CHAPTER 2: ANATOMY OF THE PERIODONTIUM KERATINOCYTE: principal cell in gingival epithelium

Non-keratinocytes:
Periodontium  Langerhans cells – antigen-presenting cells for lymphocytes
1. GINGIVAL APPARATUS: gingival fibers & epithelial attachment  Merkel cells – tactile perceptors
2. ATTACHMENT APPARATUS  Melanocytes – provide color to gingiva
 PDL: fibroblasts are the most abundant cells
o Narrower on mesial surface Gingival Epithelium
o Thinnest at the middle 1. ORAL EPITHELIUM | keratinized stratified squamous epithelium
o Thinnest at fulcrum of axis of rotation  Stratum basale
 CEMENTUM: attachment of PDL fibers  Stratum spinosum
 ALVEOLAR BONE  Stratum granulosum
 Stratum corneum
Gingival Fiber Groups: found ONLY within free gingiva 2. SULCULAR EPITHELIUM | thin, nonkeratinized W/OUT rete pegs
1. Circular fibers: resist rotational forces; bind free gingiva to tooth 3. JUNCTIONAL EPITHELIUM | collar-like band, nonkeratinized
2. Dentogingival fibers  Attached to tooth by basal lamina
3. Dentoperiosteal fibers  Formed by the confluence of oral epithelium & reduced enamel
4. Aveologingival fibers epithelium (REE) during tooth eruption
5. Transseptal fibers: DO NOT have osseous attachment  In healthy gingiva, JE is located at CEJ
 Consistent & reconstructed even after bone destruction  Epithelial attachment DOES NOT contain rete pegs & free gingiva does
 Biologic width – act as natural seal | CT + JE = 2.04 mm
PDL FUNCTIONS o Junctional epithelium = 0.97 mm | 0.25 to 1.35 mm
1. Physical: attachment via principal fibers o CT attachment = 1.07 mm
2. Formative: osteoblasts DENTOGINGIVAL UNIT: functional unit of JE & gingival fibers
3. Resorptive: osteoclasts
4. Nutritive Lamina Propria: connective tissue of gingiva
5. Sensory: trigeminal nerve (CN V)  PAPILLARY LAYER
 Free, unmyelinated nerve endings: PAIN o Rete pegs – finger-like extensions of epithelium
 Encapsulated, myelinated endings: PRESSURE  RETICULAR LAYER

Principal fibers of PDL: Type I collagen | hydroxyproline content Sources of Blood Supply to the Gingiva
*Elastic fiber system: Elastin, Oxytalan & Eluanin 1. SUPRAPERIOSTEAL ARTERIOLES
1. Horizontal: resists lateral forces 2. VESSELS OF THE PDL
2. Alveolar crest: prevent extrusion 3. ARTERIOLES
3. Oblique: resist intrusive, masticatory forces
 Most resistant to forces along the long axis Characteristics of a Healthy Gingiva
4. Apical: resist rotation of tooth; absent in incompletely formed roots  Color – coral pink | erythema: intense red, cyanosis: bluish-purple
5. Interradicular: found in furcation areas of multi-rooted teeth  Shape – knife-edged/ scalloped gingival margin
 Tone – resilient, fibrous, firm consistency
* Indifferent fiber plexus: small collagen fibers that run in all directions  Texture – stippling on attached gingiva
* Molecular configuration provides tensile strength greater than that of steel Absence of stippling is due to:
* Sharpey’s fibers: terminal portions of PDL fibers embedded into cementum & bone o Normal variation
o Inflammation
PDL Ground Substance o Edema
 Glycosaminoglycans: hyaluronic acid &proteoglycans
 Glycoproteins: fibronectin & laminin Concept of Continuous Eruption
 Does not stop when teeth meet their functional antagonists but
*Bone consists of 2/3 inorganic matter & 1/3 organic matrix continues throughout life
* Average PDL space is about 0.2 mm  Active eruption – movement of teeth in occlusal direction
* Epithelial rests of Malassez: remnants of Hertwig’s epithelial root sheath (HERS)  Passive eruption – exposure of teeth by apical migration of the gingiva
(gingival recession)
Zones of Oral Mucosa
1. MASTICATORY MUCOSA – gingiva & hard palate | keratinized CHAPTER 4: CLASSFICATION OF DISEASES AND CONDITIONS
2. SPECIALIZED MUCOSA – dorsum of tongue | nonkeratinized AFFECTING THE PERIODONTIUM
3. LINING MUCOSA – cheeks, lips, soft palate | nonkeratinized
* However, vermilion border of lips is KERATINIZED.
PLAQUE-INDUCED GINGIVAL DISEASE
 Most common, result of interaction between plaque bacteria &
Anatomical Parts of the Gingiva
inflammatory cells of host
UNATTACHED GINGIVA ATTACHED GINGIVA
Modified by systemic factors
Not firmly bounded to underlying bone Firmly bounded to underlying bone
 Endocrine changes (puberty, pregnancy, diabetes)
Demarcates from attached gingiva by Demarcates from alveolar bone by
free gingival groove mucogingival junction  Blood dyscrasias (leukemia, agranulocytosis)
Smooth appearance Stippled appearance Modified by medications
 Calcium channel blockers, Dilantin, cyclosporine
1. MARGINAL / UNATTACHED / FREE GINGIVA  Oral contraceptives
 Free gingival groove: shallow linear depression that demarcates Gingival enlargement (hyperplasia) due to medications
from attached gingiva  Anticonvulsants – phenytoin (Dilantin)
 Gingival sulcus: V-shaped space that encircles tooth  Immunosuppresants – cyclosporine
2. ATTACHED GINGIVA  Calcium channel blockers – nifedipine, verapamil, diltiazem
 Mucogingival junction present on gingival surfaces: Oral contraceptives concerns are
o Facial aspect of maxilla & mandible  Bleeding – main concern due to hormonal changes
o Lingual aspect of mandible  Thrombophlebitis / DVT – clot formation & inflammation of veins
 NARROWEST BAND of attached gingiva is found on: Modified by malnutrition
o Facial surfaces of mandibular canine & first premolar and  Vitamin C deficiency – scurvy/ scorbutic gingivitis
lingual surfaces adjacent to mandibular incisors & canines  Vit. C: needed for hydroxylation of proline & lysine for collagen formation
 Narrow gingival zones may also occur at Pyogenic granuloma (Pregnancy Tumor) | NOT a neoplasm
o MB root of maxillary first molars & at mandibular molars  Reactive hyperplasia of CT in response to local irritants, trauma of
 “Functionally adequate” zone of gingiva hormonal factors
o Keratinized, firmly bound to tooth & underlying bone, about 2  Gingiva on anterior teeth as most common site
mm or more wide, and is resistant to probing & gaping when
lip is distended NON-PLAQUE-INDUCED GINGIVAL DISEASES
3. INTERDENTAL GINGIVA  Less common
 Pyramidal (anterior teeth) In response to infections
 Col (posterior teeth)  Bacterial infections (N. gonorrhea, T. pallidum)
 Viral (herpes)
Width of attached gingiva Width of keratinized  Fungal (candidiasis)
Distance between mucogingival junction gingiva In response to allergy
& gingival sulcus Distance between  Foods, resto materials, toothpaste (sodium lauryl sulfate)
* Greatest: incisor (3.5-4.5 mm in maxilla, mucogingival junction In response to trauma
3.3-3.9 mm in mandible) & marginal gingiva  Factitious (unintentionally produced)
* Narrowest: posterior (1.9 mm in maxilla,  Iatrogenic (caused by doctor)
1.8 mm in mandibular 1st premolars)  Accidental (damage thru burns from hot foods & drinks)
Gingival lesions of genetic origin
GREATEST contour of cervical lines & gingival attachments occur on  Hereditary gingival fibromatosis
 Mesial surface of anterior teeth Hereditary gingival fibromatosis
 Maxillary central incisor has the greatest cervical line curvature  Rare benign gingival overgrowth characterized by accumulation of ECM
CEJ curves in two directions result in fibrotic enlargement of gingiva
 Toward the apex on facial & lingual surfaces  Drifting, migration of teeth, diastema, prolonged retention of primary
 Away from apex on mesial & distal surfaces teeth, poor plaque control
Etiologic Factors Associated with Periodontal Disease CHAPTER 7: STAGES OF GINGIVITIS
1. Bacterial plaque (primary) Stages Days Blood vessels Predominant Clinical findings
2. Immune/ host response cells
I. Initial lesion 2-4 Vascular dilation PMNs ↑ GCF flow
* Inoragnic constituents of bacterial plaque: Na, K, Ca, P
II. Early lesion 4-7 Vascular proliferation Lymphocytes Erythema, BOP
* Organic: polysaccharides, proteins, glycoproteins, lipids
III. Established 14-21 Same stage II, blood Plasma cells Change in size,
* Saliva: supragingival plaque | Gingival crevicular fluid (GCF): subgingival plaque
lesion stasis, anoxemia color, texture
*Parotid: Stensen’s | Submandibular: Wharton’s | Sublingual: Bartholin’s
IV. Advanced Transition to irreversible damage of periodontitis
lesion
PRIMARY/EARLY PLAQUE COLONIZERS | Gram (+) facultative anaerobe
Streptococcus Actinomyces * PMNs: first line of defense to migrate to inflamed site
SECONDARY/LATE PLAQUE COLONIZERS | Gram (-)
Capnocytophaga Fusobacterium nucleatum Porphyromonas gingivalis CHAPTER 8: CLINICAL FEATURES OF GINGIVITIS
Eikenella corrodens Prevotella intermedia Treponema denticola
Campylobacter spp. Tanerrella forsythia 2 Earliest Signs of Gingival Inflammation Preceding Established Gingivitis
1. Increased gingival crevicular fluid (GCF) production rate
* Pattern: gram (+) –> gram (-) anaerobic due to REDOX potential (oxygen-reduction) 2. Bleeding from gingival sulcus on gentle probing
* Gram (+) facultative are abundant in HEALTHY SULCUS
* Endotoxins: lipopolysaccharide (LPS) cell wall of gram (-) Effects of Toothbrushing On the Consistency of Gingiva
* Streptococcus viridans consist of variety of alpha-hemolytic streptococci, S.  Promote keratinization of oral epithelium
salivarius, mutans, sanguis, & mitis, all COMMON ORAL FLORA  Enhance capillary gingival circulation
* Oral cavity is usually sterile at birth. They appear about 10-12 hrs after birth.  Thicken alveolar bone
* By age 4-5, the oral flora resembles that of an adult
Diseases That Increase Melanin Pigmentation
GINGIVITIS PERIODONTITIS 1. ADDISON’S DISEASE – reduced cortisol production
No destruction of PDL & Destruction of PDL & alveolar bone | CAL 2. PEUTZ-JEGHERS SYNDROME – intestinal polyps
alveolar bone Severe, irreversible 3. ALBRIGHT’S SYNDROME – polyostotic fibrous dysplasia, precocious puberty
Mild, reversible Radiographic changes noted: loss of lamina dura,
NO radiographic changes horizontal/ vertical bone resorption, wide PDL space Etiologic Factors Implicated in Gingival Recession
 Faulty toothbrushing technique (abrasion)
Prognosis of The Following Forms of Periodontitis  High frenum attachment
Chronic periodontitis If px is compliant:  Gingival inflammation
SLIGHT TO MODERATE  Tooth malposition
If px is noncompliant:  Friction from soft tissues (ablation)
FAIR TO POOR  Iatrogenic (caused by dentist/ health professional)
Aggressive periodontitis POOR
Periodontitis as manifestation of FAIR TO POOR Changes in Gingival Contour
systemic disease McCall’s festoons Stillmans cleft
NUP FAIR TO POOR Rolled, thickened band of gingiva seen Narrow, triangular-shaped gingival
adjacent to cuspids recession
BLEEDING ON PROBING (BOP): measure of periodontal inflammation Due to trauma from occlusion | Tx: occlusal adjustment
CLINICAL ATTACHMENT LOSS (CAL): measure of severity of periodontitis
MOST important clinical parameters for prognosis of periodontally involved tooth CHAPTER 9: GINGIVAL ENLARGEMENT
1. ATTACHMENT LOSS
2. TOOTH MOBILITY Criteria of location & distribution
 Marginal: confined to the marginal gingiva
Chronic periodontitis Aggressive periodontitis  Papillary: confined to the interdental papilla
Age of onset > 55 yrs old < 35 yrs old  Diffuse: involving the marginal & attached gingivae and papillae
Presence of plaque Commensurate Minimal  Discrete: isolated sessile or pedunculated, tumorlike enlargement
Attachment loss Slow to moderate Rapid
Pattern of bone loss Horizontal (suprabony) Vertical (intrabony) Degree of gingival enlargement
Destruction Consistent Inconsistent Grade 0 No signs of gingival enlargement
Familial aggregation NO YES Grade 1 Enlargement confined to interdental papilla
Affected teeth Any in the arch 1st molars & incisors Grade 2 Enlargement involves papilla and marginal gingiva
Causative agent P. gingivalis A. actinomycetemcomitans Grade 3 Enlargement covers three quarters or more of the crown
T. forsythia
CHAPTER 30: CLINICAL DIAGNOSIS
Classification of Periodontitis
Oral Malodor (fetor ex ore, fetor oris, halitosis)
Distribution Severity Type
Localized: <30% Slight: 1-2 mm CAL Chronic (common)
Wasting Diseases of Teeth
Generalized: >30% Moderate: 3-4 mm CAL Aggressive (rare)
EROSION ABRASION ATTRITION ABFRACTION
Severe: ≥ 5mm CAL
Wedge-shaped, Saucer-shaped, Occlusal/ incisal Tooth flexure
Acidic food & drinks Mechanical wear wear (facets)
LAP GAP
Age of onset Puberty < 30 yrs old Principal Causes of Increased Tooth Mobility
Distribution Localized Generalized 1. Bone loss
Severity of bone loss Rapid Episodic 2. Occlusal trauma
Causative agent Aggregatibacter Porphyromonas 3. Extension of inflammation
actinomycetemcomitans gingivalis
Immunologic response Robust serum antibody Poor serum Radiographic signs of trauma from occlusion
Plaque present Minimal Marked  Widening of PDL space
Familial pattern Strong association Unclear association  Thickening of lamina dura
 Vertical rather than horizontal destruction of periodontal septum
ANUG (Trench mouth, Vincent infection, Vincent angina)  Root resorption
 Punched-out interdental papilla, crater like lesions  Hypercementosis
 Caused by: Borrelia vincentii & Fusobacterium * Reversible, if excessive occlusal forces are eliminated & there is absence of irritant
 Predominant organism found in smears: Spirochetes
 Tobacco chewing: the most common predisposing cause 2 Uses of Warm Air in Clinical Diagnosis
 Tx: Metronidazole, hydrogen peroxide mouthwash 1. Deflect the gingiva
 EXO in ANUG px can be done after 4 weeks 2. Aid in visualization of calculus: most important plaque retentive factor

Periodontitis Associated with Systemic Disease Gingival Tissue Response

DIABETES MELLITUS | Hypoglycemia: most common dental office complication of DM 1. Edematous – smooth, glossy, soft, red gingiva| Tx: scaling & polishing
1. Polyuria: frequent urination 2. Fibrotic – firm, opaque, thicker, rounded margins| Tx: gingivectomy
2. Polydipsia: excessive thirst
3. Polyphagia: excessive hunger Detection of Pockets
TYPE I DM (Children) TYPE 2 DM (Adults)  Periodontal probe – measure pocket depth from JE to marginal gingiva
Insulin-dependent Non-insulin-dependent  Gutta-percha/ silver points – used w/ radiograph to assist in determining
Require insulin therapy Can be managed by lifestyle changes level of attachment of periodontal pockets
* Presence of pockets CANNOT be determined from radiographs
DOWN SYNDROME (Mongolism, Trisomy 21)
 Less in dental caries, MORE on periodontal problems due to: Gingival pocket (pseudopocket): w/out destruction of periodontal tissues
- Mental deficiency & Manual dexterity Periodontal pocket (true pocket): w/ destruction of periodontal tissues
 Suprabony – base of pocket is coronal |bone loss: HORIZONTAL
AGRANULOCYTOSIS  Intrabony – base of pocket is apical to alveolar bone | VERTICAL
 Drug idiosyncrasy: most common cause
 Neutropenia: low no. of neutrophils How should probe be adapted in interproximal area?
 Should touch contact area & angle slightly beneath & beyond contact area
LEUKEMIA When probing & there’s resistance
 Malignant neoplasms of WBC precursors  Lift the probe away from tooth & move it apically
Most common error when probing CHAPTER 34: TREATMENT PLAN
 Excessive angling when inserting interproximally beyond long axis of tooth
 Tip should be flat & parallel with long axis of tooth Short term
 To eliminate gingival inflammation
PERIODONTAL PROBING: provides the MOST ACCURATE assessment of pocket depth  Correct conditions that cause & perpetuate disease
Critical Factors to Obtain Accuracy & Reproducibility in Probing Long term
1. PROBING FORCE = 0.75 Newton or 25 pounds  Reconstruction of healthy dentition that fulfills functional & esthetic
2. PROBING TECHNIQUE requirement
 Insert parallel to vertical axis of tooth surface & “walked”
circumferentially around each tooth surface Preliminary Phase / Treatment of emergencies
 Oblique positioning to detect interdental crater Emergency Phase  Dental or periapical abscess, Periodontal
 Naber’s probe: furcation areas | Plastic probe: implant areas abscess
3. PROBE ANGULATION 10° Extraction of hopeless teeth & interim dentures if needed
4. PROBE CALIBRATION < 1mm Phase I Therapy Plaque control & patient education
* Pocket depth: distance between base of pocket & gingival margin (Non-Surgical Phase)  Diet control
* Clinical attachment level: distance between base of pocket & CEJ
 Removal of calculus & root planning
* In healthy site, the tip of the probe stops w/in JE
 Correction of restorative & prosthetic
* In diseased site, it penetrates into connective tissue to the alveolar bone
irritational factors
* 6 probing measurements are recorded |3 buccal: DB, B, MB & 3 lingual: DL, L, ML
 Excavation of caries & restoration
 Antimicrobial therapy
EXUDATE TRANSUDATE
 Occlusal therapy
Pathogenesis Increased vascular Increased hydrostatic
 Minor orthodontic movement
permeability pressure
 Provisional splinting (stabilize loose teeth) &
Appearance Purulent, hemorrhagic Clear, serous
prosthesis
Color Yellow to red Straw colored
Specific gravity > 1.018 < 1.018
Evaluation of Response Recheck pocket depth & gingival inflammation
Bacteria HIGH LOW
to Phase I Recheck plaque, calculus, & caries
Cell type Neutrophils (acute) Few lymphocytes &
Phase II Therapy Periodontal therapy, placement of implants
Lymphocytes (chronic) mesothelial cells
(Surgical Phase) Endodontic therapy
Phase III Therapy Final restorations
CHAPTER 32: CLINICAL RISK ASSESSMENT (Restorative Phase) Fixed & removable prosthodontic appliances
Risk Factors Risk Determinants Risk Indicators Risk Markers Evaluation of response to restorative procedures
Tobacco smoking Genetic factors HIV/AIDS Previous hx of Periodontal examination
perio disease Phase IV Therapy Periodic checking
Diabetes Age Osteoporosis (Maintenance Phase)  Plaque & calculus
Bleeding on  Gingival condition (pockets, inflammation)
probing  Occlusion, tooth mobility
Pathogenic Gender Infrequent
bacteria dental visits  Other pathologic changes

Socioeconomic
CHAPTER 35: RATIONALE FOR PERIODONTAL TREATMENT
Microbial tooth status
deposits
*After perio tx, first recall visit should be scheduled at 3 months
Stress
Factors that affect healing
CHAPTER 33: DETERMINATION OF PROGNOSIS LOCAL FACTORS SYSTEMIC FACTORS
Excessive tissue manipulation during tx Age
Two aspects of prognosis Trauma to tissue Generalized infections in px w/
1. Overall prognosis Presence of foreign bodies debilitating diseases
- Concerned w/ dentition as a whole Repetitive tx procedures that disrupt Malnutrition (vit C, proteins, etc)
- Basic determinant of extent of dental tx orderly cellular activity in healing Hormones
2. Individual prognosis process Stress
- Takes into account the prognosis of each tooth in oral cavity
Types of healing after periodontal therapy
Prognosis: prediction of probable cause, duration, outcome of disease 1. REGENERATION
- Natural renewal of structure produced by growth & differentiation
Prognosis Bone loss Patient Furcation Systemic of new cells to form new tissues; MOST IDEAL but most elusive
cooperation involvement factors 2. REPAIR
Excellent None Good None None - Restores continuity of diseased marginal gingiva & reestablishes a
Good Adequate Adequate None Well normal gingival sulcus at the same level on the roots as the base of
controlled preexisting periodontal pocket
Fair (25% CAL) <Adequate Acceptable Grade I Limited - Healing by scar, does not result in gain of gingival attachment or
Poor Moderate Doubtful Grade II Present bone height
(50% CAL) to 3. NEW ATTACHMENT
advance - Embedding of new PDL fibers into new cementum & attachment of
Questionable Advance Grade II & III Present gingival epithelium to tooth surface previously denuded by disease
Hopeless Advance Present 4. EPITHELIAL ADAPTATION
- Close apposition of gingival epithelium to tooth surface w/ no gain
Factors in Determination of Prognosis in height of gingival fiber attachment
Overall Patient age - Pocket is not completely obliterated
Clinical Disease severity PERIODONTAL RECONSTRUCTION – process of regeneration of cells and fibers and
Factors Plaque control remodeling of lost periodontal structures that results in:
Patient compliance - Gain of attachment level
If px is unwilling to comply, dentist can: - Formation of new PDL fibers
1. Refuse to accept px for tx - Level of alveolar bone significantly coronal to that present before tx
2. Extract hopeless teeth
3. Perform scaling & root planning on remaining teeth Final outcome of periodontal pocket healing depends on which cells arrive first:
Systemic & Smoking 1. If oral epithelium = LONG JUNCTIONAL EPITHELIUM
Environment Systemic disease or condition  Most commonly seen result if epithelium proliferates along root
Factors Genetic factors surface before other tissues reach the area
Stress 2. If gingival connective tissue = ADHESION & ROOT RESORPTION
3. If PDL cells = NEW CEMENTUM & PDL, new attachment
Local Factors Plaque and calculus
4. If bone cells = ROOT RESORPTION & ANKYLOSIS
Subgingival restorations
Anatomic Short, tapered roots
Factors Cervical enamel projections (CEPs) CHAPTER 41: TREATMENT OF ACUTE GINGIVAL DISEASE
 Clinical implication: formation of pockets
Root concavities 1. ANUG
Root proximity - Death & sloughing of gingival tissues
Furcation involvement - Punched-out interdental papilla
Prosthetic & Abutment selection Nonvital teeth - Tx: supragingival plaque control, antibiotics (metronidazole), gentle
Restorative Caries Root resorption debridement (px w/HIV), use of chlorhexidine mouth rinse
Factors 2. PERICORONITIS
- Inflammation around crown of partially impacted tooth
Complications of ROOT PROXIMITY - Tx: Oral hygiene – rinse lukewarm water w/ salt
1. Difficulty in cleaning Medication – antibiotics & pain reliever
2. Bone loss Operculectomy – removal of operculum (gum flap)
3. Risk of tooth mobility Extraction – last resort
4. Periodontal pocket formation 3. PRIMARY HERPETIC GINGIVOSTOMATITIS
5. Increased susceptibility to periodontal disease - High fever, headache, malaise, irritability, lymphadenopathy, sore
mouth lesions
 - Affected mucosa is red, edematous w/ numerous vesicles, when Complications
ruptured, leads to shallow ulcers  Tooth loss
- Usually occurs prior to age 10  Dissemination of infection
- Tx: self-limiting (1 week) - Dissemination of bacteria inside tissue during therapy
Viscous lidocaine, Benadryl elixir, antivirals, palliative mouthrinse - Bacterial dissemination through blood stream due to bacteremia
from untreated abscess
CHAPTER 42: TREATMENT OF PERIODONTAL ABSCESS  LUNGS: may act as mechanical barrier where bacteria are trapped
 Can also lead to brain abscess
ODONTOGENIC ABSCESS Tx of periodontal abscess includes 2 stages
 Acute infections that originate from tooth, periodontium 1. Management of acute lesion
 Localized purulent inflammation, pain, swelling - Incision & drainage
- Scaling & root planning
Diagnosis of periodontal abscess - Periodontal surgery
 Palpation: check tenderness, swelling, fluctuation, hardness - Use of diff systematically administered antibiotics
 Percussion: tender to percussion - Tooth extraction
 Sensitivity test 2. Appropriate tx of original/ residual lesion, once emergency situation has
been controlled
 X-ray: dark area

Parameters Periodontal abscess Periapical abscess CHAPTER 43: PHASE I PERIODONTAL THERAPY
History Periodontal disease Caries fracture, tooth wear
Periodontal tx Resto & endo tx Rationale: reduction & elimination of causative & contributing factors by effective
Clinical Vital pulp response (+) Nonresponsive pulp test (-) plaque control through
findings Perio probing releases pus; Narrow probing defect  Complete removal of calculus
wide probing defect  Correction/ replacement of poorly fitting restorations & prosthetic
Swelling is generalized around Swelling is localized often devices
involved tooth. Seldom w/ w/ fistulous opening in  Restoration of carious lesion
fistulous tract apical area  Tx of food impaction areas
Dull pain Throbbing pain  Tx of occlusal trauma
 Extraction of hopeless teeth
Types depending on ORIGIN of infection Steps
1. Gingival – in space between gum & tooth 1. Plaque Control Instruction
2. Periapical – at the root tip as result of untreated infection 2. Removal of supragingival & subgingival calculus
3. Pericoronal – surrounding crown of impacted/ partially erupted tooth 3. Recontouring defective restorations & crowns
4. Periodontal – in periodontal pocket 4. Management of carious lesions
5. Tissue reevaluation
2 types of periodontal abscess - Periodontal tissues require approx. 4 WEEKS TO HEAL
Periodontitis-related abscess Non-periodontitis-related abscess Plaque control
Exacerbation of chronic lesion Impaction of foreign body in gingival  Most important factor in the control of hypersensitive roots
Post-therapy periodontal abscess sulcus or periodontal pocket  Regular removal of microbial plaque & prevent accumulation
Post-antibiotic abscess Root morphology alteration  Masses of plaque develop
- 1st: Proximal surfaces molar & premolar areas
Exacerbation of chronic lesion - 2nd: Proximal surfaces of anterior teeth
 Untreated perio px - 3rd: Facial surfaces of molars & premolars
 Recurrent infection during supportive perio therapy - 4th: Lingual surfaces of anterior teeth

Post-therapy periodontal abscess For px with 5 mm or more attachment loss –> REFER TO A SPECIALIST
Factors to consider:
 Post-scaling perio abscess
1. Extent of disease
- After scaling, small fragments of remaining calculus obstruct pocket
2. Root length
entrance once edema in gingiva has disappeared
3. Hypermobility
 Post-surgery perio abscess
4. Difficulty of scaling & root planning
- Result of incomplete removal of subgingival calculus
5. Restorability and importance of particular teeth for reconstruction
- Presence of foreign bodies such as sutures, regenerative devices,
6. Age of patient
perio packs in periodontal tissues
7. Lack of resolution of inflammation after scaling and planing
Post-antibiotic abscess
 Tx w/ systemic antibiotics w/out subgingival debridement in px w/ CHAPTER 44: PLAQUE CONTROL FOR THE PERIODONTAL PATIENT
advanced periodontitis
 Px who are given broad-spectrum antibiotics Toothbrush
 Occurrence of superinfection & massive inflammation  Varies in size & design w/ bristle grouped in tufts arranged in 2-4 rows
- Superinfection: antibiotics kills normal flora while pathogenic drug-  ADA recommends to replace every 3-4 months or when bristles fray
resistant organisms increase in no. due to absence of competition  2 types of bristle materials
- Natural – hogs
Diagnosis - Artificial – nylon
 Most prominent clinical sign: presence of ovoid elevation of red area
 Other findings: suppuration either from fistula or from gingiva along Toothbrush trauma (abrasion) usually occurs on
lateral side of root of pocket  Canines & premolars on left canines of right-handed persons
 Symptoms: pain, sensitivity to percussion, tenderness, swelling  More wear occurs on maxillary than mandibular teeth & on left half
 Other symptoms: tooth elevation, increased tooth mobility, elevated Effectiveness of toothbrushing is best measured by
body temp, body malaise, regional lymphadenopathy  Amount & location of plaque

Pathogenesis Brushing techniques (pattern)

 Unknown Modified stillman (roll) In gingival recession & root exposure
 Due to occlusion/ trauma to orifice of periodontal pocket Charters ( vibratory) After surgery
 Infection of pocket in soft tissues of pocket wall Bass/ Sulcular technique Most recommended technique for perio px
 Inflammatory infiltrate is formed followed by destruction of CT, (vibratory)
encapsulation of bacterial mass & pus formation Fones (circular) Recommended technique in children
 Due to lowered tissue resistance, virulence, no. of bacteria present Roll (roll) Least effective method
Scrub (horizontal) Most common method of brushing
Microbiology Leonard (vertical)
 Microflora in periodontal abscess is polymicrobial
 Non-motile, gram (-), strict anaerobe, rod-shaped species Dentifrice
 Anaerobic species are Prevotella melaninogenica, Fusobacterium  Aid in cleaning & polishing tooth surfaces
nucleatum, Bacteroides forsythus  Abrasiveness affects enamel only slightly & greater on exposed roots
 Spirochetes mostly Treponema spp.  Dentin is abraded 25x & cementum 35x faster than enamel
 Gram (+), strict anaerobes: Peptostreptococcus micros, Actinomyces spp,  Components:
Bifidobacterium spp. - Abrasives: compose 20% to 40% of dentifrices
 Gram (-), facultative anaerobes: Campylobacter spp, Capnocytophaga silicon oxides, aluminum oxides, granular polyvinyl chlorides
spp., Actinobacillus actinomycetemcomitans - Humectants: retains moisture in dentifrice
 Porphyromonas gingivalis: most virulent among all - Therapeutic agents
Fluoride (1000 – 1100 ppm to achieve caries reduction effect)
Histology Pyrophosphates (anti-calculus agent)
 Initially, neutrophils are found in central area of abscess
 At later stage, a pyogenic membrane, composed of macrophages & How can fluoride strengthen the tooth?
neutrophils is organized  By converting hydroxyapatite crystals to fluorapatite crystals which are
 Normal oral epithelium & lamina propria but inflammatory infiltrate more resistant to acids
resided lateral to pocket epithelium
 CHAPTER 45: SCALING & ROOT PLANING P1 RQS

SCALING: removal of both supragingival & subgingival plaque & calculus Palmar-plantar keratosis, destructive periodontitis, calcification of dura
ROOT PLANING: removal of embedded calculus & rough cementum o Papillon-Lefèvre syndrome

* schedule a SERIES of appointments to scale & root plane a segment or quadrant of When occlusal forces are increased, cancellous bony trabeculae?
teeth at a time o INCREASE in number & thickness
* BEST CRITERION to evaluate success of SRP is NO BLEEDING ON PROBING
Types of conditioned gingival enlargement
Main objective o HORMONAL (pregnancy, puberty)
 To remove etiologic agents from the root surface o NUTRITIONAL (vit C deficiency)
Most difficult to root plane o ALLERGIC
 Trifurcations of maxillary molars o Nonspecific conditioned enlargement

* Working stroke should begin at apical edge of junctional epithelium Localized juvenile periodontitis is ____ type of disease
o DEGENERATIVE
LATERAL WALL: most diseased part of pocket epithelium o Tx: Tetracycline

Periodontal instruments First clinical sign of localized juvenile periodontitis

1. Periodontal probe: measure the depth of pockets o Pathologic migration
2. Explorer: check root surface smoothness after root planning
3. Scalers Recent classification of periodontal disease organized by AAP was introduced in
- Hoe: remove ledges/rings of calculus| beveled at 45°| pull stroke o 1999
 Has 2-point contact w/ tooth & highest stability
- Chisel: proximal surface of anteriors| push motion Rolled, thickened band of gingiva
- File: crush large deposits of calculus| remove overhanging margin o McCall festoons
4. Periodontal endoscope: visualize into subgingival pockets & furcations
5. Cleansing & polishing instruments McCall’s festoons Stillmans cleft
Life preserver shaped enlargements of Apostrophe shaped indentations from
SICKLE SCALERS CURETTES marginal gingiva in canine & premolars & into gingival margin
For supragingival calculus For subgingival calculus Due to trauma from occlusion
Best suited for root planning
Thinnest part of PDL (hourglass shape)
GRACEY CURETTE UNIVERSAL CURETTE o MIDDLE, widens coronally & apically
Area of use Area-specific All areas
Use Work w/ outer edge only Work w/ both edges Length of junctional epithelium
Curvature Curved in 2 planes Curved in 1 plane o 0.25 – 1.35 mm
Blade angle 60-70° offset blade 90° blade not offset
Virulence factors of Aggregatibacter actinomycetemcomitans
Double-ended Gracey curettes o COLLAGENASE
 Gracey 1/2, 3/4, 5/6: anteriors o CYTOTOXIN
 Gracey 7/8, 9/10: buccal & lingual o LEUKOTOXIN
o ENDOTOXIN
 Gracey 11/12, 15/16: mesial
 Gracey 13/14, 17/18: distal
An isolated sessile or pedunculated, tumorlike enlargement
o DISCRETE
Other curettes
 Extended-shank (After Five Curettes)
Immunoglobulin found in saliva
- Allow extension into deeper periodontal pocket
o IgA
 Mini-bladed (Mini Five Curettes)
- For narrow pockets, furcation area, developmental grooves
IgA Found in saliva, tears, colostrum
 Micro Mini Five Curettes
- Smallest of all w/ blades 20% thinner than Mini Five IgD B-cell receptor that stimulates release of IgM
 Langer & Mini-Langer Curettes IgM Main antibody for primary purposes
- Set combining Gracey & Universal curettes IgG Main antibody for secondary responses; found in GCF
Ultrasonic scalers
IgE In allergic reactions, mast cells & basophils release histamine.
 For tenacious calculus | Vibrate at approx. 25 000 cycles per second In antiparasitic reactions, eosinophils release toxic proteins
 Light touch & light pressure, keep the tip parallel to tooth surface &
constantly in motion
 Optimal flow rate of coolant: 14-23 ml/min
 Contraindications: px w/ pacemaker, infectious disease
 Magnetostrictive ultrasonics
- Vibrate in elliptical pattern
 Piezoelectric ultrasonics (20 000-45 000 Hz)
- Vibrate in linear pattern

Ultrasonics have several functions to clean the pocket

1. Lavage – flushes w/ water
2. Cavitation – vacuum bubbles collapse & release energy to flush debris
3. Vibration – mechanically removes deposits & debris
4. Acoustic turbulence – agitation observed in fluids by mechanical vibrations
that disrupts bacterial cell walls

Strokes used during instrumentation: vertical & oblique (frequently used), horizontal
1. Exploratory – light, feeling stroke w/ use of probe & explorers
2. Scaling – short, powerful pull stroke to remove hard deposits
3. Root planning – light intermittent strokes w/ tip parallel to tooth surface
& in constant motion

Blade angulation
 Subgingival insertion: 0° (closed-angle)
 Scaling & root planning: 45°-90° (open-angle)