Periodontology_Bartolucci_one

Enrico G . Bartoluccifirst volume

RIOD OText by

.das

'co Bart

CONTENTSChapter 1THE MECHANISM OF PERIODONTAL DESTRUCTION Bacterial colonization of the crevic e Host defenc e Gingivitis and Periodontiti s Pocket formatio n Gingival Recession formatio n Bone resorptio n Progression of periodontal diseas e

Volume Ipage 1

Chapter 2DIAGNOSIS Classification of Periodontal diseas e Clinical examinatio n Periodontal probing Tooth mobilit y Clinical chartin g Radiographic analysi s Diagnosis page 3 9

Chapter 3TREATMENT PLANNING Initial treatment planning Reexaminatio n Definitive treatment plannin g Non surgical treatment Surgical treatment Maintenance therap y page 9 3

Chapter 4ORAL HYGIENE REHABILITATION Plaque contro l Interrelation between plaque, inflammation and tissue distructio n Instruments and instrumentatio n Supragingival scalin g Subgingival scaling and root planing Antiseptics in periodontal therap y Antibiotics in periodontal therapy Sharpening of the instrument s Reevaluation page 11 1

VI

Chapter 5 PRINCIPLES OF PERIODONTAL SURGERY Classification of surgical procedur e Local anesthesi a Incision s Flaps elevatio n Full and partial thickness flap s Flaps positionin g Suturing tchniques Periodontal dressing s Post-surgical care Instruments sterilizatio n Chapter 6 PERIODONTAL FLAP PROCEDURES Indications and controindication s Access flap Modified Widman flap Apically positioned flap Palatal flap Distal wedg e Smoking and surgical therapy

page 17 1

page 24 3

Chapter 7 RESECTIVE OSSEOUS SURGERY Osseous defects Osteoplasty Ostectomy Surgical instruments Surgical technique s Clinical case

page 29 5

Chapter 8 RESECTIVE GINGIVAL SURGERY Gingival hyperplasi a Gingivectomy Surgical instruments Surgical technique s Clinical cases

page 32 1

VII

CONTENTSChapter 9SURGERY OF FURCATION-INVOLVED TEETH Anatomy Diagnosis Radiographs Classificatio n Treatment of degree I Treatment of degree II Treatment of degree II I

Volume I I

page 345

Chapter 1 0 MUCO -GINGIVAL SURGERY

page 38 5 The function of keratinized and attached gingiv a Gingival recessio n Sullivan and Atkins Classificatio n Miller Classificatio n Surgical instrument s Frenulectomy Pedicle soft tissue grafts Coronally positioned Laterally positioned Bipapillar Free soft tissue graft s Connective tissue graft s

Chapter 1 1 GUIDED TISSUE REGENERATION Biology of GT R Barrier material s Indications Patient selectio n Surgical procedure Treatment of Intrabony defect s GTR in mucogingival surger y Bone grafts and biomaterial s Prognosis of GT R

page 46 9

Chapter 1 2PREPROTESIC SURGERY Biologic width Crown lenthenin g Intraoperatory preparation of the abutment s Preprotesic mucogingival surger y Surgical removal of exostosi s Tuber reductio n Localized ridge augmentatio n page 535

VIII

Chapter 1 3

JUVENILE PERIODONTITIS Localized Juvenile Periodontitis Generalized Juvenile Periodontiti s Batteriology Immune responce Treatment Clinical case s

page 61 1

Chapter 1 4

PERIODONTITIS AND JUVENILE DIABETES Early onset diabetes (type I) and periodontiti s Matur onset diabetes (type II) and periodontiti s Initial treatment Farmacological treatmen t Surgical rational e Surgical treatmen t Clinical case

page 63 1

Chapter 1 5

DESQUAMATIVE CHRONIC GINGIVITIS Clinical symptom s Diagnosis Immunofluorescenc e Pemphigoi d Pemphigus vulgaris Lichen Planu s Hormonal Gingiviti s Osler-Weber-Rendu Syndrom e Therapy of desquamative chronic gingiviti s

page 653

IX

Chapter 1

The mechanis m of periodonta l destruction

THE MECHANISM OF PERIODONTAL DESTRUCTION

The term "periodontal disease" describes a group of diseases initiatin g in and remaining confined to the periodontal tissue . The majority are inflammatory lesions caused by microorganisms accumulating in the pericrevicula r area. Periodontal disease can be divided into : GINGIVITIS : the inflammatory lesion is confined to the gingival tissue . PERIODONTITIS: the inflammatory lesion extends to the tooth support tis sues. Although more than 350 species of bacteria have been isolated in the mouth , human periodontal infections are apparently caused by a specific microbial infection . Less than 5% of microbial flora is, in fact, associated with disease .

--------------------------Epithelial attachment 0 .97 mm Biologic width 2 .04 m i

Ideal gingival morphology and diagrammatic representation : pink colour, scalloped margin , "orange peel" appearance, papillae in the interdental spaces, adequate band of keratinized gingiva . The gingival sulcus is shallow (0 .69 mm), the epithelial attachment is located on the enamel (0 .97 mm) , the connective attachment is inserted in the root cementum (1 .07 mm) . The distance from the bottom of the sulcus to the osseous crest is known as the biological width (2 .04 mm).

3

CHAPTER 1

HEALTHY GINGIVAL CONDITION (PRISTINE GINGIVA)uation in which there is no bacterial plaque and the gingival tissue is histologi cally perfect, without inflammatory infiltration . It can be achieved only unde r experimental conditions and through meticulous oral hygiene . A healthy gingiv a is usually characterized by the presence of modest supragingival plaque which , if removed daily, consists of Gram+ cocci-type flora only .

A healthy gingival condition (known as "pristine gingiva") is an ideal sit -

A small quantity of pericrevicular bacteria l plaque highlighted with a colorant can be seen . This consists of Gram + cocci-type flora .

If removed daily, th e plaque does not have time to proliferate an d reach the sulcus, modifying its qualitative characteristics .

4

!

THE MECHANISM OF PERIODONTAL DESTRUCTIO N

BACTERIAL COLONIZATION OF THE CREVICEIf the bacterial plaque is not constantly removed, it proliferates an d spreads in the gingival sulcus . Two subgingival plaque components have bee n identified : a part adhering to the root of the tooth and a free or fluctuating par t (Listgarten, J .Perio 1976) .PlaqueAerobic Anaerobic Supragingiva l Subgingival - adherent

Anaerobic ! Subgingival - not adheren t

Supragingival plaqu e

Gingival crevice : interior view.

Subgingival plaque.

CHAPTER 1

PERIODONTAL DISEASE

IMMUNE RESPONS E BACTERI A ! Quantity of plaqu e ! Quality of plaqu e ! Plaque retainin g factor ! Bacterial product sPositive Response

!Intact tissue s !Exudation !Phagocytosis ! Immune respons eDeficient Respons e

!PMN defect s ! Hypersensitivity reactions ! Systemic disease s

The presence of specific bacteria in the sulcus is a vital element in determining inflammatory peri odontal diseases (Loe - Theilade - Socransky - Listgarten - Newman) . On the other hand, the presence o f microorganisms is not in itself sufficient to cause the destruction of tooth support tissue. The bacterial flora, in fact, triggers off a complex immune response in the host organism and it is this response which leads to the destruction of periodontal tissues (Taichman - Page - Schroeder - Toto - Levine -Genco) .

Healthy condition .

6


Subgingival plaqu e

Disease condition .

CHAPTER 1

IMMUNE RESPONSE

Impairment of the Sulcular Epitheliu mThe enzymes produced by the subgingival bacterial plaque destroy the mucopolysaccharides in the ground substance between the cells of the junctional epithelium, allowing bacterial components acting as antigens (endotox ins, fragments of bacterial capsule, etc.) to enter the organism . This further increases vessel permeability, enabling the PMNs to leak from th e blood vessels and reach the crevice through the connective tissue and junctional epithelium. During this phase, there is an increase in crevicular fluid .

Bacterial plaque enzyme s Hyaluronidase Collagenas e Proteas e Elastas e

Collecting crevicular fluid with blotting paper .

Crevicular leukocyte s ~--- Crevicular fluid

(From Attsrom & Egelberg 1971 ) During the gingiviti s development period, a gradual increase in th e number of leukocytes i n the crevice and in the flow of crevicular flui d can be observed .

28

35

Days

8

THE MECHANISM OF PERIODONTAL DESTRUCTIO NEpithelial cells in the desquamation phase.

Epithelial cells . Ground substance.

Plaque Enzyme s

Destroy the mucopolysaccharides o f the ground substanc e

Epithelial cell in the desquamatio n phase: note the underlying groun d substance.

9

CHAPTER 1

Polymorphonuclear Leukocytes (PMNs)

Gingival blood vessel : the PMNs can be observed on the inne r surface of the vessel, attracted by the adhesins (ICAM-1 , ELAM-2) . The perivascular tissue is infiltrated . Stimulated by chemoactive substances, the PMNs migrate through th e connective tissue and accumulate in the junctional epithelium and the sulcus, pe'iforming their phagocytic function .

Polymorphonuclear leukocytes in th e non-migratory phase . 10

!


Animal histologic preparation .

Epithelial attachment and connective attachment .

Polymorphonuclear leukocytes in diapedetic phase . 11

Phagocytosis of a bacterium by a polymorphonuclear leukocyte .

CHAPTER 1

GINGIVITISInflammation localized coronally to the transseptal fibres . Probing and X-ray examination do not indicate loss of periodontal support . The PMN accumulation and activity in the pericrevicular zone lead t o the release of various enzymes with a damaging action both on the bacteri a and on the tissue of the host organism . Macrophages and lymphocytes also begin to move towards the site . The former have a phagocytic action, neutralizing the enzymes released by th e PMNs . The latter neutralize an enormous number of antigens .Supragingival plaque Gram+ filamentous rod-shaped microbe s X PMN s

Marginal gingivitis Note the plaque in the pericrevicular zone and the red and edematous gingival margin .

J . Y.CIIO

definition according to

PAGE and SCHROEDER 1976 Histologic perfectio n Normal healthy gingiva Early gingiviti s Stable gingivitis Periodontitis Initial lesion Early lesion Stable lesio n(without bone loss or apica l migration of the epithelium )

HISTOPATHOLOG Y A number of neutrophil s Slight infiltrat e(Mon. Mac) : Lymph. Neutr )

Increase in infiltrat e(appearance of a number of plasma cells)

Considerable increas e in infiltrat e(10-30% plasma cells)

Stable lesio n(with bone loss and apica l migration of the epithelium)

Considerable increas e in infiltrat e (> 50% plasma cells)


Transseptal fibres and diagrammatic representation : tissue infiltration is localized coronally to the transseptal fibres and consists mainly of neutrophils, lymphocytes, macrophages and plasma cells ; the latter make up 10-30% of the infiltrate . Marginal gingivitis in two recessions caused by traumatic toothbrushing after the patien t had stopped brushing in that zone .

CHAPTER 1

PERIODONTITISPresence of inflammatory infiltrate apically to the transseptal fibres , bone reabsorption, periodontal pocket . When the inflammatory infiltrate spreads apically and invades the transseptal fibres, bone begins to be reabsorbed, leaving more space for th e defensive cells which flow to the site in great numbers . Granulation tissue is formed . This is highly vascularized and full of plasm a cells which produce antibodies . In the meantime, while the epithelial layer s of the junctional epithelium are attacked and fragmented, new epithelium grows in a more apical position. All this leads to formation of a periodontal pocket .

The inflammatory infiltrate invades the transseptal fibres . Chronic periodontitis : with reabsoption of bone tissue .

A H 30-40'% A . Naeslundi

. Viscosu s

II Spirochete sX PMN s

Grain- rod-shaped microbes

Plasma cells

J . Y.CIIO

14


Chronic periodontitis

Chronic periodontitis is clinically characterized by the presence of a periodontal pocket (>3 mm .) When the disease is in the active phase, bleeding on probing or spontaneous bleeding is observe d

Formation of a periodontal pocket: the inflammatory infiltrate spreads apically, invading th e transseptal fibres . Bone is reabsorbed, granulation tissue is formed and new epithelium grows in c more apical positio n

15

CHAPTER 1

Formation of Gingival Recession

In the gingival morphotype illustrated characterized by thin tissu e (vestibular-lingual section), gingival recession may easily be formed as a resul t of total gingival tissue destruction caused either by traumatic toothbrushing o r by bacterial plaque . Gingival recession is always accompanied by bone tissue reabsorption .

Bacterial plaque recession

7F


Traumatic toothbrushing recessio n

Brushing traumatically or with an unsuitable brush (too hard or without rounded points) may cause surface abrasion of the gingival epithelium. In a thin gingival morphotype, persistent trauma or the onset of inflammation may lead to gingival recession .

l7

!CHAPTER 1

CELLULAR INFILTRATEPeriodontitis is accompanied by a considerable increase in cellula r infiltrate consisting mainly of lymphocytes, macrophages and plasma cells . The latter make up more than 50% of the infiltrate .

Lymphocyte sThese are white series cells deriving from lymph nodes (B lymphocytes) and the thymus (T lymphocytes) and play an extremely important rol e in the defence mechanism . One particular form of lymphocyte is the helper lymphocyte whose role is t o assist lymphocyte reproduction . Other types of lymphocyte include : killer lymphocytes responsible for elimi nating extraneous cells (cancer cells, for example) and suppressor lymphocytes which suppress the immune reaction when no longer required . Lymphocytes produce a wide variety of substances such as interferon, a growth factor, interleukines and lymphokines .

MACROPHAGE {Activates the B-cell s Memory-cells- Killer-cells Mitogenic for T-cells .

nThymus

Bone

a

marro w Memory cell s T-suppressors

*Killer cell s Spleen

Lymph nodes ..B lymphocytes -0-B and T lymphocyte s Thymus --!T lymphocytes

T-helpers

ONk/ IgA -v Secretor y Ig D - ~ Ig G Ig M I IgE.-Mast cells

nBursa equivalents

PLASMA CELL

18

THE MECHANISM OF PERIODONTAL DESTRUCTIO NB Lymphocyte

Homologous receptor s T! a few hundre d B! 50 .000 - 150 .000

T lymphocyte

In periodontitis, the majority of lymphocytes present are B lymphocytes .

19

CHAPTER 1

MacrophagesThese monocyte-derived cells have varied and extremely important functions, acting as phagocytes, B lymphocyte activators and T lymphocyte mitogen s (lymphokine production) . The phagocytic function is important in the initial stages of the disease (gingivitis) as the macrophages phagocyte the hydrolytic enzymes produced by th e PMNs, reducing cell damage . They also phagocyte the altered cells of the connective tissue . Macrophages are also important in the advanced phase of the disease (peri odontitis) when they interact with the B lymphocytes, thus maintaining the latter in a strategic position to identify and neutralise large quantities of antigens . However, they are above all important for the interaction with the lymphocyte Thelper that stimulates secretion of interleukin-1 (IL1) : this helps production o f interleukin-2 (IL2) which stimulates the T-helpers and T-killers to reproduce, trig gering the lymphokine cascade .

Macrophages

20


In the initial stages of the disease , the macrophages play a vital rol e in reducing the destructive poten tial of the hydrolytic PMN enzymes.

Phagocytosis of the connective tissue .

Connective fibre during digestion .

CHAPTER 1

Lymphocyte activatio nLymphocytes may be activated by an antigen-antibody reaction wit h the presence or otherwise of the complement. Alternatively, with the coopera tion of a T-helper, they may enter the transformation and blastogenesis phase . During this phase, the lymphocytes produce lymphokines, non-immunoglobu linic substances with numerous extremely important activation and inhibitio n functions . Antigens

r!

Blast cellT lymphocyteactivatio n

Lymphokin e

A) Antigen activation

B) Transformatio n

C) Blastogenesis Lymphokine s MIF : Macrophage inhibition factor MAF : Macrophage activation facto r OAF : Osteoclastic activation facto r CF : Chemotactic factor LT : Lymphotoxi n

B lymphocyt e activatio n

Lymphokine

A) Antigen activation

B) Transformatio n

C) Blastogenesis

22


Macrophage-Lymphocyte interactio nIn the most advanced phases of the disease (stable gingivitis - peri odontitis), the macrophages and lymphocytes interact, strengthening thei r respective defensive functions and giving rise to the lymphokine cascad e which greatly amplifies the immune response .

Periodontitis

The macrophages maintain the antigens in an accessible posi tio n B lymphocytes A number of lympho cytes can be observed approaching a non migratory macvophage.

23

CHAPTER 1

Lymphokine cascad e1) A macrophage phagocytes a microorganism 2-3) The M-T-helper complex secretes IL-1 (interleukin-1) . This activates Thelpers to produce IL-2 (interleukin-2) which stimulates the reproduc tion of T-helpers and T-killers . 4-5) T-helpers produce B-cell growth factor which stimulates the cells t o reproduce and produce antibodies . 6) T-helpers produce gamma-interferon * activates killer T-cell s * stimulates B-cell s * stimulates the M-T complex

Microorganism

acrophage phagocyte s microorganism 2) Activation of the T-helper an d bonding with a macrophag e

THE LYMPHOKINE CASCADE

6) Interferon

THE MECHANISM OF PERIODONTAL DESTRUCTIONRosette formation : macrophage surrounde d by lymphocytes (which appear) adhering t o the surface and about to be phagocytized. When the lymphocytes have concluded thei r task, they are, in fact, eliminated .

25

CHAPTER 1

BONE REABSORPTIONBone reabsorption is a complex phenomenon occurring during periodontitis an d caused by an inflammatory process triggered by bacterial plaque . There are two main pathogenic mechanisms :

A) Osteoclastic activatio nThe T-lymphocytes produce OAF lymphokine (Osteoclastic Activating Factor) , responsible for activating the osteoclasts which reabsorb the minerals from the bone an d return them to the blood circulation .

The activated osteoclasts cause bone reabsorption .9ti


B) Liberation of prostaglandins (PGE2)The cell membrane damage is caused by activation of the arachidonic acid cascade with activation of PMN chemotaxis and liberation o f prostaglandins, responsible for bone reabsorption.

Alternative pathway Bacterial plaque Bacterial endotoxi n Proteolytic enzyme s

Liberation of C3A-05 AThe bacterial plaque is responsible for bone reabsorption .

Bone reabsorption has led to exposure of the coronal third of the roo t surface.

Edema Chemotaxis Cell damage

PGE2

27

CHAPTER 1

Plasma cellsPlasma cells are large white series cells deriving from the bone mar row and numerous in chronic periodontal lesions (accounting for more tha n 50% of the inflammatory infiltrate) . The plasma cells produce immunoglobulin specific antibodies (IgA) whic h enter the sulcus together with the crevicular fluid through fenestrations in th e sulcular epithelium .

Chronic adul t periodontitis .

Presence of periodontal pocket .

28


Plasma cells make up more than 50% of th e tissue infiltrate and are also present in the crevicular fluid.

Activation of a plasma cell wit h production of immunoglobuli n antibodies . Plasma cell Antibodies

CHAPTER 1

Mast cellsIn the most severe forms of periodontitis where inflammation is pre dominant, together with spontaneous bleeding, local pain and rapid progression of lesions, cells with particular functions appear : mast cells . These cells are numerically proportional to the severity of the periodontal dis ease. Mast cells are activated via a sensitization mechanism, reacting with a n immunoglobulin (IgE) . Subsequently they fix an antigen and degranulatio n thus commences with production of histamine, heparin and serotonin . These substances are responsible for local capillary vasodilatation causing hyperemia and localized pain .

Severe form of periodontitis.

Mast cell.

The number of mast cells in the inflammator y tissues is proportional to the severity of th e periodontal disease .Zacharicson, J . Perio Res ., 1986

Qn


Vasodilatatio n T Permeability

Degranulation of th e mast cells .

A) Sensitization

B) Antigen fixation

C) Degranulatio nHistamin e Heparin Serotonin

Mast cell .z 0

0 x

W cn

Mast cell in degranulation phase.

CHAPTER 1

Pathogenesis of periodontal diseaseDiagram of the succession of events in the development of periodontitis . This condition, if not interrupted, tends to be self perpetuating with a "poussez" evolution.

FORMATION OF PLAQUE IN THE SULCUS Production of enzymes Destruction of ground substance

Passage of plaqu e products int o the gingiv a

Onset o f inflammation

' I Spreading of inflammation to deep tissue s through the vascular system

Destructio n of gingival collagen Proliferation of junctional epithelium

Formatio n of granulation tissue

THE MECHANISM OF PERIODONTAL DESTRUCTION

Immune responsePossible immune mechanism activated by the presence of bacteria l plaque in the sulcus .

BACTERIAL PLAQUE

COMPLEMENT PMN CHEMIOTAXI S MACROPHAGE ACTIVATIO N PROSTAGLANDINS B-T LYMPHOCYTE S DESTRUCTION OF FIBROBLAST S

Macrophage

CELLS INVOLVED IN TH E IMMUNE RESPONS E PMNs LYMPHOCYTE S MACROPHAGE S

33

!

CHAPTER 1

Evolution of periodontal diseas ePeriodontal diseases usually proceed with periods of exacerbation an d periods of remission . During active periods, the connective attachment syste m is destroyed and bone reabsorption takes place .

Progression of the periodonta l lesion

Motility

Activity of the disease

In this site, the attachment system has been lost and Subgingival bacterial plaque triggers destruction of the attachment system and bone tissue . bone tissue has been reabsorbed .

THE MECHANISM OF PERIODONTAL DESTRUCTIO NThe infection responsible for destruction of periodontal tissue occur s in one or more sites and may last a variable period of time. The phenomeno n may die down spontaneously or as a result of treatment . The host-parasite balance will remain stable until the same infection is re-acti vated or a new one commences .

Periodontal diseases

Gingiviti s

Periodontiti s

JuvenilePre-pubera l Localized (LIP) Generalized (JP)

Early onset (EOP )Chronic Severe (SAP ) Refractory (REF)

35

CHAPTER 1

Periodontitis can be defined as a group of diseases associated with a subgingival microbial flora varying considerably in quantity and quality fro m disease to disease . Strong evidence now exists to suggest that Actinobacillu s Actinomicetemcomitans and Porphiromonas Gingivalis are exogenous form s and represent the infective agents of periodontal diseases .

Bacterial species associated with periodontitisMicrobial species Clinical forms of periodontitis

LJPA. Actinomicetemcomitans P. Gingivalis P. Intermedi a B. Forsythus Fusobacterium spp Peptostreptococcus spp Campylobacter rectus Spirochetes

JP

EOP SAP REF

(Loesche et al . 1985; Slots and Rams 1990; Van Steenberger 1991)

Bone reabsorption in chronic adult periodontitis .


Gingival recession caused by bacterial plaque.

CONCLUSION S it must be controlled. An alternative would be to amplify the immune response aime d at combating them . However, at present this latter possibilit y does not seem feasible . Treatment thus has two main objectives : 1) Control of the periodontopatic microbial flora . 2) Surgical reconstruction of an anatomy which facilitate s maintenance of periodontal health .To eradicate periodontal infection, the microorganisms causin g

37

Chapter 2

Disease diagnosis

DISEASE DIAGNOSI S

Diagnosing a specific disease is often a complex process involvin g thorough clinical, instrumental and X-ray assessment of the patient . This chapter will describe the method used to identify the presence and exten t of periodontal disease. The etiology of periodontal diseases is varied and complex and for convenience the diseases are therefore divided into inflammatory and non-inflammatory conditions .

Classification of periodontal diseas eChronic gingiviti s Allergic gingivitis Eruptive gingiviti s Herpetic gingivitis Ulcerous-necrotic gingiviti s

Gingival

INFLAMMATORY CONDITIONSPeriodontal

Prepuberal periodontitis Juvenile periodontitis Early onset periodontitis Chronic adult periodontiti s Refractory periodontitis Gingival recession due to plaqu e

Gingival

NON-INFLAMMATORY CONDITIONSPeriodontal

Puberal gingiviti s Pregnancy gingiviti s Vitamin C deficit gingiviti s Desquamative gingiviti s Leukemia-associated gingivitis Drug-related hyperplasia Hereditary hyperplasi a Caused by occlusal traum a Atrophy caused by lack of use Gingival recession caused b y toothbrushing

41

CHAPTER 2

EXAMINATION OF THE PATIENT

apparatus possibly involved in periodontal disease or influencing the definition of pharmaceutical or surgical treatment, a questionnaire is submitted t o the patient .

Medical and stomatologic histor y To obtain a standardized assessment of the condition of organs o r

Medical historyHave you ever had : Hepatitis or liver problems Prolonged bleeding Rh ('/1 ma tie fever Heart murmur High/low pressure Chest/shoulder pain Glaucoma Contact lenses Kidney problem s Diabetes TB Emphysema/asthm a Ulcer Cancer Epileps y Venereal disease Anaemi a Blisters in the mouth Ulcers in the mouth If yes, specify If you are female : Are you pregnant ? Are you taking contraceptives ? Are you taking other hormonal drugs? _ Are you in the menopause ? Do you suffer from allergies ? To what ? ve drug s Have you ever suffere d adverse reactions to drugs ? Which ones ? Do you grind you r teeth at night ? Do you have bad breath ? Is your mouth painfu l when you wake ? Othe rYES N O

Are you taking or have you taken drugs such as: Antibiotics Aspirin Anticoagulant s Cortisone

YES N O

What kind of toothbrus h

YE S N O

Do you use a water pick ? Do your gums bleed ? Do you breath wit h

iene treatment ? dd any other information you think might be importan t

Example of questionnaire to be submitted to the patient for correct compilation of medical history .

!

DISEASE DIAGNOSI S

Clinical examinatio nThe aim of the clinical examination is to identify signs of possible disease . The signs to look for include : colour, shape, consistency and height of the gingiva and other oral structures such as the lips, mucosa, tongue, oropharynx , floor of the mouth, hard palate and soft palate . It is important to examine both the general aspect of these structures and als o any possible localized alteration . The gingiva are assessed on the basis of the following parameters :

PARAMETER S

Colour

Contours

Marginal

Festoonea

Altered festonatio n Edematous - Fibrous Fibroedematous Flat - Glossy - Stippling disappears More coronal - More apica l

junction

43

CHAPTER 2

E

-Wit!

Normal gingiv a The healthy gingiva is pink, the papillary con tour is flat and the marginal contour is festooned . The gingival margin is located at th e cemento-enamel junction . The interincisal papilla have a characteristi c "stippled" appearance . Probing identifies the presence of a gingival sulcus about 1 .5 mm deep .

Stippling Diagrammatic representation of the epitheliu m (E) with the collagen fibres (C) and anchorag e fibrils (A) . The latter give the epithelial surface of a health y gingiva a stippled appearance . If edema is present, the stippling disappears .

Position of the gingiv a In the case illustrated, the gingival margin is located apicall y to the cemento-enamel junction . This is probably caused by incorrect toothbrushing with a dam aging toothbrush .

Toothbrushing abrasio n A small toothbrushing abrasio n can be observed on the gingiva l margin vestibularly to the centra l incisor.

!

DISEASE DIAGNOSIS

Colour of the gingiv a The colour of the marginal gingiva is altered, becoming deep red, symptomatic of the presence of marginal gingivitis .

Multiple recession Bone dehiscenc e In the illustrated case, the recessions of the vestibular gingiva Recession is always accompanied are caused by two factors : thin and keratinized gingiva and by destruction of the attachmen t bacterial plaque. apparatus and bone tissue supporting the tooth.

45

CHAPTER 2

Shape of the gingiv a In the case illustrated, accumulation of bacterial plaque and chronic irritatio n have caused an inflammatory condition known as hyperplastic gingivitis . Note the bulbous appearance of the interdental papillae, the altered festonatio n of the gingival margin and the colour, now deep red becoming cyanotic .

Gingival hyperplasia caused by breathing with the mouth ope n Night-time breathing with the mouth open in adenoiditis may lead to inflammation and localized gingival hyperplasia due to chronic irritation as in the cas e illustrated. Note the change in colour and the modified shape of the gingiva i n the vestibular sector of the maxillary arch .

!!!

DISEASE DIAGNOSIS

it+ Fibrom a This fibroma affecting the mucosa of the cheek i s of irritatative-masticatory origin . Histologic examination after removal reveale d increased keratinization of the epithelial tissue , while the other malpighian layers were normal . : :1\2

nI~ORi~0~6ipiiV

i

tZ

N' ~j,4

etit lry,ryAgll

tey .

uJes,.1 i *ear

~. a

ca

J

#~ Se' f

,f 41 ' i

. 1.

v '

rA "

.j. . . ;47

.j~\

i t

CHAPTER 2

Drug-induced hyperplasi a In these two cases, gingival hyperplasia has been induced by the assumption of drugs to treat a systemic disease. The top image shows an accumulation of bacterial plaque, aggravating the hyperplasia . In the absence of periodontitis, the pocke t explored by probing is a pseudopocket (caused by coronal growth of the gingiva and not attachmen t loss).

Vitamin C deficiency Ascorbic acid (vitamin C) deficiency cause s scurvy, a systemic disease characterized b y accentuated weakness, anaemia, capillary dis ease and a tendency for both the skin an d mucosa (gingiva) to bleed, with the appearanc e of petechiae on the limbs .

49

CHAPTER 2

Instrumental examinatio n A ) Periodontal probingThe periodontal probe enables the presence and severity of a periodontal lesion to be verified simply and immediately . A periodontal probe can be used to reveal : 1. 2. 3. 4. 5. 6. 7. The depth of a periodontal pocke t The depth of a pseudopocke t The height of the keratinized gingiv a The height of the attached gingiv a The quantity of attachment loss The depth and width of recession The presence or absence of bleeding .

Periodontal prob e University of Michigan .

Periodontal probing The sulcus is about 3 mm deep.

Periodontal prob e color probe 11mm

(CP11).

DISEASE DIAGNOSI S

The periodontal probe is inserted into the gingival sulcus (the virtua l space existing between the gingiva and the tooth enamel) . The penetration depth depends on various factors : the shape and diameter o f the probe, the insertion force, tissue resistance, the convexity of the crow n and the insertion direction . Histologic research by Schroeder and Listgarten (1971) demonstrated that periodontal probing may not correspond to the actual depth of the sulcus o r periodontal pocket . Later, Listgarten (1976) demonstrated that, after crossing the epithelial attach ment, the point of a probe consistently penetrates at least 0 .3 mm further int o the more coronal part of a healthy connective attachment . On the basis o f these studies, it has been established that the sulcus or histologic pocket doe s not coincide with the clinical pocket . The histologic depth of a pocket is determined by the distance between th e gingival margin and the bottom of the pocket (corresponding to the corona l margin of the junctional epithelium) . The clinical depth (or probing depth) of a pocket corresponds to the penetration depth of the probe into the pocket .

POCKET > 3 mm.

Periodontal pocke t Note the periodontal pocket (4 mm) and the tissu e edema, indicated by the mark (fovea) left by th e probe on the gingiva . 51

The periodontal pocke t is about 6 mm deep.

CHAPTER 2

A pathological condition is known to cause proliferation of the junctional epithelium . This grows apically, replacing the connective attachmen t destroyed by the disease, interposing between the gingival connective tissu e and the root surface, where it attaches itself . The epithelium may reach a length of 4-5 mm and in these cases is known a s long junctional epithelium (Listgarten - Rosenberg, 1979) . In the presence of inflammation, the probing depth will differ from the histo logic pocket depth . The probe penetrates the inflamed epithelial attachmen t easily, coming to a halt in the coronal part of the healthy connective attach ment . Poison (1990) demonstrated that the point of the probe is stopped by the firs t healthy connective fibres still attached to the root cementum .

Long junctiona l epitheliu m Note the proliferation of the junctional epithelium as far as the roo t cementum .

Junctional epitheliu m Diagrammatic representation of the structure of the junctional epitheliu m adhering to the surface of the enamel via hemidesmosomes . In drawing 1, the yellow line corresponds to the basal lamina and denta l cuticle . In drawing 2, note the cemento-enamel junction with a small are a of afibrillar cementum (A), the beginning of the root cementum (C), the dentine (D) and the enamel (E) .

Probing dept h In the presence of inflammation, the probe penetrates as far as the first health y fibres of the connective attachment apparatus .

DISEASE DIAGNOSIS Force applied to the prob eIn 1967, Glavind and Loe demonstrated that application of a non-standardized force resulted in variable probing depths, both in health and inflame d tissues. Using calibrated pressure periodontal probes, Van der Velden and De Vrie s (1978), found that the optimum pressure to apply to a round pointed 0 .36 mm diameter probe was 0 .75 Newtons (one pound = 0 .0098 Newtons = about 25 grams) . Using this type of probe and this constant pressure, pocket depth measurements were reproducible, even when performed by different operators .

Bleeding on probing

In 1979, Van der Velden introduced the concept of "bleeding on probing " in diagnosing between a healthy and a diseased condition . 53

CHAPTER 2 Probing techniqueThe dental probe should be held as though it were a pen . Keeping it parallel to the long axis of the tooth, it should be delicately inserted betwee n the free gingival margin and the tooth . Three readings are taken for each tooth : distal, intermediate and mesial . Particularly in the case of molars with a convex clinical corona, for the mesia l and distal readings, the instrument should be held at an angle of about 25 (Ziegler - Allen 1980) .

When probing the vestibular su'iface, the probe should be held parallel to the long axis of the tooth . Probe angle

TPS Probe Vivacare " Calibrated pressure probe .

In the mesial and distal interproximal spaces, the probe should be held at an angle of 25 .

DISEASE DIAGNOSIS

After delicately inserting the instrument into the sulcus or pocket, a pressure of 25 grams is exerted until the first resistance is encountered. It is important to verify that this resistance is not caused by solid concretion (cal culus) on the root surface of the tooth . Once the probing depth has been reached, the instrument should be slightl y raised and moved around the circumference of the tooth (walking the probe) .

Incorrec t

The presence of subgingival calculus may stop the probe and lead to a faulty reading of pocket depth .

Walking the probe When the probing depth is reached, the probe should be slightly raised and moved around the circum ference of the tooth.

55

CHAPTER 2

Probing sitesFor each tooth, three vestibular and three palatal or lingual readings should be taken : distal (1), intermediate (2) and mesial (3) .

Deep periodontal pocket (>7 mm .) in the vestibular surface of the central incisor . Note the accompanying gingival recession and presence of subgingival calculus .

!!!!"!

DISEASE DIAGNOSI S

The probings (in millimetres) for each tooth should include vestibular and lingual readings, starting from the maxillary arch and proceeding in succession from no . 18 to no . 28 . The examination then continues with th e mandibular arch, starting with vestibular probing in succession from no . 38 to no . 48, followed by lingual probing first of the mandibular arch from no . 48 to no . 38 and then the maxillary arch from no . 28 to no . 18 .

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57

CHAPTER 2

B) MeasurementsMeasuring the keratinized gingiv aThe periodontal probe is indispensable for measuring the quantity o f keratinized and attached gingiva . To assess the keratinized gingiva, the mucogingival junction must first be iden tified. The periodontal probe is then used vertically to measure the distanc e between the free gingival margin and the mucogingival junction .

A periodontal prob e (CP11) is used to identify the mucogingival junction. The height of the keratinized gingiv a from the free gingival margin to the mucogingival junction is then measured .

DISEASE DIAGNOSI S

Measuring the attached gingiv aThe attached gingiva is the part of the keratinized gingiva attached to the tooth (epithelial attachment + connective attachment) and bone tissue . To verify the quantity of attached gingiva, the height of the keratinized gingiv a and the depth of the sulcus must be measured and the latter subtracted fro m the former.

A periodontal prob e (CP11) is used to measure the height of th e keratinized gingiva and depth of the sulcus . The latter is subtracted from the former to calculate the quantity of attached gingiva .

59

CHAPTER 2 Measuring gingival recessionThe term gingival recession describes the apical migration of the gingival margin with respect to the cemento-enamel junction . This phenomenon may be caused by bacterial plaque or damaging toothbrushing .Bacterial plaqu e derived recession .

Toothbrushing derived recession.

DISEASE DIAGNOSI S

Gingival recession is measured using a periodontal probe. The length (A-B) is the distance between the cemento-enamel junction an d the apical part of the exposed root . The width (C-D) is measured in correspondence with the cemento-ename l junction.

61

CHAPTER 2 Measuring furcation involvementFurcation involvement is diagnosed by probing with a special periodontal probe, the Nabers 2N .

Classification Degree Furcation involvemen tHorizontal loss of bone tissue not exceeding 2-3 rum of the depth o f the furcation .

A: Horizontal loss of bone tissue for less than half the furcation . B: Horizontal loss of bone tissue for more than half the furcation . C: Almost complete horizontal loss of bone tissue . A small diaphragm remains .

Total loss of interradicular bon e (otherwise known as a through-and-through furcation) .

Nabers 2N probe .

C)

DISEASE DIAGNOSI S

Degree I

Horizontal loss of bone tissue no t exceeding 2-3 mm of the depth of the furcation .

63

CHAPTER 2

Degree II

Type A Horizontal loss of bon e tissue for less than half the furcation.

Type B Horizontal loss of bone tissue for more than half the furcation.

Type C Almost complete hori zontal loss of bone tissue . A small diaphragm remains .

DISEASE DIAGNOSI S

Degree III

Total loss of interradicular bone . Degree III is also known as a "through-and-through" furcation .

65

CHAPTER 2

C) Tooth mobilityTooth mobility is caused by absorption of alveolar bone as a result o f bacterial plaque or occlusion damage . Tooth mobility is an early symptom of occlusion damage and a late sympto m of periodontitis. It is assessed using the ends of two instruments .

Classificatio nDegree 0 Degree 1 Degree 2 Degree 3

Absent

Tooth mobility in a vestibular-lingual direction by up to 1 m m

Tooth mobility in a vestibular-lingual direction by more than 1 m m Tooth mobility in a vestibular-lingual direction by more than 1 m m and/or depressibility in the alveolus .

Classification criteria of dental mobility .

!

DISEASE DIAGNOSIS

Tooth mobility Presence of disease in progress (Occlusion trauma) (Inflammatory) Poor bone support .Stabilized : Ingravescent:

Occlusion traum aBone reabsorption caused by excessive occlusal accompanied by attachment loss . (Glossary of Periodontic terms . American Academy of Periodontology, 1986 )

Orthodontic traumaMono-directional forces exerted on individual teeth produce pressure and tension fields within the periodontal space . As a result, the tooth becomes progressively more mobile and starts migrating in the direction of th e force . When the tooth leaves the influence of the trauma, the periodontium is reorganized and the tooth becomes stable in its new position.

ressure zone Tightened ligament . Thrombosis, hemorrhage, collagen destruction . Bone and cementum reabsorption .67

Tension zon e 0 Stretched ligament. 0 Bone apposition. Dilated vessels . 0 Torn periodontal fibres .

CHAPTER 2 Jiggling traumaThe combined effect of pressure and tension forces in the periodontal tissues causes thrombosis, hemorrhage, collagen destruction and reabsorption of bone and cementum . This leads to progressive enlargement of the periodontal space and subsequent hypermobility of the tooth . Subsequently, the larger periodontal space neutralizes the trauma and there fore blocks bone reabsorption .

Occlusion trauma alon e When the periodontal space i s enlarged, the trauma is neutralize d and bone reabsorption is halted .

Various experiments carried out first on animals then on humans have demonstrated that neither mono-directional orthodontic forces nor jiggling force s cause pockets or periodontal attachment loss in a healthy periodontium . However, if the trauma is accompanied by bacterial plaque-derived periodontal disease, the disease progresses more rapidly . From a clinical point of view , the fundamental moment in treating inflammatory periodontal diseas e involves elimination of the bacterial plaque as this will halt periodontal tissu e destruction, even in the presence of trauma from occlusion .

Occlusion trauma + inflammatio n When the trauma is accompanie d by an infection, the disease progresses more rapidly.

Junctional epitheliu m in the migratory phase Occlusio n trauma-derived bone lesio n

0

DISEASE DIAGNOSI S

CLINICAL CAS EThe clinical case illustrates a typical diagnostic and therefore therapeutic error . A young patient (male, aged 15) presented mobility of the left upper latera l incisor and a diastema between the central and lateral incisors . The initial diagnosis was : occlusion damage and night grinding of the teeth for psychological reasons . Dental treatment consisted of selective grinding and construction of a resi n "bite" to wear at night . The youth (with divorced parents) was also referred t o a psychologist. After a year of psychotherapy, "bite" and selective grinding, the patient - still a long way from being cured - was referred for a second opinion . The diagnosis was : juvenile periodontitis . The correct diagnosis was followed by suitable and successful treatment (se e chapter 13) .

The reddened and collapsed interdenta l papilla is a symptom of reabsorption of the underlying bone.

69

!"!

CHAPTER 2

The clinical recordclinical and instrumental data and the patient's medical histor y should be gathered together in a clinical record .

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DISEASE DIAGNOSI S

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CHAPTER 2

X-ray analysisIf well performed, a set of intraoral and periapical X-ray images pro vide valuable information on the condition of the patient's bone tissue . 1. Height of alveolar bone . 2. Characteristics of the bone trabeculae . 3. Localized areas of bone destruction. 4. Bone loss from the furcations . 5. Extent of the periodontal space . 6. Crown - root relationship .

Note the difference between the photographic details in the X-ray and in the orthopantomography .

DISEASE DIAGNOSIS 7. Shape and length of roots . 8. Periapical lesions. 9. Decay, quality of restoration work, presence of root calculus . 10. Identification of the maxillary sinus . 11. Missing teeth, supernumerary teeth, impacted teeth . It should be remembered that a radiographic image is a two-dimensional representation of three-dimensional structures . To reach a correct diagnosis, the radiographic status should always be correlated with a thoroug h clinical examination and correct periodontal probing .

Note the difference between the photographic details in the X-ray and in the orthopantomography .

73

CHAPTER 2

Radiographic status (14 X-r) In the incisor sectors, only three X-ray images (no . 1) per arch were used .

Radiographic status (18 X-r) In this status, the "bite-wing" X-rays were also included (2 on the right and 2 on the left) .

DISEASE DIAGNOSI S

Dig italic orthopantomograph y Note the high definition of the details and the excellent contrast obtained with this typ e of X-ray analysis .

Limitations of intraoral X-ray 1.They do not identify periodontal pockets . 2.A successfully treated case is no different from an untreated case . 3.They do not distinguish the number of walls in bone defects . 4.They do not identify the vestibular and lingual structures of the root surface . 5.Tooth mobility is not recorded . 6.It is not possible to identify dormant periodontitis until six months after the disappearance o f inflammation (calcified lamina dura) .

75

CHAPTER 2

X-ray techniqu e

The seated patient should be covered with a lead apron to protect th e gonads and thyroid. The Extension Cone Paralleling Technique is used . The most commonly used X-ray positioner is the Rinn Corporation XC P " . This is available in two types, one for the front upper and lower sectors of th e mouth and one for the rear upper and lower sectors . A plastic "bite" is positioned in the patient's mouth . This is connected via a metal arm to a plastic ring representing the target for correct positioning of the cathode tube . The most commonly used films are Kodak ultra-speed DF-58 (size 2) for th e molar and premolar sectors and Kodak ultra-speed DF-56 (size 1) for th e canine and incisor sectors . Once exposed, the radiographs should be developed, preferably using an auto matic system . After fixing and drying, the radiographs are mounted in a fram e and represent the X-ray status .

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DISEASE DIAGNOSIS

Positioner for intraoral X-ray s

Rear right positioner with collimato r mrnwted on the target, .

Collimator . Metal disc to reduce dispersion of X-rays and concentrate them on the radiograph .

Rear left positioner:

Plastic bite. A spacer (cotton roll) is inserted in the mouth t o guarantee patient comfort and the stability of the positioner.

Front positioner with disposable expande d polystyrene "bite".

77

CHAPTER 2

Positioning the X-ray film s

Intraoral status with 16 film s Maxillary arc h Four films vertically DF-56 no .1 (from the front) Position between : 1 - 2 right and left 3 - 4 right and left

Four X-ray films horizontally DF-58 no . 2 (from the rear)

Position between : 5 - 6 right and left 7 - 8 right and left

c

Mandibular arch Four X-ray films vertically DF-56 no .1 (from the front) Position between : 1 - 2 right and left 3 - 4 right and left

Four X-ray films horizontally DF-58 no .2 (from the rear)

Position between 5 - 6 right and left 7 - 8 right and left

An intraoral status may consist of 21 X-ray films if four bite-wing films and 1 film for the interincisor sector between the upper sectors are included (11-21) .

~o

DISEASE DIAGNOSIS

uaituttlitti'mai

Film Dentaire Zahnfil m Pelicula Denta l

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Incorrec t

The X-rays must hit the films at right angles to avoid superimposition of the points of contact with the teeth and obtain correct images of the bon e tissue.

79

CHAPTER 2

X-RAY ANALYSIS OF THE MAXILLARY ARCH

Front secto r

For the incisor sector, if five X-ray images are to be taken, the bite must be positioned between th e central incisors . Alternatively, if four X-ray images are required, the bite must be placed between th e central and lateral incisor, first on the right, then on the left . The series of X-rays is completed b y positioning the bite between the canine and lateral incisor ; once again, first on the right, then on the le,

Note the longitudina l bone reabsorptio n affecting the entire upper front sector:

,zn

!

DISEASE DIAGNOSI S

Lateral secto r

The positioner is inserted between the two premolars . A cotton rol l can be used if necessary.

Normal The crestal and radicular laminae dura are intact. The trabeculae are in the norm . 81

Diseased The crestal laminae dura of the premolars are decalcified . Calculus can be observed on the roo t surfaces.

CHAPTER 2

Rear sector

In the molar sectors, the positioner bite should be inserted i n correspondence a'ith the first molar :

A cotton roll is inserted under th e bite to guarante e patient comfort and the stability of the positioner :

Normal The crestal and radicular laminae dura ar e intact. The trabeculae are in the norm .

Diseased Note the deep distal bone reabsorption corresponding to the first molar and the intraosseou s pocket identified by probing .

#DISEASE DIAGNOSIS

X-RAY ANALYSIS OF THE MANDIBULAR ARCH

Front sector

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In the incisor sector ; the positioner bite should be inserted between the central incisors, then betwee n the canine and lateral incisor, first on the right, then on the left .

Norma l No bone lesions are identified.

Diseased Bone reabsorption ca n be noted for more than 50% of the length of the roots . The crestal lamina dura has disap peared . An accumulation of calculus can b e observed on the roo t surfaces.

8

CHAPTER 2

Lateral sectorIn the premolar sector, the positioner bite should be inserte d between the two premolars, first on the right, then on the left . O

In the molar sector, the positioner bite should be inserted between the two molars, first on the right, then on the left . If a third molar is present, the bite should be placed on the second molar.

84

!

DISEASE DIAGNOSI S

Normal Calcification of the crestal laminae dura is normal.

Disease d Bone reabso'iption prevents identification of the crestal laminae dura. A large quantity of calculus can be observed on the root su ifaces.

Normal Calcification of the crestal laminae dura is normal.

Diseased Considerable bone reabsorption can be observe d corresponding to the molars with possibl e damage to the furcations (degree 2) .

85

CHAPTER 2

Lamina dur aThis X-ray image was produced by directing Roentgen rays to the sec tor where they were partly blocked by calcification of the cortical plate . In the presence of inflammation, the calcification disappears and the greate r quantity of X-rays crossing the cortical plate prevents the lamina dura fro m being detected.

The diagram illustrates the relationship between the crestal lamina dura and the cemento-enamel junction of the two neighbouring teeth . In a normal situation, the crestal lamina dura i s always parallel to th e line between the cemento-enamel junctions of two neighbouring teeth.

RA

DISEASE DIAGNOSI S

Bone defect

X-ray image of a bon e defect of the interdenta l septum between th e first and second mola? :

By lifting a mucope riosteal flap and remov ing the granulation tis sue, the bone defec t shown in the top X-ray image can be observed to have three walls .

87

CHAPTER 2

DISEASE DIAGNOSISFrom a clinical point of view, periodontal diseases can be divided int o gingivitis and periodontitis . These are differentiated by loss of connectiv e attachment and bone reabsorption, two phenomena confined to periodontitis , classifiable as slight, severe or complicated according to the degree of damag e to anatomical structures.

Periodontal diseasesDISEASE 'TYPE LESTnNInflammatory infiltrate above the transseptal fibres Bone reabsorption limite d to the coronal third of the root only Bone reabsorption extended beyond the coronal third Angular bone reabsorptio n and 2nd or 3rd degree furcation involuement Bleeding on probin g Pocket Possible tooth mobilit y Bleeding on probin g Pocket Possible tooth mobility Furcation involvement

SYMPTOM SBleeding on probing No pocke t

Slight Periodontitis Severe Complicated

GingivitisShis term is used to describe localized or generalized inflammation o f the gingiva . The clinical system of this disease is "bleeding on probing" . Gingivitis is diagnosed in the absence of a periodontal pocket and when X-ra y examination does not indicate bone reabsorption. Pseudopockets may b e present .

Margina l gingivitis .

QQ

DISEASE DIAGNOSI S

Slight periodontitisProbing depth, attachment level and X-ray analysis indicate a unifor m loss (horizontal reabsorption) of bone tissue not exceeding a third of th e length of the root (coronal third) . Inflammation is present . Probing to the bottom of the pocket causes bleeding.

Chronic adul t periodontitis (slight) .

Severe periodontitis (Advanced periodontitis)Probing depth, attachment level and X-ray analysis indicate a unifor m loss (horizontal reabsorption) of bone tissue exceeding a third of the lengt h of the root. Probing to the bottom of the pocket causes bleeding .

Chronic adult periodontitis (severe) .

89

CHAPTER 2

Complicated periodontitisThis diagnosis is reached when angular (vertical) bone reabsorption is present, accompanied by 2nd to 3rd degree furcation involvement .

Chronic adult periodontiti s (complicated) with tooth mobility, damage to a number of furcations and angular bone defects.

Complicated periodontitis in an adult suffering from diabetes mellitus with tooth mobility, damage to all bifurcations and trifurcations and angular bone defects .

DISEASE DIAGNOSI S

Severe gingival inflammation and the accumulation of bacterial plaque can be observed .

CONCLUSION S Periodontal disease is diagnosed by means of a thorough assessment of th e patient based on clinical, instrumental and radiographic data . Only a correc t diagnosis can enable a suitable treatment plan to be drawn up .

91

TREATMENT PLANNIN G

The treatment of a patient with periodontal disease consists of thre e fundamental phases : 1) Complete removal, or at least control, of bacterial plaque, the etiologica l agent of the disease. 2) Surgical correction of alterations to the soft and hard tissues caused by th e disease . Restoration of functional form facilitates plaque control an d improves aesthetics. 3) Prevention of possible relapses with a personalized programme of follow up appointments .

Chronic adult periodontitis .

95

CHAPTER 3

TREATMENT PLANNING

0 Initial treatment plan 0 Presentation of alternative

plans

REEVALUATIO N

Hygienic treatment phas e 0 Treatment of carie s 0 Endodontic treatment 0 Extractions 0 Minor orthodontic s #> Construction of temporary prosthese s

Patient cooperatio n

40-

4PERIODI C FOLLOW-UP APPOINTMENTS Supportive therapy

DEFINITIVE TREATMENT

o Periodontal surgery 0 Implant surgery o Peri-implant surgery 0 Construction of definitive prosthese s

TREATMENT PLANNIN G

Initial treatmen tThe aim of initial treatment is to eliminate, or at least control, bacterial plaque. It involves implementation of the following phases : 1) Oral hygiene instruction . The patient is instructed in correct home use of oral hygiene instruments an d attempts are made to motivate him or her towards positivecompliance .

Before scaling .

2) Scaling and root planing . These manual or mechanical operations enable bacterial plaque to be completel y removed from the crown and root surfaces of the tooth.

Immediately after scaling.

During initial treatment, other measures may be required. These include : 1)Removal and restoration of caries . 2) Endodontic treatment. 3) Extraction of hopeless teeth. 4) Minor orthodontics. 5) Construction of temporary prostheses .

Together, these measures neutralize the bacterial infection, eliminat e pain and re-establish a certain degree of masticatory, phonetic an d aesthetic functionality.

97

CHAPTER 3

Reevaluatio nreasonable period of time (possibly several months) after the end of initial treatment, the patient undergoes a thorough examination to check th e state of gingival inflammation (which should have disappeared), periodonta l pocket depth and residual tooth mobility. The level of patient cooperatio n must also be verified . The examination covers every tooth and the result s determine the choice of definitive treatment .

A

Before initia l treatment .

At reevaluation .

nQ

TREATMENT PLANNIN G

Reevaluation: periodontal pocket and bleeding on probing .

Probing reveals a pocket (>6 mm .) between the first and second molars .

A modest degree of bleeding on probin g is present .

Raising a mucoperiosteal flap, bone reabsorption of the interdental septum can be observed .

99

CHAPTER 3

Definitive treatmen tIf the patient cooperates, surgical treatment can commence .

PERIODONTAL FLAP SURGERY to eradicate any periodontal pockets (>4 mm) still present after the hygienic phase .

BONE RESECTIVE SURGERY to eliminate intraosseous defects by resecting one or more bone walls .

1 nn

TREATMENT PLANNING

GINGIVAL RESECTIVE SURGER Y to eliminate hyperplastic gingival formations and pseudopockets and reconstruct a functional and aes thetically satisfactory gingival profile .

ROOT RESECTIVE SURGER Y involves the sectioning and removal of one or two roots of a multirooted tooth .

101

CHAPTER 3

BONE REGENERATIVE SURGER Y to regenerate bone tissue in angular defects using guided tissue regeneration (GTR) .

PRE-PROSTHETIC SURGERY to modify the length of the clinical crown, the shape and length of tooth abutments and the shape o f bone and soft tissues, enabling a functional and aesthetically satisfactory prosthesis to be constructed .

1r)

TREATMENT PLANNIN GMUCOGINGIVAL SURGERY to reconstruct the gingiva, improve appearance and reduce root sensitivity .

DENTAL IMPLANT SURGERY to reconstruct dental elements in partially totally toothless patients .

103

CHAPTER 3

Surgical treatmen t of periodontitis

Modified Widman flap Apical flap Bone resective surgery Gingivectomy Root resection surgery

Provides access to roots and bon e defects Reduces or eliminates the pocket Facilitates plaque contro l Facilitates restorative and cosmetic dentistry

Increase in gingival recessio n Long term success not guarantee d without maintenanc e

Mucogingival surgery Free grafts Pedicle graft s Pedicle grafts + GT R

Improves aesthetic s Reconstructs gingival defects Reduces root, sensitivity

Clinical variability Results linked to surgical techniqu e

GT R Non-reabsorbable membran e Reabsorbable membrane

Significant increase i n attachment level s The best results are obtained with Class II mandibular furcations an d intraosseous defects

Results linked to surgical techniqu e

Autologous bone Increase in bone level The osteogenetic capacity of demin e alized bone grafts is variabl e Alloplastic bone (synthetic) Increase in bone level Synthetic grafts act as fillers withou t regeneratio n

(Modified from World Workshop in Periodontics 1996) .

If the patient is not cooperative or does not wish to or cannot undergo surgery, non-surgical treatment can be administered, followed by the maintenance phas e with a cycle of periodic follow-up appointments .

!!

TREATMENT PLANNIN G

Non-surgical treatment of gingivitis and periodontitis

Treatment

Indications

Contraindication s

i

Manual or mechanical scaling and root planing

Gingiviti s Periodontiti s

Non e

Chemical treatment of bacterial plaqu e Mouth washes Gel Irrigation

Gingivitis

No long term benefits in periodontitis

Topical antibiotics Tetracycline impregnated fibres

Periodontitis

Allergy Recessions Candid a

Systemic antibiotic s Tetracyclin e Metronidazol e Amoxicilli n Clavulanic aci d Clindamycin Spiramycin

Aggressive destructive periodontitis

Gingiviti s Adult periodontitis

(Modified from World Workshop in Periodontics 1996 )

Manual scaling . 105

Mechanical scaling .

!

CHAPTER 3

CLINICAL CASEMale patient aged 48 fitted with two cardiac by-passes. The periodontal examination led to a diagnosis of chronic periodontitis . The clinical file reproduced below indicates tooth mobility, pocket depth and furcatio n involvement.Maxillary arc h

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Medical alert: aorta-coronary by-pas s Diagnosis : complicated chronic periodontitis

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#TREATMENT PLANNIN G

TREATMENT PLAN

HYGIENIC PHASE

1 gross-scaling sessio n 4 scaling and root planing session s

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REEVALUATION

1SURGERY

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MAINTENANCE Periodical follow-up appointment s every three month s

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CHAPTER 3

MaintenanceAt the end of treatment, the patient is included in a programme of peri odic follow-up appointments formulated to prevent possible relapse . The appointment schedule is established in relation to the patient's ability to maintain a high standard of oral hygiene . Longitudinal studies have shown that a maintenance programme with appointments every three months is optimu m for preventing relapse in the majority of cases . During each session, oral hygiene is assessed and scaling is performed for the entire mouth, usually associated with polishing. If necessary, the patient is remotivated to maintain positive compliance . At least once a year, bone level should be assessed via X-ray analysis .

The image shows a cas e after a year in the maintenance phase (follow-u p appointments every fou r months) . Note the absence of periodontal pocket and inflammation.

Compliance The patient's behavioural response in relation to his/he r health and the means at his/he r disposal to maintain it .

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TREATMENT PLANNING

At the end of periodontal treatment, the patient is included in a pro gramme of periodic follow-up appointments .

Follow-up programm e After one mont h Subsequently every three month s Every three months Personalized (every 4-6 months )

CONCLUSION SA treatment plan is a sequence of therapeutic measures aimed at healing o r halting periodontal disease. It is vital that the phases are applied according to this algorithm . Each play s a vital role in determining the success of the treatment. It is important to emphasise that it is impossible to prevent bacterial colo nization and thus avoid relapse of the disease without effective maintenance .

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Chapter 4

Oral Hygien e Rehabilitation'ow

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ORAL HYGIENE REHABILITATIO N

The aim of Oral Hygiene Rehabilitation (OHR) is to eliminate bacteria l plaque infection by removing all local irritative stimuli . During this initial phase of periodontal treatment, the patient must be motivated and instructed in th e use of home oral hygiene instruments . The patient must be made aware of th e close relationship between his or her active participation and the successfu l outcome of the treatment .

Oral hygiene instruction MotivationToothbrush (manual, electric, sonic, interdental) Dental floss (floss, tape, super floss ) Toothpaste Antiseptics (chlorhexidroe) Manual instruments (curettes, scalers) I-Iyposonic and ultrasonic instrument s Rotary instruments Alternating movement instrument s

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BACTERIAL PLAQUE CONTROLBacterial plaque must be controlled daily (2-3 times) by the patient using a toothbrush and dental floss .

ToothbrushNone of the toothbrushes currently available on the market is better than th e others. The best brush is probably the one used with the most effective technique . The advantages of electric toothbrushes over normal toothbrushes are con fined to patients with reduced manual ability. Sonic toothbrushes (Sonicare 0) supplement the electrical movement with cavitating vibration and a water je t to facilitate removal of plaque and stains from the supragingival surface of the teeth.

Conventional toothbrush.


Electric toothbrush . Does not remove bacterial plaque more efficiently tha n conventional toothbrushes.

Brushing methodsNumerous brushing methods have been described, but none ha s proved more efficient than the others . The Bass Method effectively removes bacterial plaque from the supragingival and subgingival pericrevicular zone . The head of the toothbrush is placed on th e gingival margin at an angle of 45 with respect to the axis of the tooth and move d from the front towards the back, in association with short pulses of vibration . In the Charter Method, the bristles of the toothbrush are placed at an angle o f 45 in the interdental spaces and moved backwards and forwards with a rotat ing movement . This method is particularly effective in removing bacteria l plaque in the presence of open interdental spaces caused by papillary recession . Other techniques include: Roller Circular Vertica l Horizontal

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Too thbrushing

duration and sequenc e

The patient must learn to brush his or her teeth according to a sequence which must become automatic and routine . Toothbrushing starts in a vestibular position in the molar sector of one arc h (about 10 seconds for each sextant) and then proceeds to the lingual position . It continues with the other arch following the same sequence . The occlusal surfaces are the last to be brushed .

Toothbrushing techniqu e Step 1The toothbrush is positioned at 45 to the axis of the tooth and the bristle s are pushed into the gingival sulcus .

Step 2The toothbrush is moved in a mesial-distal or circulatory-vibratory directio n to remove bacterial plaque from the pericrevicular or inter-proximal areas .


Step 3The same movements are repeated for th e other sectors of the mouth following an established sequence (about 10 second s for each sextant) .

Step 4In the front palatal and lingual sectors, th e toothbrush must be held perpendicularly to the arch .

Step 5To conclude, first the lower and then the upper occlusal surface s are brushed .

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Plaque disclosing dyesBacterial plaque, often difficult to detect, may be highlighted by usin g either single colour or two colour dyes . Two-colour plaque detectors differentiate between newly formed and less recently formed plaque . Dyes containing fluorescein can be used to make the plaque visible in ultraviolet light only. Plaque disclosing dyes are extremely useful during the initial phase of OHR to motivate the patient and indicate where it is necessary to brush correctly. They are also important to verify the home hygiene programme and monitor correc t removal of bacterial plaque .

SINGLE COLOUR PLAQUE DISCLOSING AGEN T

Plaque can be observed in the pericrevicular zone . Invisible to the naked eye , it is highlighted by the dye .

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ORAL HYGIENE REHABILITATIO NTWO COLOUR PLAQUE DICLOSING AGEN T

r

Note the different gradation s of colour: the dark colouring identifies less recently formed plaque .

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The same clinical case as i n the previous image treated with single colour plaqu e detector. Recent plaque canno t be distinguished from less recent plaque .

MARGINAL GINGIVITI S

. T.TTNote the modest quantity of bacterial plaque in the pericrevicular region, highlighted b y single colour dye .119

CHAPTER 4PLAQUE DICLOSING AGENT WITH FLUORESCEI N This diclosing agent avoids staining the patient's mouth . When the surface is exposed to ultraviolet rays, the zones covered with bacterial plaque are fluorescent .

Flake Lite r equipment.


Complianc e The patient's behavioural response in relation to his healt h and the means at his disposal to maintain it .

ACTIVE PATIENT MOTIVATIO N

By placing a small quantity of bacterial plaque taken from the patient's mouth on a slide and using a phase contrast microscope, the composition and amoebic movements of the mobile life-forms in th e plaque can be displayed on a television screen . This method is effective in active patient motivation .

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Dental flossDental floss effectively removes bacterial plaque from between the teeth and under the papillae and is an indispensable part of the daily ora l hygiene programme . Various types are available : single thread, multi-thread, ribbon and super floss ; waxed or unwaxed and in various flavours .

Use of a toothbrush alone is not sufficient t o remove the bacterial plaque from the interdenta l spaces .

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Using dental floss

Step 1A length of dental floss approximately 30 cm lon g is taken and rolled around one finger of eac h hand, leaving about 20 cm free .

Step 2For the maxilla, the index finger and thumb are used . For the mandible, the two index fingers are used .

Step 3The floss is passed delicately acros s the contact point with a backwards an d forwards movement .

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Step 4The floss is curved into a "C" around the tooth and moved delicately in an apical direction . Then with a single rapid movement, it is move d in an occlusal direction , scraping the plaque .


Step 5Using clean sections of the floss, the operation is repeated for the othe r interproximal surfaces .

BLEEDIN G

If the floss is used correctly without damaging the epithelial attachment, any papillary bleeding ca n be attributed to the presence of plaque or subgingival calculus . 125

CHAPTER 4

Proxa- brushPatients with papillary recession or with a prosthesis may effectivel y replace the dental floss with an interdental toothbrush (proxa-brush) to completely remove interdental plaque . Two shapes of proxa-brush exist, conical and cylindrical, the latter being avail able in various sizes .

CONICAL PROXA-BRUSHAfter periodontal surgery, the space between the premolar an d molar is wider as a result of papillary recession . Use of a conica l proxa-brush is therefore recommended .

Its shape makes the conical proxa-brush ideal for removin g bacterial plaque from the interproximal spaces of a prostheti c reconstruction .

ORAL HYGIENE REHABILITATIO NCYLINDRICAL PROXA-BRUS H

Access to the interdental spac e between the two roots of a hemi sectioned tooth can be obtained only by using a cylindrica l proxa-brush .

Only a small diameter cylindrical proxa-brush is able to penetrate the upper front interdental spaces of a temporary prosthesis which, for aesthetic reasons, are always very narrow . 127

CHAPTER 4

ToothpasteUsed in combination with the toothbrush, toothpaste makes brushin g more pleasant, facilitates bacterial plaque removal and may contain antisepti c substances, etc . Some toothpastes are more abrasive than others . The toothpaste should contain calibrated abrasion particles (75 RDA-25 RDA) to protect the enamel and, in the case of gingival recession, also the neck and root of th e tooth .

CONTROLLED ABRASION TOOTHPAST E 75 RDA* 25 RDA* Dental enamel Necks and roots

"Radioactive Dentine Abrasion .


Relation between bacterial plaque, inflammation and tissue destructio nThe ability of bacterial plaque to cause gingivitis and possibly peri odontitis has already been discussed in chapter one . If performed correctly and constantly, oral hygiene measures enable the gums to be maintained in a healthy state . This has been incontrovertibly demonstrated by numerous researchers .

Lindhe et al. (1975) eliminated gingival inflammation from the mouths of a group of beagles by applying a hygiene regime based on toothbrushin g twice a day and prophylactic polishing once a week . The group of dogs was subsequently divided into two sub-groups . The control group (dotted line) was kept free of local inflammation (zero plaqu e index) for a period offour years just by brushing twice a day . The dogs in the second group (test dogs) were left without oral hygiene . Bacterial plaqu e accumulated rapidly, followed immediately by gingival inflammation . After six months, the dogs began progressively to lose periodontal attachment . During the four year experiment, the test group lost a mean 2 .9 mm of attachment.

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SCALING AND ROOT PLANINGScaling: involves the use of instruments to remove plaque and calculus fro m the supragingival and subgingival surfaces of the teeth . Root planing : involves the use of instruments to remove softened cementu m from the root surfaces . Scaling and root planing are usually carried out without incision an d therefore without a direct view of the deposits on the roots . The manual o r mechanical instruments used for these operations must have very fine point s and an extremely sharp cutting edge . In the case of single root teeth, irritative stimuli can be completely remove d and the roots planed . However, this is not possible with multi-root teeth an d scaling and root planing must therefore be completed with the tooth and roo t exposed during periodontal surgery . Calculus: hard, widely distributed calcareous deposit adhering tenaciously t o the surface of the teeth, formed by calcification of bacterial plaque by certai n groups of Gram+ bacteria . From a topographical point of view, it is divided into supragingival calculu s and subgingival calculus .

Supragingival calculus : yellowish and friable, it is located mainly on th e lingual and vestibular aspects of the mandibular sector of the mouth .


Subgingival calculus : dark and hard, it occurs everywhere in the mouth . Th e colour is caused by the deposit of hematic pigments resulting from ulceratio n of the soft wall of the periodontal pocket .

CHAPTER 4

InstrumentsThe instruments used for scaling and root planing include : Manual instruments (scalers - curettes ) Mechanical instruments (sonic, hyposonic ) Rotary instruments (burrs ) Alternating movement instrument s MANUAL INSTRUMENT S Manual instruments are made up of three parts : blade, shaft and handle . SCALER Triangular section instrument with two cutting edges, a back and a point . Its particular shape makes it strong and rigid enough to remove thick calculu s deposits. Scalers may be straight or curved . Use: supragingival scaling, shallow pockets .

Scaler M23 (Deppeler) Tl.1Q

ORAL HYGIENE REHABILITATIO NCURETT E Semicircular instrument with two cutting edges and a rounded point . The rounded back enables the instrument to be inserted into deep pocket s without damaging surrounding soft tissues . The particular curved blade of cer tain curettes ensures optimum adaptation of the instrument to the surface o f the tooth . Use : subgingival scaling, root planing .

Curette M23 A (Deppeler) TI

Scaler M23 (Deppeler) TI Curetta M23 A (Deppeler) TI

The ideal curette should have a very small blade enabling it to be inserted easil y into the pocket . It should also be shaped in such a way that it can be used in al l sectors of the mouth.

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CHAPTER 4

Holding the instrument sThe way an instrument is held is crucial to stability, control and efficiency. The most common techniques are : Pen grip: the instrument is held between the thumb and index finger of th e operating hand and rested on the side of the middle finger . Modified pen grip : the instrument is held between the thumb and index finge r of the operating hand ; the fingertip of the middle finger is rested on the instrument in such a way as to act as a pivot . This grip is more powerful an d improves the instrument's stability during lateral movements .

Pen grip

Modified pen grip

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ORAL HYGIENE REHABILITATION

Resting the han d To maintain control of the instrument, a point must be found to res t the operator's hand, thus improving stability and efficiency while minimizin g the risk of damage to surrounding tissues . The hand is usually rested inside the mouth (teeth) as close as possible to the working area, using the fingertips of the ring and little finger . These fingers should be perfectly dry to avoid slippage .

Resting point in the same arch .

Resting point in the opposite arch . 135

CHAPTER 4

Mechanical instruments (ultrasonic - sonic)Clinical research has consistently failed to demonstrate the superiority of manual instruments over mechanical instruments . Although the latter produce a rougher root surface, they enable the junctional epithelium to readapt perfectly to the surface of the root cementum . A number of studies (Leon et al . 1987 - Ainamo et al . 1991) have demonstrated the superiority of mechanical instruments over curettes in subgingival scalin g of multi-root teeth . The latest generation of mechanical instruments, hyposonic instrument s (2,300-6,300 cycles/second), produce a less rough root surface than ultrasoni c instruments (25,000-42,000 cycles/second) .

Titan-S

Note the point of the Titan-S a , similar in size to that of a very small curette (M23A-TI) . In the furcation area, the point of a soni c instrument removes bacterial plaque more efficiently via vibration and the cavitatin g effect of the water used for cooling .


Rotary instrument sThe use of diamond burrs mounted on rotary instruments to remov e residues of calculus and softened root cementum is confined to devitalize d teeth transformed into prosthetic abutments . This operation is carried ou t exclusively with the tooth exposed during pre-prosthetic surgery .

During the surgical preparation of abutments , calculus and softened root cementum residue s are removed using a diamond stone mounted on a rotary instrument .

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A lternating movement instrumentsAlternating movement instruments are extremely useful in removing calculus and planing the approximal surfaces of the roots . They are also use d to remove the excess contours of iatrogenic interproximal fillings which wil l subsequently have to be redone to enable optimum control of bacterial plaqu e in the meantime.

DENTATUS EUA TIPS no . 4-3- 1 CONTRA-ANGLE EUA with TIP no. 20

Note the calculus deposit on the approxi mal surfaces of the molars and premolars . After calculus removal , root planing can easily be performed using alternating movement instruments.


DENTATUS EVA TIPS no . 4-3- 1

DENTATUS EVA TIP no . 20

Iatrogenic filling . The interproximal exces s contour must be remove d (EVA TIPS no. 20-21) fo r optimum hygiene i n these areas . 139

CHAPTER 4

Supragingival scalingDefinition : removal of all accretions (plaque, calculus, stains) fro m the supragingival surface of the teeth . Supragingival scaling can be carried out using manual instruments (curettes , scalers) and/or mechanical instruments (sonic, hyposonic) .

TECHNIQUE Manual instruments : the blade is rested on the tooth and adequate pressur e is applied . The instrument is then moved in a coronal direction with a movement repeated across the entire supragingival surface of the tooth until all visible accretions have been removed . Magnifying glasses (x 2-3) can be used to facilitate this operation .

Supragingival scaler DEPPELER M23.

Note the blade of the instrument resting on the surface of the tooth t o perform supragingival scaling .14Q


Supragingival scaling . Mechanical instruments : the point of the instrument (sonic, hyposonic) is held flat on the surface of th e tooth with a very light pressure and moved backwards and forwards . To break very thick calculus concretions, the point of the instrument may be positioned perpendicularly to the surface of the tooth . If this is not successful, rather than persist, manual scalers should be used . The Titan- S 12 sonic instrument is also highly effective in tooth surface planing, using its rhomboid-sectio n point flat and performing brush-type movements .

If thick calculus concretions are present, th e point of the instrument may be positione d perpendicularly to the sus face of the tooth .

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CHAPTER 4

Pre-hygienic phas e

Post-hygienic phas e

Note the considerable reduction i n recession after completion of the hygienic phase (supragingival scaling) . If the patient controls bacterial plaque adequately, mucogingiva l reconstruction of the central incisors can be avoided . l /,


Pre-hygienic phas e

On completion of the hygienic phas e (supragingival scaling), the local inflammation has receded, but the larg e recession is unaltered . In this case, reconstruction of the gingiva wit h mucogingival surgery is recommended. 143

CHAPTER 4

Subgingival scaling and root planing are presented together as they are both performe d at the same time . Subgingival work must be carefully targeted and performed under local anaesthetic following identification of pocket depths and the presence of subgingival deposits .

Subgingival scalingDefinition: removal of all accretions (plaque, calculus) from the sub gingival surface of the teeth . Subgingival scaling may be performed using manual instruments (curettes ) and/or mechanical instruments (sonic/hyposonic) .

Note that the subgingival concretion of calculus has bee n completely removed by the curette . During subgingival scaling, root planing is also completed .

Subgingival curette Deppeler M23 A Tl.


Root planingDefinition : involves the use of instruments to remove the final residues of calculus, the softened and infiltrated cementum and smooth th e root surface . Root planing is normally carried out using manual instruments (curettes) . Th e same result can also be obtained using certain hyposonic mechanical instruments (Titan-S) with a particular shaped point .

The very fine rhomboid-section point of the Titan-S enables it to be used for subgingival work .

Titan-S .

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Subgingival scaling and root planing technique Step 1The pocket is probe d and the solid concretio n is identified .

Step 2The curette is reste d on the tooth with th e rounded back toward s the gingiva.

Step 3The curette is pushed under

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