PERIODONTICS: Recent Episodes
Dr.Mayakha Mariam
PERIODONTIUM
1 Gingiva
2 Attachment apparatus*
a. Pdl
b. Alveolar bone
c. Cementum (has dead cells) acellular cementum
PERIODONTAL TISSUE : (has living cells)
a) Gingiva
b) Periodontal ligament
c) Alveolar bone
PARTS OF GINGIVA
Normal range of gingival sulcus depth is- 2-3mm
Colour of normal gingiva is an interplay between – keratin layer, melanine, blood vessels, epithelial thickness.**
FREE GINGIVA – Also known as unattached / marginal gingiva. From the gingival margin till the free gingival groove / base of the sulcus.
(sulcus is in healthy gums, whereas pocket is in unhealthy / diseased
gums) KERATINIZED
ATTACHED GINGIVA- From free gingival groove (base of the sulcus) to the
mucogingival junction. KERATIINIZED
o Healthy one shows stippling.
o Best views by drying the gingiva.
o Highest width is seen in incisors-
Maxillary : 3.4-4.5
Mand - 3.3-3.9**
o Narrowest seen in molars
Max 1.9mm
Mand 1.8mm
ALVEOLAR MUCOSA
o From mucogingival junc to fold
o Non keratinized
INTERDENTAL GINGIVA
a) Anterior – pyramidal
b) Posterior — col shape
c) Midline diastema — triangular
FREE GINGIVAL GROOVE
MUCOGINGIVAL JUNCTION
BIOLOGICAL WIDTH
Biological width — junctional epithelium + connective tissue = 2 mm***
ORAL MUCOUS MEMBRANE:-
KERATINIZED MUCOSA
Hard palate
Gingiva (70% para & 30% ortho)
NON – KERATINIZED (stratum cornea absent)
Soft palate
Floor of mouth
Alveolar mucosa
Sulcular epithelium
Buccal mucosa
SPECIALISED MUCOSA
Dorsum of tongue
LAYERS OF MUCOSA
EPITHELIUM
LAMINA LUCIDA
BASEMENT MEMBRANE (contains TYPE IV COLLAGEN)
LAMINA DENSA
CONNECTIVE TISSUE
Basement membrane connections to epithelium
Via — desmosoms and hemidesmosomes
LAYERS OF EPITHELIUM
Stratum cornea (surface layer)
Stratum granulosum
Stratum spinosum
Stratum basalis (innermost layer)
Most common epithelium – squamous epithelium
No blood supply
How does epithelium get Nutrition? By diffusion from connective tissue
a) Stratum basalis – highly dividing cells
b) Odland bodies (reserve bodies) – stratum spinosum
c) Stratum granulosm – contains granules that get activated from enzymes and produce keratin for the cornea layer of the epithelium
d) Stratum cornea – keratin deposition
KERATINIZATION
a) Para keratinized (with nuclei) — 70% gingiva
b) Ortho keratinized (devoid nuclei) — 30% gingiva
NON KERATINOCYTES:-
Free nerve cells
Melanocytes
Langerhan cells
CEMENTUM
With age cementum on root end become thicker & irregular.
This increase in the width of cementum is greater in the APICAL & LINGUAL areas.**
COLOUR
o VITAL – YELLOW
o NON – VITAL — GREY OR GREEN
Cementum starts formation from cervical area
Cementum in cervical2/3rd acellular extrinsic fiber,
In coronal acellular intrinsic,
In apical mixed cellular
Acellular – cervical region A x C
Cellular – apex region C x A
Thickness
o Thickest at apex
o Thin at CEJ
Age changes – content increases with age at apex
SHARPEY’S FIBRES – connection from cementum to
alveolar bone. Parallel to bone and parallel to
cementum?
Transseptal fibers are Fibers which completely
embedded in cementation and pass from cementum
of one tooth to the cementum of adjacent tooth.
HYPERCEMENTOSIS
o Low grade periapical infection
o Excessive occlusal force, bruxism
The end of PDL fibers that are embedded in the alveolar bone and cementum are called - Sharpey's
fiber is the dominant type of fibers found in cementum.
Nb: dental tissue similar to bone – DENTINE (histologically) not cementum
BONE
PDL attachment is to : alv. Bone proper or called bundle bone
The crest of INTERDENTAL BONE is said to be parallel to the marginal gingiva
Or you could also say it id parallel to the line drawn from the CEJ of adjacent teeth.
Now if the position of CEJ of the neighboring tooth is variable, then the bone will be angulated towards the line.***
PERIODONTAL LIGAMENT
Cells
o Fibroblast
o Osteoblast
o Cementoblast
o Cell rest of malassez
Lateral periodontal cyst from rest of serres ,while apical periodontal cyst from rest of malassez.
Fibres
o Collagen
o Elastic fibres
Cementoblasts present in pdl
Cell rest of malassez seen commonly at apex
FIBRES OF PDL
COLLAGEN 1,3,7
Most dental tissue type I collagen fibres
o Eg: pdl,alveolar bone, cementum, gingiva, dentin
o They are most abundant
Anchoring fibres are type 7, seen in pdl
Type 3 also seen in pdl
Ageing OF PDL
Elastic fibres increase and cells decreases
Function of pdl
Formative, nutritive, anchorage, cushioning (type 7)
PRINCIPLE GROUP OF PDL FIBRES:
a) Alveolocrestal fibres – prevents extrusion of teeth
b) Horizontal fibres – prevents lateral movement of teeth
c) Oblique fibres – withstands masticatory forces, most abundant
QN. Periodontal ligament fibers in middle third of root is oblique.
d) Apical fibres – absent in young permanent teeth , because of open apex
e) Intraradicular fibres – absent in single rooted teeth
TRANSEPTAL FIBRES
Transseptal fibers are Fibers which completely embedded in cementation and pass from cementation of one tooth to the cementation of adjacent tooth.
the only fibers present in cementum only
Not a pdl group of fibres
Responsible for orthodontic relapse
This fibre is removed in pericision(surgical Rx to prevent ortho relapse)
Dentogingival fibre — the 1st fibre lost during extraction
In pulp :- - Cell rich zone inner most pulp layer contain fibroblast
– Cell free zone rich in capillaries & nerve networks
- Odontoblastic layer contain odontoblast.
PATHOGENESIS
Subgingival plaque is the initiating factor her- the microorganism in it release toxins
Our immune system sends response in the form of white blood cells, cytokines,
prostaglandins, Matrix Metalo Protein (mmp)
Then cause tissue distruction
BLOOD CELLS
All born / formed in bone marrow
RBC
No nucleus
Life span is 120 days
PLATELETS
No nucleus
Below 80,000 — no surgery possible
Below 50,000 — no injury at all
o 50,000 cells/mg — critical count of platelets
WBC
GRANULOCYTES
o NEUTROPHIL
Predominant inflammatory cells in pdl pockets
o BASOPHIL
Allergy
o EOSINOPHIL
Allergy
Least abundant WBC
AGRANULOCYTES
o T
o B – plasm cells
- NEUTROPHIL
a. POLYMORPHO NEUTROPHIL LEUKOCYTES
b. PMNL cells present in acute infection and suppurative cases-pdl abcess , while
chronic lymphocytes.
c. Most abundant WBC in pdl pockets
d. Acute inflammatory cell
e. It is the cell that will become defective in diabetes mellitus
f. Destroys PDL membrane in periodontitis
g. Diabetes condition, weak activity of PMNL
h. Action – phagocytosis eg: macrophage
OTHER NEUTROPHIL DEFECTIVE CONDITIONS:-
i. Neutropenia
j. Granulocytosis
k. Chediak – Higashi syndrome
l. Papillon – Lefevre syndrome
m. Leukocyte adhesion deficiency
n. DM most importantly!
Phagocytosis is the process of engulfing particles.
Chemotaxis is attraction of neutrophils to site of local injury.
2. CELLS OF SPECIFIC RESPONSE
a. T cells
b. B cell or Plasma cells
i. Produce immunoglobins Ig G A M E
ii. Most dominant in perio pockets.
- INNATE IMMUNE CELLS
a. Neutrophils
b. Monocytes
c. Macrophages
d. Mast cells
e. Dentrite cells - LANGERHANS CELL DISEASE
a. Eosinophil infiltrate to pdl — cause early loss of 1° tooth
IMMUNOGLOBINS:- (produced by B lymphocytes) (G-A-M-E)
IgG
— most abundant Ig in blood and in GCF
— passive immunity through placenta
IgA
— all secretion of body contains this eg: saliva (lacrimal)
— passive immunity through milk (colestrum breast milk)
IgM
— first Ig to reach site of infection
IgE
— abundant in allergy and anaphylaxis
MMPS — MATRIX METALO PROTEINASES
Most important proteinase involved in destruction of
periodontal tissue
EG: MMP – 8, MMP – 13
GINGIVAL CREVICULAR FLUID
GCF has most abundance of IgG
CONTAINS
o Components of CT
o Epithelium
o Inflammatory cells
o Serum
o Microbial flora living there in the sulcus
More neutrophils to defend the gingiva.
Most drug concentration
o 1st tetracycline/doxycycline
o 2nd metronidazole
DOXYCYCLINE – similar to tetracycline
QN Tetracycline cause brownish discoloration in all teeth & appear yellowish with UV light
Pedo —20mg
Therapeutic value — 100mg /day (Antibacterial dose)
Sub antimicrobial dose = 20mg — bacteriostatic at GCF
PLAQUE INDUCED GINGIVITIS:-
STAGES ----------- FINDINGS ------------- CELLS INVOLVED
INITIAL GCF ----- 1ST sign of gingivitis --- PMNL or neutrophils
ACUTE ------------ bleeding on probing, definitive sign of gingivitis ---- T - lymphocytes
CHRONIC / ESTABLISHED ----- edematous or fibrous – smokers plasma / B – lymphocytes (7-
21 days)
ADVANCED -------- onset of PDL destruction plasma/B lymphocytes
CONDITIONAL GINGIVITIS :-
All these plaque induced gingivitis
Systemic conditions — pregnancy, DM, Leukemia, puberty
PREGNANCY GINGIVITIS:-
P.intermedia – orange complex
Begins 2nd/3rd
Disappears in 9th month.
PREGNANCY TUMOUR
EPULIS GRAVIDIUM:— kind of Angio-granuloma or pyogenic granuloma (old name) ie bleeding on touch
o Irritation of interdental papilla results in tumor like growth at papilla
Rx
o Scaling best time is 2nd trimester (remove irritant)
NB: safest antibiotic in pregnancy – Amoxycillin *
NON – PLAQUE INDUCED CONDITIONS:
STD
Herpes infection
Candida infection
Hereditary
Food/paste/restoration allergy
Iatrogenic
Traumatic
Foreign body in sulcus
DRUG INDUCED GINGIVAL ENLARGEMENT
Dilantin (phynotoin )don't give with metronidazole
Gingival hyperplasia – drug induced
Gingival enlargement by plaque
Drugs:
o Phenytoin antiepileptic
60% chances – most common cause for DIGE
o Nifedipine
Antihypertensive
Ca-channel blockers
o Cyclosporins – immunosuppresants
20% chances – for organ transplants
Management
o 1st line Rx – scaling and replacement of drugs
o 2nd line Rx – gingivectomy
ANUG /TRENCH MOUTH ULCER/ VINCENT STOMATITIS
o Pseudomembrane
o Acute necrotising ulcer gingivitis
o Organisms causing
Fusiform
Treponima denticola (spirochete) }red complex gram -ve
Borelia Vincenti
o Precipitating factors
Smoking, pericoronitis(infection)
DOWN’S SYNDROME, bed ridden patients
o C/F
Multiple punched out ulcers in Interdental papilla + marginal gingiva
Halitosis
Dull pain
Sometimes fever
Pt. physiological stress, smoker before 1 yr he reported to the clinic, he has necrosis gingival , redness, no attachment loss , treated by mechanical debridement and systemic antimicrobial therapy.**
o If not treated, it will lead to complications
Necrotising ulcerative periodontitis
Cancrum oris / NOMA
Investigations required – dark field microscope
o Rx
Antibiotic if required – amox 500 mg + metro 400 mg
Mouth wash – H2O2 + CHX
1st step in Rx – removal of pseudomembrane
Then medication + mouth wash
Surgery
Extraction of offending tooth done only after 4 weeks ie after ANUG
subsides
Anterior – gingivoplasty shaping of gingiva done as cosmetic
correction of ANUG
PERIODONTITIS
If pt c/o pain on chewing, cold test is normal, but sensitivity otherwise and pain on biting !
o Here pulp is normal acc to pulp test
o Pdl is affected –pain on biting
o Sensitivity is due to the cementum tear in th epdl- through which dentine is exposed and hence the sensitivity (its not the pulp that is affected here so no pulpitis here okay )
WIDENING OF PDL SPACE
Periodontitis
Osteosarcoma
TFO
Scleroderma – bilateral bone loss at angle of mandible also seen
NARROWING OF PDL SPACE
Ankylosis
Hypofunction of tooth
Hypercementosis – seen in Paget’s disease
NB: feature that distinguish periodontits from gingivitis – presence of clinically
detachable attachement loss in periodontits
TRAUMA FROM OCCLUSION
Trauma from occlusion
C/F – mobility of tooth (most common)
No pocket formation – differentiating from periodontitis
TOP +VE ,erythema gingiva
R/F – widening of PDL – most important diagnosis
Type of bone loss seen in 2° TFO is – vertical /angular bone loss
RX
o 1° TFO coronoplasty
o 2° TFO coronoplasty + splinting
PRIMARY TFO
o Excessive occlusive forces that exceeds the adaptive capacity of normal periodontitis
SECONDARY TFO
o Normal occlusive forces that excedes the adaptive capacity of diseased
periodontium
PERIODONTAL POCKET & DIAGNOSIS:-
Patient with healthy gingiva , upon insertion of perio probe , it should stop at --> Most coronal of junctional epithelium
Best measurement of periodontitis by attachment level*,
While BLEEDING ON PROBING
o To detect tissue response to oral hygiene measures – will see less bleeding.
o It is the best to measure the inflammation
Slightly bleeding increase capillary fragility..... This is due to vit k deficiency**
PERIODONTAL POCKET DEPTH – FROM GINGIVAL MARGIN TO BASOE OF THE POCKET
CLINICAL ATTACHMENT LOSS – FROM CEJ TO BASE OF THE POCKET
Pocket depth measurable by probing at 25g force
GINGIVAL RECESSION – FROM CEJ TO GINGIVAL MARGIN
TYPES OF POCKETS
Isolated pockets can be seen in :
o Vertical root fracture,
o Palatogingival groove
Types
o True
o Pseudo
Pseudo pocket
o Seen in gingivitis QN: gingival tumor
o Rx is scaling fibroma
True pocket QN: pericoronitis
o Supra
o Infra
o Suprabony
Rx – gingivectomy
o Infrabony
Base of pocket is below alveolar bone
Attachment of the epithelium is below the crest of alveolar bone.
Divided into 3 types based on the no.of walls present /left
3 walled defect
Rx: regenerative osseous surgery\ treated with which autogenous osseous coagulum that contain: Mixed intraoral cancellous & cortical bone mixed with patient blood**
3 wall defects in adult : mixed cortical and cancellous from his own intraoral mixed with his blood.
good prognosis
2 walled defect / osseous crater (most common)
Rx regenerative osseous surgery or resective osseous surgery
Best graft to treat this is Cancellous freeze dried bone allograft****
1 walled defect resective osseous surgery
poor prognosis
FURCATION INVOLVEMENT :- NABER’S PROBE
QN Nabers probe is Probe used to detect
furcation
GRADE 1
No inter radicular bone loss
Suprabony pocket
Rx – gingivectomy
GRADE II
Also known as CULL – D – SAC
Bone loss present at furcation
No through and through probing
Rx – regenerative and resective osseous surgery
GRADE III
Through and through probing
Rx – hemisection and bicuspidisation QN
Dividing the M into 2 halves + removing a portion of crown and root(hemisection)
Dividing the M into 2 halves and preserving the both
In case of maxilla Rx- root resection(other indication : long standing radiolucency with one of the root of maxillary molar)
— interdental aids – proxa brushes***
GRADE IV
Through and through probing + furcation visible , poor prognosis
LOCALIZED AGGRESSIVE PERIODONTITIS
Organism – A A comitants ( actinomycetem comitants)
C/F – minimal plaque
o Spacing and proclination of anteriors
o Mobility of 1st molar
R/F – arc shaped and mirror shaped bone loss
Pathology – defective neutrophils function
Syndrome – pappilone Lefevre Syndrome
C/F –
LAP
Calcification of duramater
Palmar and plantar keratosis
Drug of choice –
o tetracycline /doxycycline
o Also Ciprofloxacin
o In order to increase the success rate of treating local juvenile periodontitis, we need
to give local antibiotic treatment (pouches n all)**
PERICORONITIS
Pericoronitis by streptococcus gram +ve
SYMPTOMS OF PERICORONITIS
Pain in mouth
Halitosis
Lymph node enlargement
CALCULUS
Calculus induce further periodontal lesion due to:
o More plaque adhere to it
a) SUPRA GINGIVAL CALCULUS:-
a. Mineralized by saliva
b. Easy to detach
c. Calculus differ in their composition
d. Yellow in colour,
e. Usually seen near major salivary glands
b) SUB GINGIVAL CALCULUS
a. Mineralized by GCF
b. Composition is hydroxy apetite crystals
PLAQUE
Main cause in gingivitis + periodontitis
DENTAL PLAQUE COMPOSITION
o SUPRAGINGIVAL-
Aerobic
Starts on the tooth surface as gram +ve then stacks G- on outer surfaces
There are more detached plaques within supragingival plaques than subgingival plaques. *
o SUBGINGIVAL-
Anaerobic
Coronal portion is G+ve and apical most is filled of G-ve bacteria
The detached plaques within subgingival area are the ones that are more toxic to tissue than attached plaques*
CONSTITUENTS :
o Bacteria
o Inorganic material- CALCIUM, SODIUM, PHOSPHORUS & FLUORIDES
o Organic components-polysacharrides, proteins, glycoproteins and lipids, Food-GLUCANS AND FRUCTANS
PLAQUE FORMATION
1. PELLICLE FORMATION –
a. A thin layer of salivary glycoprotiens (ie. Made of saliva, mainly composed of
proteins, not carbohydrates okay!) is formed on the tooth surface within minutes of polishing.
b. They serve as attachment sites for bacteria
-
ADHESION AND ATTACHMENT OF BACTERIA
a. Within minutes
b. Initial adhesion is due to weak reversible VAN DER WAALS forces
c. Firm attachment is due to strong irreversible interactions btwn the molecules on bacteria(adhesion molecules on them) and host pellicle receptors on tooth -
COLONIZATION AND PLAQUE MATURATION
a. Within 24-48hrs
b. Firmly attached primary people provide new receptors for other bacteri through a process called CO-ADHESION
c. As the bacteria grow in number and the biofilm that is formed in the process matures, there is a shift from G+ve to anaerobic G-ve
Materia Alba – unorganised structure DIFFERS FROM
Plaque – organised matrix
Plaque formation in a cleansed tooth begins – after 1 hour** - bacteria starts coming back and building colonies.
24 hours is to compete maturation- the take taken to form plaque
MICROORGANISMS & THE COMPLEXES
Yellow complex – leads to gingivitis and periodontitis (seen in years old patient)
Or purple complex –
o most abundant
o Color complex of calculus in 18 y yellow or purple.**
o fusobacterium nucleatum – bridging micro- organisms
Secondary colonization :RED,GREEN , ORANGE
o Grame -ve facultative anaerobes
o Rods nd filaments
Complexes seen:
o Red complex:
Bleeding on probing +ve
P gingivilis – chronicgeneralised periodontitis
Treponima denticola(spirochetes) – ANUG / ANUP**
T Forsythia
o Green complex
AA comitans – localized aggressive perio (LAP)**
Capnocytophagem – puberty gingivitis(18 year old female)
o Orange complex*
P intermedia – pregnancy gingivitis
Fusiform – ANUG
Campylobacter
o Pregnancy – orange complex
o Smokers = red+orange+tannernella forynthe
PLAQUE AND OHI
Seen in – hard tissue + prosthetic appliance
Can only be removed by Mechanical means, Eg: brushing, flossing
Plaque cannot be removed chemically but only be prevented it will not wash off the
plaque!**
The benefit of rinsing mouth with water is to prevent plque formation by washing off the
food debris.
How will you asses oral hygiene / efficiency of oral hygiene methods prescribed to the
patient? Plaque index** not Calculus index
PLAQUE CONTROL : MECHANICAL
a) Tooth paste
a. Fluoride in toothpaste – 1000pm – above 4 years
b. Anti – tartar agents or anti plaque — Triclosan , Zn compound and pyrophosphate**
b) Tooth brush
a. For pedo small head and long handle
b. 1st powered toothbrush – 1939 *
c) Mouthwash
a. Fluoride mouth wash — above 6 years age**
BRUSHING TECHNIQUE
Best Tq – modified bass technique. Modified Bass tooth brushing is
o the best method because it enter interproximal area &cervical, can be used with
gingival recession, & advice to all types of pt. with or without periodontal
involvement.- UNIVERSAL
o Type of brushing bristles works as active part
Best Tq for pedo — Fones Tq
Best Tq in periodontitis — sulcular Tq
Best Tq in gingival recession — modified stillman’s (side of bristles) used with edematous, inflamed , loss of contour, & progressive recession .
Best Tq after periodontal flap surgery — charters Tq
FLOSS
o Main use of floss.: to destroy interdental plaque matrix*
o Acute injury to tissue during improper flossing - Laceration of interdental papilla*
INTERDENTAL AIDS
Type I embrassure — dental floss of ideal length – 18 inch
Type II embrasure — proxa brush**, also for grade III furcation
Type III embrasure — unified brush
STIM U DENT
Orange coloured stick
Best interdental aid
Help in plaque removal + gingival massage
WATER FLOSSER
Can dilute bacterial toxins only**
INSTRUMENTS
QN Schwartz periotriever To remove broken instrument from gingival sulcus
PROBES
Technique – walking the probe
Force applied – 0.25 N*
Most common – Williams probe
Missing pts on probe – 4 and 6
WHO probe
o Tip diameter of 0.5mm
o Black marking for 3.5 and 5.5 mm
o Used in CPIT index America
o Light weight
Most common for furcation – Nabers probe
Pressure sensitive probe – FOSAT – MILLER PROBE
o RECORDS – CEJ
SCALER
Supra gingival scaling
Short, powerful pull motion
After scaling and root planning, healing happens by long junctional epithelium
TYPES
o Piezoelectric,
o Magnetostrictive*
This scaler is used with elliptical motion **
o Sonic,
o Ultrasonic
CURETTE
Subgingival scaling
Root planning
Long, light pull motion
UNIVERSAL CURRETTE
Two cutting edge
Not area specific
90°
Blade of a pdl instrument should be perpendicular to the shank****
Shank should be parallel to the tooth surface, but blade/cutting edge should be perpendicular ok?
GRACEY CURETTE
One cutting edge
Area specific
70° or offset
#11 #12 mesial surface of posterior
#13 #14 distal surface of posterior
All currettes (gracey/universal) are semi – circular in cross section
Best angulation of activation of any perio instrument - 70° (45°- 90°)
Angulation : the relationship b/w the instrument blade and the tooth surface
The part of instrument that should be parallel during calculus removal is the shank **
PERIO SURGERIES: FLAPS AND GRAFTS
GINGIVECTOMY
After gingivectomy, surface epithelium occurs in 7-14 days
They heal by secondary intention, because there is no tissue approximating.
INDICATIONS FOR GINGIVECTOMY:
o DIGE cases
o To eliminate suprabony pocket
o To remove pseudopocket,* in fibrous enlargement cases
o To eliminate gingival abscesses
o For suprabony pdl abscess !
CONTRA INDICATIONS TO GINGIVECTOMY
o Anterior aesthetic zone.
o If there is defect in the alveolar bone!!!*
o Infrabony pockets
o Osseous reconstruction cases.*** (tricky one)
FLAP SURGERY
A portion of marginal periodontal tissue that has been surgically separated coronally from its underlying support and blood supply and attached apically by a pedicle of supporting vascular connective tissue
Perio surgery miscellaneous
Wait 6 months after perio surgery for maturation of entire periodontium
Periodontitis prognosis – depends on loss of clinical attachment QN
Success of perio Rx – depends on good oral hygiene QN
Best indication for successful perio Rx is --> NO bleeding on probing QN
Indications : accessibility and visualization
Best to access a bony defect
After perio surgery, re-attachment happen as soon as in a week.
evaluation of improved periodontal health: no bleeding on probing/ decreased plaque score attachment level***
FLAP DESIGN
Wide base to ensure adequate blood supply.
Most commonly used flap --> modified Widman flap
Classification if papilla id preserved or not
Conventional technique-splitting the interdental papilla.
Papilla preservation flap used in graft placement in aesthetic zones, to preserve the esthetic look of papilla. So that the “black triangle” is not formed after the perio surgery
Classification acc to placement of flap after surgery
APICALLY DISPLACED FLAP
o It is almost impossible to perform on maxillary lingual area.
o Advantage- it convert unattached gingiva to attached gingiva **
o Indication —
increase width of attached gingiva
No pocket formation
o Disadvantage —
Cannot be used in anterior aesthetic zone
Coz root visibillity
CORONALLY AND LATERALLY DISPLACED FLAP
o Indication – to correct resection
o Disadvantage – pocket formation
Classification according bone exposure after flap / thickness
Full thickness mucoperiosteal flap
Includes surface mucosa (consisting of epithelium, basement membrane, and
connective tissue lamina propria) and the contiguous periosteum of the underlying alveolar bone.
Mucoperiosteal flap
Bone exposure required – osseous surgery, heals by primary intention.
Also used in apically repositioned flaps,
DIASADVANTAGE OF FULL THICKNESS FLAP
o Interdental papilla integrity can be compromised.
ADVANTAGES OF FULL THICKNESS FLAP
o Primary intention healing
Incisions :-
o INTERNAL BEVEL INCISION
First incision
To remove pocket lining
o CREVICULAR INCISION
To use No:12 blade
Only used in perio
o INTERDENTAL INCISION
Partial thickness flap
Includes only the mucosa,
Mucosal flap
Used for mucogingival surgeries, bone exposure is not required here.
GUIDED TISSUE REGENERATION
Placing a membrane to increase the growth of periodontium
Function – to present long junctional epithelium
BONE SWAGGING
Pushing of bone into contact root surface without fracturing bone at its base
(done if edentulous area present near the wall defect)
BONE GRAFTS
A. AUTOGENOUS GRAFTS – AUTOGRAFT
a. From same individual – different donor site
b. Best graft For osseous defect– cancellous graft (since they have pores for blood vessels to pass)*
c. Eg: bone coagulum
d. Best extraoral donor site:
i. Post surface of iliac bone (nerve supply here is iliogastric nerve)
ii. Best graft for condyle of mandible
1. 5th and 6th costocondral graft
2. 6th and 9th rib graft for ridge augmentation
B. ALLOGENOUS GRAFT – HOMOGRAFT
a. From same species – different individual
b. DFDBG – Decalcified Freeze dried Bone Graft
i. For grade 2 furcation involvement
ii. Best for osseous defect is – DECALCIFIED CANCELLOUS FREEZE DRIED BONE GRAFT*
C. XENOGRAFT GRAFT
a. Graft from different species, POVINE GRAFT FOR EG.
D. ALLOPLASTIC GRAFT
a. From inorganic substance
b. Eg: hydroxyapatite
E. Graft from identical twins – ISO GRAFT
F. Condyle : post chondral graft
G. Child for alveolar process : iliac crest
H. 3 wall defects in adult : mixed cortical and cancellous from his own intraoral mixed with his blood.
I. 2 wall defect in perio --> Cancellous freeze dried bone allograft*
GINGIVAL RECESSION & GRAFTS
Caused by tooth brush trauma or plaque deposits
Stages – MILLER’S CLASSIFICATION
CLASS I
Marginal gingival recession (MGR), that does not extend up to mucogingival junction (MGJ)
Rx : coronally / laterally displaced flap or Free gingival graft
CLASS II
MGR that extends up to mucogingival junction with no loss of interdental soft tissue and bone
Rx : CONNECTIVE TISSUE FLAP/GRAFT WITH PARTIAL SPLIT****
NB: difference between I & II GR is width of attached gingiva
CLASS III
o MGR extended up to MGJ with mild to moderate interdental soft tissue + bone loss
o Rx : regenerative or resective osseous surgery
NB: difference between II & III GR is interdental bone loss
CLASS IV
o Severe interdental soft tissue + bone loss
o Poor prognosis
o Rx : extraction
o DEPTH OF ATTACHEMENT LOSS = GINGIVAL RECESSION + SULCULS DEPTH