etiologic factors

plaque (primary), calculus, restoration contour, malocclusion, smoking, diabetes, general systemic health, toothbrush abrasion

why do we need classifications?

not all individuals are equally susceptible to disease or responsive to prevention/ management, help distinguish patients who may not respond to standard therapies, necessary to properly diagnose and treat patients,

what do classifications do?

provide framework to study the etiology/ pathogenesis/ and treatment options in ordered fashion, scheme based on disease severity fails to capture individual differences that influence outcomes

history of periodontal classifications: 1989 workshop changes

distinct clinical presentations, different ages of onset (pre-pubertal, juvenile, adult), rates of progression (rapidly progressive)

history of periodontal classifications: 1999 classification major changes

chronic vs aggressive (localized and generalized), necrotizing, periodontitis as a manifestation of a systemic disease

history of periodontal classifications: major changes 2018

specific criteria for periodontal health, gingivitis, reduced but healthy periodontium (successfully treated periodontitis), gingival inflammation in a periodontitis patient, periodontitis as a manifestation of systemic diseases

Major Changes 2018

removal of distinction between chronic and aggressive periodontitis; due to lack of evidence for specific treatments between chronic and aggressive

highlights of new classifications

well-defined clinical entities linking diagnosis with prevention and treatment, individualized treatment, sensitive screening to differentiate health (gingivitis vs periodontitis), assess severity and complexity of periodontitis cases (staging), assess the risk profile of cases (grading)

3 new case diagnoses

periodontal health, reduced but healthy periodontium, gingival inflammation in a periodontitis patient (treated case w/ persistent inflammatory response)

is reversible following treatment that resolves inflammation

transition from gingivitis to periodontal health

attachment loss, irreversible

transition to periodontitis

periodontitis patient in the “green”

stable case of periodontal health 

periodontitis patient in the “yellow”

case with some gingival inflammation

periodontitis patient in the “red”

unstable case of recurrent periodontitis

periodontal and gingival health

A. clinical gingival health on intact periodontium B. clinical gingival health on a reduced periodontium (stable periodontitis patient or non-periodontitis patient)

gingivitis - dental biofilm induced

associated with biofilm alone, mediated by systemic or local risk factors, drug influenced gingival enlargement

gingival diseases - not biofilm induced

genetic/ developmental disorders, specific infections, inflammatory/ immune conditions, reactive processes, neoplasms, endocrine/ nutritional/ metabolic disease, traumatic lesions, gingival pigmentation

clinical gingival health on intact periodontium

BOP <10%, PPDs = or < 3mm

intact periodontium 

no probing attachment loss, PPDs = or < 3mm, BOP <10%, no radiographic boneloss

reduced periodontium non-periodontitis patient (ex. toothbrush trauma induced generalized gingival recession)

possible probing attachment loss, PPDs = or < 3mm, BOP <10%, possible radiographic bone loss

successfully treated stable periodontitis patient (ex. pt w/ a past hx of 4 quads osseous surgery)

probing attachment loss evident, PPDs = or < 4mm, BOP <10%, radiographic bone loss present

gingivitis - dental biofilm induced : change from 1999

addition of description of extent (localized or generalized) and severity (mild, moderate, severe) of inflammation

plaque induced gingival diseases

most common, pt. presents w/ swelling/ bleeding/ redness of gingiva, caused by interaction of microorganisms in plaque and inflammatory response in host tissues

plaque/ host interaction can be modified by local factors, systemic factors, medications, malnutrition 

plaque induced gingival disease

drug-induced gingival enlargement

antiepileptic drugs, calcium channel blockers, high-dose oral contraceptives

systemic or local risk factors of biofilm induced gingivitis

sex steroid hormones, hyperglycemia, hematological conditions, smoking, nutritional factors, pharmacological agents, oral factors enhancing plaque accumulation

staging of periodontitis

attempt to classify severity and extent of disease, asses contributing factors, explore reasons for previous tooth loss to identify periodontitis, initial stage should be determined using clinical attachment loss (CAL)

periodontitis stage I

interproximal clinical attachment loss 1-2mm, radiographic bone loss at coronal third (<15%), no tooth loss, max PPD = or < 4mm, mostly horizontal bone loss

periodontitis stage II

interproximal clinical attachment loss 3-4mm, radiographic bone loss at coronal third (15%-33%), no tooth loss, max PPD =or < 5mm, mostly horizontal bone loss

periodontitis stage III

interproximal clinical attachment loss = or > 5mm, radiographic bone loss extending to middle third of root or beyond, tooth loss = or < 4 teeth, probing depths = or > 6mm, vertical bone loss = or > 3mm, furcation involvement Cl II or III, moderate ridge defects

periodontitis stage IV

interproximal clinical attachment loss = or > 5mm, radiographic bone loss extending to middle third of root and beyond, tooth loss = or < 5 teeth, probing depths = or > 6mm, vertical bone loss = or > 3mm, furcation involvement Cl II or III, moderate ridge defects

extent and distribution to add as stage descriptor, for each stage describe extent as:

localized (<30% of teeth involved), generalized, or molar/incisor pattern

stage IV need for complex rehabilitation due to:

masticatory dysfunction, secondary occlusal trauma, tooth mobility (degree = or > than II), severe ridge defects, bite collapse/ drifting/ flaring, <20 teeth remaining

stage I: initial periodontitis 

early-stage attachment loss, develops in response, to persistent inflammation/ biofilm dysbiosis, CAL at early age may indicate heightened susceptibility, probing of early disease may present challenges due to inaccuracy, salivary biomarkers/ new imaging technology may increase detection  

stage II: moderate periodontitis

responds well to standard periodontal treatment and frequent monitoring, case grade and treatment response may guide for more individualized management

stage II: severe periodontitis

protentional/ additional tooth loss in absence of treatment, presence of deep periodontal lesions that extend to middle portion of the root, complicated by deep intrabony defects/ furcation involvement/ ridge defects

stage IV: advanced periodontitis 

extensive tooth loss, considerable damage to periodontal support, presence of deep periodontal lesions, frequent hypermobility due to secondary occlusal trauma

how to manage “gray zones”

select 2 worst teeth to assess, is there a presence or absence of furcation involvement? are there other contributing factors? (non-periodontitis?) is it localized, generalized, or molar/ incisor pattern?

aim of grading of periodontitis

rate of progression, responsiveness to standard therapy, potential impact on systemic health

grading of periodontitis (primary criteria): direct evidence of progression

radiographic bone loss or clinical attachment loss

grading of periodontitis (primary criteria): indirect evidence of progression

% bone loss/ age; case phenotype

grade modifiers: risk factors

smoking and diabetes

grade A : slow rate

no bone loss or CAL over 5 years, % bone loss/ age is less than 0.25, case phenotype is heavy biofilm deposits with low level of destruction, non-smoker, no diagnosis of diabetes

grade B: moderate rate

bone loss or CAL <2mm over 5 years, % bone loss over age is 0.25-1.0, case phenotype is destruction commensurate with biofilm deposits, <10 cigarettes/day, A1c < 7.0% in patients with diabetes

grade C: rapid rate

bone loss or CAL = or > 2mm over 5 years, % bone loss/ age >1.0, case phenotype is destruction exceeds expectations given biofilm deposits, = or or> 10 cigarettes/day, A1c = or > 7.0% in patients with diabetes

periodontitis as a manifestation of genetic disorders: immunologic

Down’s Syndrome, Papillion Lefevre Syndrom

periodontitis as a manifestation of genetic disorders: oral mucosa and gingival tissues

Epidermolysis bullosa

periodontitis as a manifestation of genetic disorders: connective tissue

Ehler’s Danlos Syndrome

periodontitis as a manifestation of genetic disorders: endocrine

glycogen storage diseases

periodontitis as a manifestation of acquired immunodeficiencies 

acquired neutropenia, HIV infection

periodontitis as a manifestation of inflammatory diseases

inflammatory bowel disease

necrotizing periodontal diseases (NPD)

necrotizing gingivitis (NG), necrotizing periodontitis (NP), infections, host immune response is critical to pathogenesis, occur with low frequency, require immediate attention

NPD diagnostic criteria: NG

painful, necrosis and ulceration of papilla, spontaneous bleeding, pseudo membrane formation, halitosis, adenopathy or fever

NPD diagnostic criteria: NP

painful, necrosis and ulceration of papilla, spontaneous bleeding, pseudo membrane formation, halitosis, adenopathy or fever, AND bone destruction/ sequestrum

other condition affecting the periodontium

periodontal abscess, gingival abscess, pericoronal abscess, endo/ perio lesions, mucogingival deformities, traumatic occlusal forces

mucogingival deformities

gingival recession, lack of keratinized gingiva, frenum pull

traumatic occlusal forces

occlusal force resulting in injury to teeth and/ or attachment apparatus

trauma from occlusion can cause

fremitus, tooth mobility, thermal sensitivity, excessive wear, tooth migration, pain to chewing, fractured teeth, widened PDL space, root resorption, hypercementosis

primary occlusal trauma

injury from excessive force to tooth or teeth with normal periodontal support

secondary occlusal trauma

normal or traumatic force applied to teeth with reduced support resulting in injury

orthodontic forces

root resorption, pulpal disorders, gingival recession, alveolar bone loss

tooth and prosthetic related factors

tooth anatomy, root fractures, restorations