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CHAPTER 24 Breath Malodor DA N IE L V A N S TE E N B E R G H E A N D MA R C Q UI R Y N E N Socio-economic aspects Clinical and laboratory examination Etiology and pathophysiology Treatment Diagnosis Conclusions Patient history Breath malodor means an unpleasant odor of the expired air, whatever the origin may be Oral malodor specifically refers to such odor originating from the oral cavity itself A term like halitosis is synonymous with breath malodor but is not always understood by the general population Breath malodor has long been a matter of concern There are references to it in the Bible and in the Koran Surprisingly enough, until recently breath malodor has not been a matter of much interest in periodontology, although its most frequent causes are plaque-related gingivitis and periodontitis Even the literature concerning this subject is scarce There was only one book on this topic in the nineteenth century (Howe 1898) and it was not until the end of the twentieth century that two more books were devoted to the subject (Rosenberg 1995, van Steenberghe & Rosenberg 1996) Joe Tonzetich from the University of British Columbia unfolded the biologic basis for oral malodor (Tonzetich 1977) but his observations received only limited attention from clinicians, even if oral or breath malodor is frequently encountered in any dental and especially periodontal office SOCIO-ECONOMIC ASPECTS A transient breath malodor is noticed when waking up in the morning in more than half the adult population (Morris & Read 1949) It does not deserve special attention since it is due to the xerostomia developed during sleep, i.e when salivary flow is reduced to a minimum This with the ongoing intra-oral putrefaction explains the malodor when waking up Morning breath odor disappears soon after the intake of food or fluid The intra-oral placement of a toothpaste containing zinc salts and triclosan has the capacity to reduce the odor for several hours, even in the absence of toothbrushing (Hoshi & van Steenberghe 1996) The real concern of the population is the breath malodor which remains during the day and which can cause social and/or relational problems Unsubstantiated press releases claim that breath malodor may concern as many as 25 million people in the US alone Everyone has sometimes experienced, when a person is speaking to them at close proximity, breath odor that is unpleasant if not unbearable Subjects who believe they produce malodor can adopt avoidance patterns such as keeping a distance when speaking to others or holding their hand in front of the mouth while speaking There is also a tendency to constantly use rinses, sprays, chewing gums or pills to mask the breath odor, although many such items have no effect whatsoever or at least no lasting effect Even more disturbing is the fact that a number of subjects imagine they have breath malodor when they may not have This imaginary breath odor, also called halitophobia (Oxtoby & Field 1994), has been associated with obsessive-compulsive disorders or hypochondria It has even led to suicide (Yaegaki 1995) There are well-established personality disorder questionnaires such as the SCL-90 (Derogatis et al 1973) which allow the clinician to assess the tendency for illusionary breath malodor among those where no objective diagnosis of breath malodor can be made (Eli et al 1996) For such patients, the presence of a psychologist/psychiatrist at the multidisciplinary malodor consultation is essential Epidemiological investigations concerning breath malodor are rare There is a large-scale Japanese study involving more than 2500 subjects aged 18 to 64 years in which the malodor was measured by a portable sulfide monitor (see section on diagnosis later in this chapter) at several times during the day The volatile sulfur components reached high levels several hours BREATH MALODOR • 513 after food intake and increased with age, tongue coating and periodontal inflammation About one out of four subjects exhibited volatile sulfur components ( VSC) values higher than 75 ppb, which is considered the limit for social acceptance Thus one can conclude that the socio-economic impact of breath malodor is considerable ETIOLOGY AND PATHOPHYSIOLOGY Findings from different investigations have documented that the vast majority of causes of malodor relate to the oral cavity, with gingivitis (Persson et al 1989, 1990), periodontitis (Yaegaki & Sanada 1992a) and tongue coating (Yaegaki & Sanada 1992b) as predominant factors On the other hand, since more than 90% of the population suffers from gingivitis and periodontitis, there is a risk that such plaque-related inflammatory conditions are always considered to be the cause, while in fact more important pathologies, such as a hepatic or renal insufficiency or a bronchial carcinoma, may be the main etiological factor In a multidisciplinary breath odor clinic, it appeared that 87% of the etiologies were intra-oral, 8% in the oto-rhino-laryngological field and 5% from elsewhere in the body or unknown (Delanghe et al 1997) Members of the oral anaerobic microbiota, especially species such as Treponema denticola, Porphyronrrnras gingivalis and Prevotella intermedia, can produce hydrogen sulfide and methylmercaptan from L-cysteine or serum (Tonzetich 1977), i.e proteins which are consistently present in the oral cavity and in the crevicular fluid Chromatography (see section on diagnosis later in this chapter) revealed that crevicular fluid contains hydrogen sulfide, methylmercaptan and also dimethyl sulfide and even dimethyl disulfide (Coil 1996) When deep pockets are present the relationship with methylmercaptan/HZS increases (Coil 1996) One should never forget that many components besides sulfide components, e.g diamines (putrescine, cadaverine) in the crevicular fluid and in saliva can be malodorous (Goldberg et al 1995) It is important to realize that the latter odor-inducing components cannot be detected by a portable sulfide monitor (see section on diagnosis later in this chapter), which is often used in breath odor consultations All such malodor-inducing components can only be perceived when they become volatile This means that as long as they are dissolved in the saliva, they will not be expressed – just as a perfume only evaporates when the skin becomes dry This explains why xerostomia reveals a strong breath malodor, which otherwise might only be a faint odor While on the one hand periodontitis favors the production of malodorous components, the latter may in their turn play a role in the ongoing periodontitis Volatile sulfur components, such as methylmercaptan, enhance the interstitial collagenase production, the IL-1 production by mononuclear cells and the cathepsin B production (Lancero et al 1996, Ratkay et al 1996) and thus mediate connective tissue breakdown Brunette et al (1996) found that human gingival fibroblasts grown in vitro showed an affected cytoskeleton when exposed to CH3SH The same gas altered cell proliferation and migration These potent biologic effects can be blocked by Zn", at least for the influence of VSC on protein synthesis The tongue dorsum, because of its large surface, is a prominent host for products that can cause malodor Desquamated cells, food remnants, bacteria, etc accumulate on the tongue and putrefy under the action of bacteria (Bosy et al 1994) There is six times more tongue coating in patients with periodontitis than in subjects with a healthy periodontium (Yaegaki & Sanada 1992b) Saliva plays a predominant role in the control/expression of malodorous components After drying, sulfur and non-sulfur-containing gases such as cadaverine, skatole, indole, etc are released (Kleinberg & Codipilly 1995) The oral microbiology involved in VSC production is well identified; Porphyromonas gingivalis, Prevotella intermedia, Fusobacteriurn nucleatum, Porhyromonas endodontalis, Prevotella loesclrii, Haemophilus para influenzae, Treponema denticola, Enterobacter cloacae and many others have been associated with malodoros gas production (Persson et al 1990, Kleinberg & Codipilly 1995, Niles & Gaffar 1995) The above are members of the oral microbiota, are anaerobic and are Gram-negative The ear-nose-throat causes include chronic pharyngitis, purulent sinusitis and postnasal drip The latter, rather frequent condition is associated with regurgitation oesophagitis and is perceived by patients as a liquid flow in the throat which originates from the nasal cavity (Rosenberg 1996) Ozena, which is an atrophic condition of the nasal mucosa with the appearance of crusts, leads to a very strong breath malodor but is a rare disease Pulmonary causes include chronic bronchitis, bronchiectasis, and bronchial carcinoma (Lorber 1975, McGregor et al 1982) Gastro-intestinal tract causes include: • The Zenker diverticle: the accumulation of food and debris in the pouch of the esophagus, not separated from the oral cavity by any sphincter, can cause a significant breath odor (Crescenzo et al 1998) • A gastric hernia can, especially when reflux esophagitis occurs, lead to a disturbing breath odor Otherwise, the stomach never causes breath malodor, contrary to a common opinion among the public and even some clinicians (Norfleet 1993) • Intestinal gas production can also play a role, probably because some gases such as dimethylsulfide are poorly resorbed by the intestinal endothelium and when transported by the blood they can reach 514 • CHAPTER 24 Fig 24-1 The periodontologist, the oto-rhino-laryngologist and the psychologist listen to the patient Fig 24-2 Two calibrated judges evaluate the expired air and com pare their rating the lung tissue and be exhaled in the breath air ( Suarez et al 1999) Other systemic causes (Leopold et al 1990, Preti et al 1995) of breath malodor include renal (uremia) ( Simenhoff et al 1977), pancreatic (acetone) (Booth & Ostenson 1966) and liver (ammonium) (Chen et al 1970) insufficiencies which appear as breath malodors with different characteristics that can be detected by experienced clinicians Some medications such as metronidazole can by themselves cause some breath malodor Periodontologists should keep these possible nonoral causes in mind Their role may be masked to the clinician by the fact that a patient with such a disease may also present, as the vast majority of adults do, with gingivitis or periodontitis DIAGNOSIS Patient history There is a saying "Listen to the patient and he will tell you the diagnosis" This is very true for patients with breath odor complaints Besides what is spontaneously told, the clinician should question about the frequency of odor (e.g does it happen only some weeks), the time of appearance within the day (e.g after meals, which can indicate a hernia), whether others (non-confidants) have identified the problem ( imaginary breath odour?), what kind of medications are taken, whether dryness of the mouth is noticed, etc (Fig 24-1) Several of the points retrieved from this case history, which because of the emotional character of the matter cannot be obtained by a written questionnaire, must be used in the (differential) diagnosis of the problem BREATH MALODOR • 515 Fig 24-3 Nasal examination should be done routinely when the air expired through the nose is malodorous Fig 24-4 The oropharyngeal air is sampled by an electronic apparatus which measures the volatile sulfur components Clinical and laboratory examination causing the problem The judge will smell a series of different air samples (Fig 24-2): Organoleptic Even though some instruments are now available, the best method in the examination of breath malodor is still the organoleptic assessment made by a judge, who has been tested and calibrated for his/her smelling acuity This testing is done by determining the threshold level for detecting a series of dilutions of a malodorous compound such as isovaleric acid The discrimination power of the judge is evaluated by presenting to him/her a series of odors for identification (Doty et al 1984) The use of any fragance, shampoo or body lotion, and smoking, alcohol consumption or garlic intake are strictly forbidden 12 hours before the assessment is made This involves both the patient and the judge The judge will not wear rubber gloves, the odor of which may interfere with the organoleptic assessments Assessments should be performed at several appointments on different days, since breath odor fluctuates dramatically from one day to the next The patient should be encouraged to bring a confidant to the consultations to help him/her identify the odor • Oral cavity odor: the subject opens his/her mouth and refrains from breathing; the judge places his nose close to the mouth opening • Breath odor: the subject breathes out through the mouth; the judge smells both the beginning (determined by the oral cavity and systemic factors) and the end (originating from the bronchi and lungs) of the expired air • Tongue coating scraping: the judge smells the tongue scraping and also presents it to the patient or the accompanying confidant to evaluate whether they associate the smell from the scraping with the malodor complaint • Breath odor when breathing out through the nose: when the air expired through the nose is malodorous, but the air expired through the mouth is not, a nasal/paranasal etiology should be suspected In the oro-pharyngeal examination, the clinician must look for inflammation of the gingiva, or in the mucosa under a prosthesis Fresh extraction wounds or inter- 516 • CHAPTER 24 dental food entrapment can cause breath malodor The pharynx should be thoroughly inspected for the presence of inflamed tonsils The tonsils often present with crypts which may harbor anaerobic bacteria, pus and even calculus (tonsilloliths) Less obvious for a dentist is the examination of the nostrils, although this is essential if the breath malodor is noticed more clearly when the subject breathes out through the nostrils (Fig 24-3) Portable volatile sulfide monitor This is an electronic device that aspirates the air of the mouth or expired air through a straw and analyses the concentration of H2S (hydrogen sulfide) and CH3SH ( methylmercaptan), without discriminating between the two (Fig 24-4) It can also be used to measure the headspace above incubated saliva (Rosenberg et al 1991) The monitor is good for the detection of hydrogen sulfide but less good for methyl mercaptan It needs regular calibrations It should be stressed that this machine will not detect malodorous components such as cadaverine, putrescine, urea, indole, skatole and several others which have been described in salivary headspace ( Kostelc 1981) Cadaverine (produced by bacteria through decarboxylation of lysine to counteract the unfavorable acidic growth conditions during glycolysis) and putrescine (from decarboxylation of ornithine or arginine) are both diamines the level of which in air expired from the mouth does not, evidence shows, correlate with VSC scores (Goldberg et al 1994) but does correlate to a certain extent with tongue coating and/or periodontitis Gas chromatography This can analyse air or incubated saliva or crevicular fluid for any volatile component (Goldberg et al 1994) Some hundred components were isolated, and mostly identified, from saliva and/or tongue coating, from ketones to alkanes and from sulfur-containing compounds to phenyl compounds (Claus et al 1996) Gas chromatography is only available in specialized centers and for identifying non-oral causes such as intestinal (Suarez et al 1999) or bronchial/pulmonary causes TREATMENT An etiologic treatment is to be preferred The treatment of oral malodor consists of the elimination of the pathology present, such as deepened and inflamed periodontal pockets and/or tongue coating If another underlying disease is suspected, or if clinical experts in the different disciplines (internal medicine, periodontology, ENT, psychology, etc.) are not available, it is possible to rapidly (within 1-2 weeks) make a differential diagnosis by performing a full-mouth onestage disinfection of the oro-pharynx, including the use of chlorhexidine spray to deal with the pharynx ( Quirynen et al 2000) Since all oral diseases which cause malodor relate to microorganisms, this onestage professional approach reinforced by stringent home care will dramatically reduce the oro-pharyngeal microbiota and the putrefraction they cause and thus the malodour (Quirynen et al 1998) If the symptoms not disappear, the patient should be referred to a specialized multidisciplinary center where gas chromatography can help in the differential diagnosis Masking of breath malodor should be distinguished from etiological treatment It is well established that zinc-containing mouthrinses have the property to complex the divalent sulfur radicals, reducing this important cause of malodor Thus it appears that the application of a zincchloride/triclosan-containing toothpaste on the tongue dorsum reduces the oral malodor for some hours (Hoshi & van Steenberghe 1996) Baking soda containing dentifrices (> 20%) confers a significant odor-reducing benefit for up to hours (Brunette et al 1998) The use of hydrogen peroxide rinse also offers positive perspectives (Suarez et al 2000) To deal with the tongue coating it appears that tongue brushing with chlorhexidine, be-sides oral rinses with the same antiseptic, reduces the organoleptic scores significantly (Loesche & De Boever 1996) Whether the beneficial effect of tongue brushing is related to the removal of bacteria and/or to the reduction of their substratum, remains an open question Hardly efficient are mints and other short acting " anti-breath" odor components Most of them have not been properly tested in a blind way against a placebo A recent review compared the efficiency of oral rinses, toothpastes and cosmetics for breath odor therapy ( Quirynen et al 2002) When dryness is at stake, any measure to increase the salivary flow may be beneficial This can mean a proper fluid intake or the use of chewing gum to trigger the periodontal-parotid reflex, which originates from the mechanoreceptors in the periodontal ligament of molar teeth (lower) and has the parotid gland as a target (Hector & Linden 1987) The presence of these molars is therefore crucial before advocating the use of chewing gum to enhance salivary secretion The pH of the saliva can also be reduced to increase the solubility of malodorous components (Reingewirtz et al 1999) Evidence shows that the effect is short-lived CONCLUSIONS Breath malodor has important socio-economic consequences A proper diagnosis and determination of the etiology allows the proper etiological treatment to be instituted quickly Although gingivitis, periodontitis and tongue coating are by far the most common causes, other more challenging diseases should not be BREATH MALODOR • 517 overlooked This can be dealt with either by a trial therapy to deal quickly with intra-oral causes (the full-mouth one-stage disinfection) or by a multidisciplinary consultation REFERENCES Booth, G & Ostenson, S (1966) Acetone to alveolar air, and the control of diabetes Lancet II, 1102-1105 Bost' A., Kulkarni, G.V., Rosenberg, M & McCulloch, C.A.G ( 1994) Relationship of oral malodor to periodontitis: evidence of independence in discrete subpopulations Journal of Periodontology 65, 37-46 Brunette, D.M., Ouyang, Y., Glass-Brudzinski, J & Tonzetich, J ( 1996) Effects of methyl mercaptan on human gingival fibroblast shape, cytoskeleton and protein synthesis and the inhibition of its effect by Zn" In: van Steenberghe, D & Rosenberg, M., eds Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, pp 47-62 Brunette, D.M., Proskin, H.M & Nelson, B.J (1998) The effects of dentifrice systems on oral malodor Journal of Clinical Dentistry 9, 76-82 Chen, S., Zieve, L & Mahadevan, V (1970) Mercaptans and dimethyl sulfide in the breath of patients with cirrhosis of the liver Effect of feeding methionine The Journal of Laboratory and Clinical Medicine 75, 628-635 Claus, D., Geypens, B., Rutgeers, P., Ghyselen, J., Hoshi, K., van Steenberghe, D & Ghoos, Y (1996) Where gastroenterology and periodontology meet: determination of oral volatile organic compounds using closed-loop trapping and high-resolution gas chromatography-ion trap detection In: van Steenberghe, D & Rosenberg, M., eds Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, pp 15-27 Coil, J.M (1996) Characterization of volatile sulphur compounds production at individual crevicular sites In: van Steenberghe, D & Rosenberg, M., eds Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, pp 3138 Cresecenzo, D.G., Trastek, V.F., Allen, M.S., Descamps, C & Pairolero, P.C (1998) Zenker's diverticulum in the elderly: is operation justified? Annals of Thoracic Surgery 66, 347-350 Delanghe, G., Ghyselen, J., van Steenberghe, D & Feenstra, L ( 1997) Multidisciplinary breath-odour clinic The Lancet 350, 187 Derogatis, L.R., Lipman, R.S & Covi, L (1973) SCL-90: an outpatient psychiatric rating scale – preliminary report Psychopharmacology Bulletin 9, 13-28 Doty, R.L., Shaman, P., Dann, M (1984) Development of the University of Pennsylvania Smell Identification Test: a standardized microencapsulated test of olfactory function Physiological Behaviour 32, 489-502 Eli, I., Baht, R., Kozlovsky, A & Rosenberg, M (1996) The complaint of oral malodor: possible psychopathological aspects Psychosomatic Medicine 58, 156-159 Goldberg, S., Kozlovsky, A., Gordon, D., Gelernter, I., Sintov, A & Rosenberg, M (1994) Cadaverine as a putative component of oral malodor Journal of Dental Research 73, 1168-1172 Goldberg, S., Kozlovsky, A & Rosenberg, M (1995) Association of diamines with oral malodor In: Rosenberg, M., ed Bad Breath: Research perspectives Tel-Aviv: Ramot Publishing, TelAviv University, pp 71-85 Hector, M.P & Linden, R.W (1987) The possible role of periodontal mechanoreceptors in the control of parotid secretion in man The Quarterly Journal of Experimental Physiology 72, 285-301 Hoshi, K & van Steenberghe, D (1996) The effect of tongue brushing or toothpaste application on oral malodor reduction In: van Steenberghe, D & Rosenberg, M., eds Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, pp 255-264 Howe, J.W (1898) The breath and the diseases which give it a fetid odor, 4th edn New York: D Appleton and Co Kleinberg, I & Codipilly, M (1995) The biological basis of oral malodor formation In: Rosenberg M, ed Bad Breath: Research perspectives Tel-Aviv: Ramot Publishing, Tel-Aviv University, pp 13-39 Kostelc, J.G (1981) Volatiles of exogenous origin from the human oral cavity Journal of Chromatography 226, 315-323 Lancero, H., Niu, J & Johnson, P.W (1996) Thiols modulate metabolism of gingival fibroblasts and periodontal ligament cells In: van Steenberghe, D & Rosenberg, M., eds Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, pp 63-78 Leopold, D.A., Preti, H.J., Monzell, Youngentob, S.L & Wright, H.N (1990) Fish-odor syndrome presenting as dysosmia Archives of Otolaryngology – Head and Neck Surgery 116, 354355 Loesche, W J & De Boever, E (1996) Strategies to identify the main microbial contributors to oral malodor In: van Steenberghe, D & Rosenberg, M., eds Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, pp 41-54 Lorber, B (1975) Bad breath Presenting manifestation of anaerobic pulmonary infection American Reviews of Respiratory Diseases 112, 875-877 McGregor, I.A., Watson, J.D., Sweeney, G & Sleigh, J.D (1982) Tinidazole in smelly oropharyngeal tumours Lancet I, 110 Morris, P.P & Read, R.R (1949) Halitosis: variations in mouth and total breath odor intensity resulting from prophylaxis and antisepsis Journal of Dental Research 28, 324-333 Niles, H & Gaffar, A (1995) Advances in mouth odor research In: Rosenberg, M., ed Bad Breath: Research perspectives TelAviv: Ramot Publishing, Tel-Aviv University, pp 55-69 Norfleet, R.G (1993) Helicobacter halitosis Journal of Clinical Gastroenterology 16, 274 Oxtoby, A & Field, E.A (1994) Delusional symptoms in dental patients: a report of four cases British Dental Journal 176, 140-142 Persson, S., Claesson, R & Carlsson, J (1989) The capacity of subgingival microbiotas to produce volatile sulfur compounds in human serum Oral Microbiology & Immunology 4, 169-172 Persson, S., Edlund, M.B., Claesson, R & Carlsson, J (1990) The formation of hydrogen sulfide and methylmercaptan by oral bacteria Oral Microbiology & Immunology 5, 195-201 Preti, G., Lawley, H J & Hormann, C.A (1995) Non-oral and oral aspects of oral malodor In: Rosenberg, M., ed Bad Breath: Research perspectives Tel-Aviv: Ramot Publishing, Tel-Aviv University, pp 149-173 Quirynen, M., Mongardini, C., De Soete, M., Pauwels, M., Coucke, W & van Steenberghe, D (2000) The role of chlorhexidine in the one-stage full-mouth disinfection treatment of patients with advanced adult periodontitis Long-term clinical and microbiological observations Journal of Clinical Periodontology 27, 578-589 Quirynen, M., Mongardini, C & van Steenberghe, D (1998) The effect of a 1-stage full-mouth disinfection on oral malodor and microbial colonization of the tongue in periodontitis patients A pilot study Journal of Periodontology 69, 374-382 Quirynen, M., Zhao, H & van Steenberghe, D (2002) Review of the treatment strategies for oral malodour Clinical Oral Investigations (in press) Ratkay, L.G., Tonzetich, J & Waterfield, J.D (1996) The effect of methyl mercaptan on the enzymatic and immunological activity leading to periodontal tissue destruction In: van Steen- 518 • CHAPTER 24 berghe, D & Rosenberg, M., eds Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, pp 35-46 Reingewirtz, Y., Girault, O., Reingewirtz, N., Senger, B & Tenenbaum, H (1999) Mechanical effects and volatile sulfur compound-reducing effects of chewing gums: comparison between test and base gums and a control group Quintessence International 30, 319-323 Rosenberg, M (1995) Bad Breath: Research Perspectives Tel-Aviv: Ramot Publishing, Tel-Aviv University, Tel-Aviv, pp 237 Rosenberg, M (1996) Clinical assessment of bad breath: current concepts Journal of American Dental Association 127, 475-482 Rosenberg, M., Kulkarni, G.V, Bosy, A & McCulloch, C.A.G ( 1991) Reproducibility and sensitivity of oral malodor measurements with a portable sulfide monitor Journal of Dental Research 11, 1436-1440 Simenhoff, M.L., Burke, J.F., Saukkonen, J.J., Ordinario, A.T & Doty, R.L (1977) Biochemical profile of uremic breath New England Journal of Medicine 297, 132-135 Suarez, F.L., Furne, J.K., Springfield, J & Levitt, M.D (2000) Morning breath odor: influence of treatments on sulfur gases Journal of Dental Research 79, 1773-1777 Suarez, F., Springfield, J., Furne, J & Levitt, M (1999) Differen- tiation of mouth versus gut as site of origin of odoriferous breath gases after garlic ingestion The American Journal of Physiology 276, G425-430 Tonzetich, J (1977) Production and origin of oral malodor: a review of mechanisms and methods of analysis Journal of Periodontology 48, 13-20 van Steenberghe, D (1997) Breath malodor Current Opinion in Periodontology 4, 137-143 van Steenberghe, D & Rosenberg, M (1996) Bad Breath: a multidisciplinary approach Leuven: Leuven University Press, p 287 Yaegaki, K (1995) Oral malodor and periodontal disease In: Rosenberg, M., ed Bad Breath: Research perspectives Tel-Aviv: Ramot Publishing, Tel-Aviv University, pp 88-108 Yaegaki, K & Sanada, K (1992a) Biochemical and clinical factors influencing oral malodor in periodontal patients Journal of Periodontology 63, 783-789 Yaegaki, K & Sanada, K (1992b) Volatile sulfur compounds in mouth air from clinically healthy subjects and patients with periodontal disease Journal of Periodontal Research 27, 233-238 CHAPTER 25 Periodontal Surgery: Access Therapy JAN L WENNSTROM, LARS HEIJL AND JAN LINDHE Techniques in periodontal pocket surgery Gingivectomy Flap procedures Regenerative procedures Distal wedge procedures Osseous surgery General guidelines for periodontal surgery Objectives, indications, contraindications Local anesthesia Since most forms of periodontal disease are plaqueassociated disorders, it is obvious that surgical access therapy can only be considered as adjunctive to cause -related therapy (see Chapter 20) Therefore, the various surgical methods described below should be evaluated on the basis of their potential to facilitate removal of subgingival deposits and self-performed plaque control and thereby enhance the long-term preservation of the periodontium The decision concerning what type of periodontal surgery should be performed and how many sites should be included is usually made after the effect of initial cause-related measures has been evaluated The time lapse between termination of the initial cause-related phase of therapy and this evaluation may vary from to months This routine has the following advantages: • The removal of calculus and bacterial plaque will eliminate or markedly reduce the inflammatory cell infiltrate in the gingiva (edema, hyperemia, flabby tissue consistency), thereby making assessment of the "true" gingival contours and pocket depths possible • The reduction of gingival inflammation makes the soft tissues more fibrous and thus firmer, which facilitates surgical handling of the soft tissues The propensity for bleeding is reduced, making inspection of the surgical field easier Instruments Selection of surgical technique Root surface instrumentation Root surface conditioning/biomodification Suturing Periodontal dressings Postoperative pain control Postsurgical care Outcome • A better basis for a proper assessment of the prognosis has been established The effectiveness of the patient's home care, which is of decisive importance for the long-term prognosis, can be properly evaluated Lack of effective self-performed care will often mean that the patient should be excluded from surgical treatment TECHNIQUES I N P E R I O D O N T A L POCKET SURGERY Over the years, several different surgical techniques have been described and used in periodontal therapy A superficial review of the literature in this area may give the reader a somewhat confusing picture of the specific objectives and indications relevant for various surgical techniques It is a matter of historical interest that the first surgical techniques used in periodontal therapy were described as means of gaining access to diseased root surfaces Such access could be accomplished without excision of the soft tissue pocket (" open-view operations") Later, procedures were described by which the "diseased gingiva" was excised ( gingivectomy procedures) The concept that not only inflamed soft tissue but also "infected and necrotic bone" had to be eliminated called for the development of surgical techniques by 520 • CHAPTER 25 Fig 25-1 Gingivectomy The straight incision technique (Robicsek 1884) a Fig 25-2 Gingivectomy The scalloped incision technique (Zentler 1918) b Fig 25-3 Gingivectomy Pocket marking (a) An ordinary periodontal probe is used to identify the bottom of the deepened pocket (b) When the depth of the pocket has been assessed, an equivalent distance is delineated on the outer aspect of the gingiva The tip of the probe is then turned horizontally and used to produce a bleeding point at the level of the bottom of the probeable pocket which the alveolar bone could be exposed and resected (flap procedures) Other concepts such as (1) the importance of maintaining the mucogingival complex (i.e a wide zone of gingiva) and (2) the possibility for regeneration of periodontal tissues have also prompted the introduction of "tailor-made" surgical techniques In the following, surgical procedures will be described which represent important steps in the development of the surgical component of periodontal therapy Gingivectomy procedures The surgical approach as an alternative to subgingival scaling for pocket therapy was already recognized in the latter part of the nineteenth century, when Robicsek (1884) pioneered the so-called gingivectomy procedure Gingivectomy was later defined by Grant et al ( 1979) as being "the excision of the soft tissue wall of a pathologic periodontal pocket" The surgical procedure, which aimed at "pocket elimination", was usu- ally combined with recontouring of the diseased gingiva to restore physiologic form Robicsek (1884) and, later, Zentler (1918) described the gingivectomy procedure in the following way: The line to which the gum is to be resected is determined first Following a straight (Robicsek; Fig 25-1) or scalloped (Zentler; Fig 25-2) incision, first on the labial and then on the lingual surface of each tooth, the diseased tissue should be loosened and lifted out by means of a hook-shaped instrument After elimination of the soft tissue, the exposed alveolar bone should be scraped The area should then be covered with some kind of antibacterial gauze or be painted with disinfecting solutions The result obtained should include eradication of the deepened periodontal pocket and a local condition which could be kept clean more easily Technique The gingivectomy procedure as it is employed today was described in 1951 by Goldman • When the dentition in the area scheduled for surgery has been properly anesthetized, the depths of the pathologic pockets are identified with a conven- PERIODONTAL SURGERY: ACCESS THERAPY • 521 Fig 25-4 Gingivectomy (a) The primary incision (b) The incision is terminated at a level apical to the "bottom" of the pocket and is angulated to give the cut surface a distinct bevel Fig 25-5 Gingivectomy The secondary incision through the interdental area is performed with the use of a Waerhaug knife Fig 25-6 Gingivectomy The detached gingiva is removed with a scaler Fig 25-7 Gingivectomy Probing for residual pockets Gauze packs have been placed in the interdental spaces to control bleeding Fig 25-8 Gingivectomy The periodontal dressing has been applied and properly secured tional periodontal probe (Fig 25-3a) At the level of the bottom of the pocket, the gingiva is pierced with the probe and a bleeding point is produced on the outer surface of the soft tissue (Fig 25-3b) The pockets are probed and bleeding points produced at several location points around each tooth in the area The series of bleeding points produced describes the depth of the pockets in the area scheduled for treatment and is used as a guideline for the incision • The primary incision (Fig 25-4), which may be made by a scalpel (blade No 12B or 15; Bard- Parker®) in either a Bard-Parker handle or an angulated handle (e.g a Blake's handle), or a Kirkland knife No 15/16, should be planned to give a thin and properly festooned margin of the remaining gingiva Thus, in areas where the gingiva is bulky, the incision must be placed at a level more apical to the level of the bleeding points than in areas with a thin gingiva, where a less accentuated bevel is needed The beveled incision is directed towards the base of the pocket or to a level slightly apical to the apical extension of the junctional epithelium In areas where the interdental pockets are deeper than 1030 • CHAPTER 45 application of different prophylaxis procedures Clinical Oral Implants Research 7, 64-72 Mombelli, A., Feloutzis, A., Bragger, U & Lang, N.P (2001) Treatment of peri-implantitis by local delivery of tetracycline Clinical, microbiological and radiological results Clinical Oral Implants Research 12, 287-294 Mombelli, A & Lang, N.P (1992) Anti-microbial treatment of peri-implant infections Clinical Oral Implants Research 3, 162168 Mombelli, A., Miihle, T., Bragger, U., Lang, N.P & Burgin, W.B (1997) Comparison of periodontal and peri-implant probing by depth-force pattern analysis Clinical Oral ho plants Research 8, 448-455 Mombelli, A., van Oosten, M.A.C., Schiirch, E & Lang, N.P (1987) The microbiota associated with successful or failing ossoeintegrated titanium implants Oral Microbiology and Irnmunolaq-rI 2, 145- 151 Persson, L.G., Araujo, M., Berglundh, T., Grondahl, K & Lindhe, J (1999) Resolution of peri-impatitis following treatment An experimental study in the dog Clinical Oral Implants Research 10, 195-203 Taylor, A.C & Campbell, M.M (1972) Reattachment of gingival epitheolium to the tooth Journal of Periodontology 43, 281-293 Wetzel, A.C., Vlassis, J., Caffesse, R.J., Hammerle, C.H.F & Lang, N.P (1999) Attempts to obtain re-osseointegration following experimental peri-implantitis in dogs Clinical Oral Implants Research 10,111-119 Index abscesses, 240 periodontal, 240-66, 333 classification, 240-41 complications, 266 diagnosis, 262-4 microbiology, 262 pathogenesis and histopathology, 261-2 prevalence, 261 treatment, 264-5 abutment selection, 863 access therapy, 519-58 anesthesia, 538-40 comparison with non-surgical therapy, 552-8 contraindications for, 537-8 distal wedge procedures, 531-4 dressings, 549-50 flap procedures, 522-31, 544 general guidelines, 535-46 gingivectomy, 52022, 543-4, 550-51 healing after, 550-52 indications for, 535-7 instruments, 540-43 objectives, 535 osseous surgery, 534 outcome, 550-58 postoperative pain, 539, 550 postsurgical care, 550 regenerative procedures, 531 root surface conditioning/biomodification, 546-50 root surface instrumentation, 545-6 selection of technique, 543-5 suturing, 546-9 acidified sodium chlorites, 475 Actinobacillus actinomycetemcornitans, 70, 71, 107, 113, 114 -16, 120, 127, 129, 133, 134-5, 136, 137, 138, 172, 375, 389, 494, 497, 681 aggressive periodontitis, 169, 217, 225, 226-7, 228, 235, 238 antibiotics and, 499, 500, 501, 502-3 chronic periodontitis, 169 diabetes and, 182 effects of therapy on, 563, 568, 571 linear gingival erythema (LGE) and, 274 peri-implantitis and, 1020 periodontal abscesses, 262 virulence, 164 Actinomyces spp., 84, 126-7, 262, 266, 568 A naeslundii, 129, 133, 136 A odontolyticus, 127, 565 A viscosus, 111 acute necrotizing ulcerative gingivitis (ANUG), 108-9, 110, 111, 130, 189, 205-7, 243 additional (corrective) therapy, planning, 420-22 adrenal function, 538 adrenaline (epinephrine), 539 adult periodontitis, 54-7 advanced flap procedures, 597-601 aesthetics, see esthetics age chronic periodontitis and, 211 implants and, 853-4 necrotizing periodontal disease and, 255 aggressive periodontitis, 54, 216-38 classification and clinical syndromes, 217-18 diagnosis, 2337 epidemiology, 218-25 permanent dentition, 220-21 primary dentition, 219-20 screening, 221-5 etiology and pathogenesis, 225-32 generalized (GAP), 217, 227-8, 234, 235 genetic predisposition, 231-2, 237, 388 immune system and, 226, 228-30, 235-7 localized (LAP), 58, 60-61, 217-18, 234, 235, 502-3 pathogens, 225-32, 235, 238 radiography, 223-4 treatment, 237-8 antibiotic therapy, 238, 501-3 agranulocytosis, 538 AIDS, see HIV infection and AIDS alcohol amine alcohols, 475 necrotizing periodontal disease and, 255 allergic reactions, 286-7, 400 alveolar hone, 3, 27, 34 42 angular bone defects, 557-8, 731 infrabony pockets, 752-4 assessment of loss, 52 basic bone biology, 866-7 defect closure, 885 dehiscence, 36, 889 examination of patients, 409-10 fenestration, 36, 889 formation, 866-94 grafts, 654, 663-7, 876-7 guided tissue regeneration (GTR), 877-84 bone regeneration with GTR, 892-4 clinical applications, 885-92 healing, 867-77 osseous surgery, 534 radiography, 52, 409-10 regeneration adjacent to implants, 879 regenerative capacity of bone cells, 657 1032 • INDEX alveolar bone (contd) ridge augmentation, 631—44, 767—8, 880—83, 885—9, 897— 913 sequestrum formation in necrotizing periodontal disease, 246 see also implants alveolar crest, 28 alveolar mucosa, 5, ameloblastoma, 306—7 amine alcohols, 475 amoebae, 108 amoxicillin, 499, 500, 501, 502, 503, 566—8, 571 anatomy furcation involvement, 706—8 gingiva, 5—27 periodontium, 3—49 anchoring implants, 1004—12 direct and indirect orthodontic implant anchorage, 1009—12 orthodontic implant anchorage (OIA), 1007—9 orthodonticprosthetic implant anchorage (OPIA) technique, 1006—7 anemia, 538 anesthesia, 538—40 angina pectoris, 537 angular bone defects, 557—8, 731 infrabony pockets, 752—4 angulated abutments, 970 ankylosis, 336 anterior single-tooth replacement, 917—18, 919—31 antiadhesive agents, 468 antibiotics, 494—507 aggressive periodontitis, 238, 501—3 biofilms and, 124—5 characteristics of infection and, 495—6 clinical trials, 501—6 local therapy, 503—6 systemic therapy, 501—3 comparison of treatment methods, 506—7 delivery routes, 497—9 effects of treatment, 565—8 evaluation for periodontal therapy, 499—507 infection concepts and treatment goals, 496—7 necrotizing periodontal disease, 256 plaque control agents, 471 post-therapy periodontal abscesses, 261 principles for antibiotic therapy, 494—9 treatment of periodontal abscesses, 265 use in pregnancy, 186 anticoagulant therapy, 537, 854 antiseptics for supragingival plaque control, 464—87 agents, 471—5 approaches, 468—9 chlorhexidine, 473, 475, 476—81 clinical trial design, 485—7 evaluation of, 481—5 history, 466—7 rationale for, 467—8 vehicles for delivery, 469—71 apically repositioned flap, 525—6, 551 arterial hypertension, 537 articain, 538—9 atheromatic plaque, 71, 375 atherosclerosis, periodontal disease and, 70—72, 370, 375 attached gingiva, 6, 7—8, 10—11 augmentation gingiva, 577—92 healing after, 589—92 indications for, 586—7 procedures, 587—9 ridge augmentation, 631—44, 767—8, 880—83, 885—9, 897— 913 bacteria antiseptics against, 468—9 atheroma tic plaque, 71 dental plaque, 63—4, 66, 81—2, 87, 89—90, 92—3, 95, 97—8, 111, 190 effect of therapy on, 561—72 gingival lesions, 269 peri-implantitis, 1020—21 periodontal disease, 63—4, 66, 72, 82, 106—39 aggressive periodontitis, 225—32, 235, 238 chronic periodontitis, 211 current suspected pathogens, 112—22 historical perspectives, 108—12 mechanisms of pathogenicity, 135—9 necrotizing periodontal disease, 251—3 periodontal abscesses, 261—2 prerequisites for disease initiation and progression, 132—5 transmission, 129—31 pneumonia, 380 vaginosis, 376 see also individual species Bacteroides forsythus, 64, 66, 70, 71, 72, 73, 107, 114, 117—18, 126, 127, 129, 138 aggressive periodontitis and, 227 effects of therapy on, 563, 564, 565, 568, 571 peri-implantitis and, 1020 periodontal abscesses, 262 Bacteroides melaninogenicus,110, 252 barrier materials guided tissue regeneration (GTR), 673—4 root coverage combined with membrane barriers, 601—3 basic periodontal examination (BPE), 416 benign mucous membrane pemphigoid (BMMO), 280—82 benzylconium chloride, 473 beta-tricalcium phosphate, 666 beveled flap, 527 Bifidobacterium spp., 262 bioactive glasses, 666 biofilms, 85, 107, 122—32, 368, 496, 1020 antiadhesive agents, 468 dental plaque as, 85, 107, 125—32, 175, 449, 561, 571—2 factors affecting composition, 127—32 microbial complexes, 126—7 properties of, 123—5 bisbiguanide antiseptics, 473 chlorhexidine, 473, 475, 476—81 blood clotting, 869 blood supply to periodontium, 43—6 Bohn's nodules, 313 bone alveolar, see alveolar bone basic bone biology, 866—7 bone multicellular unit, 41, 867 grafts, 654, 663—7, 876—7 healing, 867—77 lining cells, 866 INDEX • 1033 bone (contd) modeling and remodeling, 867 osteoblasts, 21, 39, 40, 866 osteocytes, 38–9, 40, 858, 866 regeneration adjacent to implants, 879 Borrelia spp., 252 breath malodor (halitosis), 457–8, 512–17 diagnosis, 514–16 etiology and pathophysiology, 513–14 socio-economic aspects, 512–13 treatment, 516 bronchitis, 380 brushing, 450–53, 465–6 electric toothbrushes, 453, 466 frequency and effectiveness, 452–3 interproximal brushes, 455–7 methods, 451–2 toothbrush wear and replacement, 453 trauma from, 459, 579, 580 buccal nerve, 48 bundle bone, see alveolar bone burns, 291 calcifying fibroblastic granuloma, 300–301 calcium channel blockers, 203, 204 calculus, see dental calculus Campylobacter spp., 107, 226, 262 C concisus, 127 C gracilis, 127, 135 C rectus, 107, 120, 127, 134, 135, 182, 274, 565 C shozaae, 127, 129 cancer, see tumors cancrum oris, 243 Candida spp., 272–4, 275 C albicans, 181, 252, 272–4 candidosis, 272–4, 480 cantilever units, 952–4 Capnocytophaga spp., 127, 134, 137, 182, 225, 262, 319, 565 C sputigena, 227 cardiovascular disease contraindication for surgery, 537 implants and, 854 periodontal disease and, 70–72, 370–76, 382–3 caries, see dental caries case presentation, 418–19 cause-related therapy, 432–47 evaluation of effects, 446–7 healing after, 441–6 methods, 432–41 objectives, 432 planning, 414, 419 cell mediated immune response, 170–71 cemented multiple-unit posterior implant prostheses, 968–70 cementoblastoma, benign, 308 cementoblasts, 21 cementoma, 302 cementum, 3, 31–4 cephalosporins, 499 ceramic implant restorations, 970–71 cerebrovascular disease, periodontal disease and, 70–72 cervical root resorption, 201 cetylpyridinium chloride, 471, 473 Chediak Higashi syndrome, 168 chemical injuries, gingival lesions and, 289 chemical treatments, see antiseptics chemotactic cytokines, 167 chemotherapy, 854 chewing gum, 470 children /adolescents implants and, 853-4, 1011–12 periodontal disease in, 57–61 aggressive periodontitis, 219–24, 388 Chlamydia pneumoniae, 375 chlorhexidine, 473, 475, 476–81, 506 clinical uses, 479–81 mechanism of action, 478 products, 478–9 staining, 477–8 toxicology, safety and side effects, 476–7 chronic obstructive pulmonary disease (COPD), 380 chronic periodontitis, 209–15 genetic predisposition, 213, 388 pathogens, 211 risk factors, 211–13 treatment, 213–15 antibiotic therapy, 501–2 scientific basis, 213–14 cigarettes, see tobacco smoking ciprofloxin, 499, 501 clavulanic acid, 499, 501, 502 clear cells, 11 clindamycin, 499, 500, 501, 502 Clostridium difficile, 501, 502 col, collagen fibers, 21, 22, 28–30, 42, 166 Community Periodontal Index for Treatment Needs (CPITN), 52, 53–4, 61, 73 complement, 165 computed tomography, 845 connective tissue, see lamina propria contraceptives, hormonal, 187–8 coping behaviors, 68 copper salts, 474 coronally advanced flap procedure, 597, 598–9, 600–601 coronary heart disease, see cardiovascular disease Crohn's disease, 287 cross-arch bridge restoration, 991–6 cross-sectional tomography, 841, 842–5 crown lengthening procedures, 619–30 ectopic tooth eruption, 628–30 excessive gingival display, 619–22 exposure of sound tooth structure, 622–8 cumulative interceptive supportive therapy (CIST), 1026–9 curettes, 433, 542 cyclic neutropenia, 168, 203 cyclosporin A, 203, 204, 537–8 cystic fibrosis, 391–2 cysts, 298, 312–16 cytokines, 166–7, 170–71, 174, 182 cytomegalovirus, 121 dehiscence, alveolar bone, 36, 889 delmopinol, 475 dental artery, 43 dental calculus, 98–103 attachment to tooth surfaces and implants, 100 clinical appearance, 98 clinical implications, 102–3 diagnosis, 99–100 • INDEX dental calculus (contd) distribution, 98–9 mineralization, 100, 101 structure, 101–2 dental caries, 107, 480 tooth loss and, 61 dental organ, dental plaque, 81–98, 150 bacteria, 63–4, 66, 81–2, 87, 89–90, 92–3, 95, 97–8, 111, 190 as biofilm, 85, 107, 125–32, 175, 449, 561, 571–2 factors affecting composition, 127–32 chemical control, 464–87 agents, 471–5 approaches, 468–9 chlorhexidine, 473, 475, 476–81, 506 clinical trial design, 485–7 evaluation, 481–5 history, 466–7 rationale for, 467–8 vehicles for delivery, 469–71 chronic periodontitis and, 211 disclosing agents, 459–60 factors affecting composition, 127–32 formation, 83-4, 465 gingivitis and, 198–207, 465, 782 non-specific plaque hypothesis, 82, 110 orthodontics and, 749 peri-implant, 98 removal of plaque-retention factors, 441 scaling, 432, 563 structure, 85–98 subgingival, 82, 90–98 removal, 434–8 supragingival, 82, 85–90 removal, 433, 449–61, 568–71 tobacco smoking and, 190 trauma from occlusion and plaque-associated periodontal disease, 352–65 see also dental calculus dental restorations, 793 allergic reactions to, 286 distally shortened arch with fixed implant-supported prostheses, 950–57 furcation involvement and, 723 gingival dimensions and, 586 gingivitis and, 200–201 radiography after installation, 847 removal of plaque-retention factors, 441 ridge augmentation and, 630, 633–4, 643 root separation and resection (RSR) and, 720, 723 see also implants dentifrices/toothpastes, 458–9, 466–7, 469–70, 479 dentin hypersensitivity, 341–4, 651 dento-gingival epithelium, 16–19 denture stomatitis, 480 desmosomes, 13–14 detergents, 474–5 diabetes mellitus, 179–83, 791 clinical symptoms, 180 gingivitis and, 203 implants and, 854 periodontal disease and, 67–8, 73, 134–5, 180–83, 378–80 chronic periodontitis, 212 surgery and, 538 types, 180 diagnosis breath malodor (halitosis), 514–16 cysts, 298, 312–16 dental calculus, 99–100 endodontic lesions, 344–6 furcation involvement, 708–11 differential, 711–12 gingivitis, 410 implant maintenance, 1024–6 periodontal disease, 410–12, 416 aggressive periodontitis, 233–7 necrotizing periodontal disease, 249–50 periodontal abscesses, 262–4 tumors, 298–312 digital intraoral radiography, 850 disclosing agents, 459–60 distal wedge procedures, 531–4 distally shortened arch, implants and, 950–57 doxycycline, 501, 502, 504 dressings, 549–50 drugs, see medication dysplasia, periapical cemental dysplasia, 302–3 ectomesenchyme, 3–4, ectopic tooth eruption, 628–30 edentulous ridge deformed, 630–44 correction of ridge defects with soft tissue grafts, 631–44 prevention of soft tissue collapse following tooth extraction, 630–31 Eikenella corroders, 120, 127, 135, 225, 389, 502 elastase, 169 elastic fibers, 22 electric toothbrushes, 453, 466 embryonic development, periodontium, 3–5, 24, 34, 37 enamel enamel pearls, 200 mesiodital enamel reduction, 771–2 endodontic lesions, 318 combined with periodontal lesions, 346–7 differential diagnosis, 344–6 in marginal periodontium, 323–6 endodontic treatment impact on periodontium, 326–33 root separation and resection (RSR) and, 720 endogenous infections, 82 endopeptidases, 165, 166 endothelial cells, leukocytes and, 169 Enterobacter agglornerans, 121 Enterobacter cloacae, 121, 513 environmental factors aggressive periodontitis and, 232 see also tobacco smoking enzymes, 471–2 epidemiology of periodontal diseases, 50–74 aggressive periodontitis, 218–25 permanent dentition, 220–21 primary dentition, 219–20 screening, 221–5 methodological issues, 50–54 critical evaluation, 52–4 examination methods, 50–52 index systems, 50–52 prevalence, 54–61, 73 INDEX • 1035 epidemiology of periodontal diseases (contd) adult periodontitis, 54—7 children/adolescent periodontitis, 57—61 tooth loss and periodontitis, 61 risk factors, 61—70, 387 chronic periodontitis, 211—13 diabetes mellitus, 67—8 HIV infection, 68 hormonal changes, 179, 183—8 longitudinal studies, 68—70 multiple factors, 61, 63—4 other factors, 68 tobacco smoking, 64—7, 70, 135, 189—92 systemic disease and periodontal disease, 70—73, 74, 203, 212—13 epilepsy, 538 epinephrine (adrenaline), 539 epinutin ( phenytoin sodium), 203, 204 epithelium dento-gingival, 16—19 epithelial mesenchymal interaction, 24—7 innate defense system, 165, 175 oral, 8—15 periodontal wound healing and, 659 Epstein Barr virus, 121 Epstein's pearls, 313 epulis, 298 pregnancy granuloma, 185, 202 eruption ectopic, 628—30 forced, 756—9 erythema multiforme, 283—4 erythromycin, 499 Escherichia coil, 107, 376—7 essential oils, 473 esthetics implants, 766—8, 915—40 orthodontics and, 751, 766—8 estrogen (oestrogen), 183, 186, 187 ethnicity, necrotizing periodontal disease and, 255 Eubacterium spp., 121, 319 E nodatum, 107, 121, 127 examination of patients, 50-52, 403-13, 798 alveolar bone, 409—10 diagnosis of periodontal lesions, 410—12 gingiva, 404—6 oral hygiene status, 412 periodontal ligament and root cementum, 406—9 prior to implants, 852—7 exopeptidases, 165 Extent and Severity Index, 51—2 external inflammatory root resorption (EIRR), 337, 339 extraction of teeth furcation involvement and, 726 implants immediately after, 853, 879—80, 889—92, 975—6 prevention of soft tissue collapse following tooth extraction, 630—31 extravascular circulation, 46 extrusion of single teeth (forced eruption), 756—9 felypressin, 539 fenestration, alveolar bone, 36, 889 fever, necrotizing periodontal disease and, 248 fiberotomy, 772 fibroblasts, 19 fibroma calcifying fibroblastic granuloma, 300—301 focal fibrous hyperplasia, 298—300 fibromatosis, gingival, 275—6 fillings, see dental restorations flap procedures access therapy, 522—31, 544—5 advanced flap, 597—601 apically repositioned flap, 525—6, 551 beveled flap, 527 implants, 857—8 modified flap operation, 524 modified Widman flap, 528, 529, 551—2 Neumann flap, 522—3 original Widman flap, 522 papilla preservation flap, 530—31 ridge augmentation, 897 roll flap procedure, 633—4 root coverage, 597—610 rotational flap, 597 suturing, 546—9 flossing, 454—5 fluorides, 474 focal fibrous hyperplasia, 298—300 focal infection theory, 74 food, allergic reactions, 287 forced eruption, 756—9 foreign bodies gingival lesions, 291 periodontal abscesses and, 261 fractured roots, 201, 330—33, 1002—3 free gingiva, 6, free gingival groove, free gingival margin, 5, 6, frenotomy, 772—4 fungal diseases, gingival lesions, 272—5 furcation involvement, 651, 705—29, 793 anatomy, 706—8 assessment of, 409 diagnosis, 708—11 differential, 711—12 orthodontics and, 766 prognosis, 726—9 terminology, 705-6 treatment, 712-26 extraction, 726 furcation plasty, 712 guided tissue regeneration (GTR), 683—9, 724—6 prosthetic restoration, 723 regeneration of furcation defects, 683—9, 723—6 root separation and resection, 714—23 scaling and root planing, 712 tunnel preparation, 713—14 fusiform bacteria, 108—9, 110 Fusobacterium spp., 84, 252, 319, 565 F nucleatann, 107, 119—20, 127, 134, 135, 138, 262, 266, 274, 389, 513, 1020 F periodonticum, 127 gastro-intestinal diseases breath malodor (halitosis) and, 513—14 gingival lesions and, 287 gels, 478—9 generalized aggressive periodontitis (GAP), 217, 227—8, 234, 235 • INDEX genetics and genetic disorders, 391–2, 791 gingival lesions, 275–6 human genes and polymorphisms, 390–91 periodontal disease, 387–97 aggressive periodontitis, 231-2, 237, 388 chronic periodontitis, 213, 388 cytokine gene polymorphisms, 392–6 evidence, 388–90 FCy gene polymorphisms, 396–7 gene modification, 392 major gene associated with, 392 twin model, 388–90 giant cell fibroma, 299 giant cell granuloma, 301–2 gingiva, 3, 5–27, 152 attached gingiva, 6, 7–8, 10–11 augmentation, 577–92 healing after, 589–92 indications for, 586–7 procedures, 587–9 blood supply, 43, 44 dento-gingival epithelium, 16–19 dimensions and periodontal health, 577-9, 586 enlargement, 204–5 epithelial mesenchymal interaction, 24–7 examination of patients, 404–6 excessive gingival display, 619–22 free gingiva, 6, inflammation, see gingivitis lamina propria, 19–24 macroscopic anatomy, 5–8 microscopic anatomy, 8–27 nerves, 48, 49 oral epithelium, 8–15 recession, 556–7, 579–86, 594, 650 orthodontics and, 583–6, 768–72 symptoms of periodontal disease, 403 transmucosal attachment of implants, 829–37 gingival cysts, 313 Gingival Index, 51 gingival invaginations, removal of, 774–6 gingival lesions, 269–91 bacterial origin, 269 fungal origin, 272-5 genetic origin, 275-6 systemic origin, 277–89 trauma, 289–91 viral origin, 269–72 Gingival Sulcus Bleeding Index, 51 gingivectomy, 520–22, 543–4, 550–51, 776–8 gingivitis, 54, 81, 82, 84–5, 151, 154, 155, 175 dental plaque and, 198–207, 465, 782 diagnosis, 410 histopathological features, 155–7, 200 hormonal changes and, 184-6, 201–2 local contributing factors, 200–201 malnutrition and, 202–3 medication and, 203–5 necrotizing periodontal disease and, 254 necrotizing ulcerative gingivitis (NUG/ANUG), 108-9, 110, 111, 130, 189, 205–7, 243 stages, 155–63 supportive periodontal therapy (SPT) and, 786 systemic conditions and, 203 treatment, 201 grafting procedures bone grafts, 654, 663–7, 876–7 correction of ridge defects with soft tissue grafts, 631–44 gingival augmentation, 588–9, 592 regenerative therapy and, 662–7 allogenic grafts, 664–5 alloplastic materials, 665–7 autogenous grafts, 663–4 biologic concept, 667 xenogenic grafts, 665 root coverage, 597–610 combined with membrane barriers, 601–3 free soft tissue graft procedures, 605–10, 616 healing, 613–16 pedicle soft tissue graft procedures, 597–604, 613–16 granuloma calcifying fibroblastic granuloma, 300–301 peripheral giant cell granuloma, 301–2 pregnancy, 185, 202 pyogenic granuloma, 301 greater palatal nerve, 48 greater palatine artery, 43 growth regulatory factors, 668–9 guided tissue regeneration (GTR), 669–94, 695, 762–3, 877 84 barrier materials, 673–4 bone regeneration with GTR, 892–4 clinical applications, 885–92 combined with other regenerative procedures, 689–92 evaluation of, 692–4 furcation involvements, 683–9, 724–6 intrabony defects, 674–83 procedural guidelines, 671–3 halitophobia, 512 halitosis, see breath malodor (halitosis) hand instruments, 433–9 healing after cause-related therapy, 441–6 after implants, 862–3 after insertion of osseointegrated implants, 810–18 bone, 867–77 following surgery, 550–52, 589–92, 613–16 regenerative therapy and, 652–61 tobacco smoking and, 192 transmucosal attachment of implants, 829–37 heart disease, see cardiovascular disease Helicobacter pylori, 571 hemangioma, 303 Henrophilus influenzae, 106, 380 Hemophilus parainfluenzae, 513 herbal products, 474 hereditary gingival fibromatosis, 275–6 herpes viruses, 121, 269–72 herpes zoster, 270, 272 primary herpetic gingivostomatitis (PHG), 249–50, 270–72 Hertwig's epithelial root sheath, hexetidine, 475 high-strength all-ceramic implant restorations, 970–71 histiocytosis X, 311–12 histopathology benign neoplasms of periodontal hard tissues, 307, 308 benign neoplasms of periodontal soft tissues, 303, 304, 305 INDEX • 1037 histopathology (coutd) cysts, 313, 314, 315-16 focal fibrous hyperplasia, 299 gingivitis, 155-7, 200 granulomas, 301, 302 malignant neoplasms of periodontal hard tissues, 311, 312 malignant neoplasms of periodontal soft tissues, 309, 310 necrotizing periodontal disease, 250-51 periapical cemental dysplasia, 303 periodontal abscesses, 261-2 symptoms of periodontal disease, 403 Histoplasma capsulatum, 275 histoplasmosis, 275 HIV infection and AIDS, 107, 571 implants, 854 Kaposi's sarcoma and, 310 linear gingival erythema (LGE) and, 274 periodontal disease and, 68, 134 chronic periodontitis, 212 necrotizing periodontal disease, 244, 252, 253-4, 256 hoes, 433 hormonal changes, 179, 183-8 chronic periodontitis and, 212 contraceptives, 187-8 hormone replacement therapy, 68, 186, 187 menopause, 179, 183, 186-7, 212 menstruation, 184, 202 pregnancy, 179, 183, 184-6, 201-2 puberty, 179, 183, 184, 202 humoral immune response, 169-70 hydrogen peroxide, 474 hydroxyapatite, 665-6, 826 hygiene, see oral hygiene hyperplasia focal fibrous, 298-300 gingival, 204, 275-6 hypersensitivity root dentin, 341-4, 651 to antibiotics, 500 see also allergic reactions hypertension, 537 immune system, 154-5, 163, 164, 165-75 acute necrotizing ulcerative gingivitis (ANUG), 206-7 adaptive defense system, 169-75 aggressive periodontitis and, 226, 228-30, 235-7 cell mediated immune response, 170-71 chronic periodontitis and, 212 diabetes mellitus and, 182-3 humoral immune response, 169-70 innate defense system, 165-9, 172, 175 necrotizing periodontal disease and, 253 overcoming host defense mechanisms, 137 protective role, 172 regulation processes, 172-5 specific antibody responses, 172 tobacco smoking and, 190-91 implants, 809-18, 821 angulated abutments, 970 anterior single-tooth replacement, 917-18, 919-31 basic concepts, 915-18, 945-50 bone regeneration adjacent to, 879 cantilever units, 952-4 cemented multiple-unit posterior implant prostheses, 968-70 clinical applications, 965-75 clinical reality, 817-18 combination of implant and natural tooth support, 954 development, 809-10 distally shortened arch, 950-57 early tissue response, 810-13 esthetics of, 766-8, 915-40 excessive load, 1014 failures, 1014 future, 818 high-strength all-ceramic implant restorations, 970-71 immediately after extraction of teeth, 853, 879-80, 889 -92, 975-6 impressions, 968 indications for, 947-50 load carrying, 945-76 excessive load, 1014 maintenance, 1024-9 cumulative interceptive supportive therapy (CIST), 1026-9 diagnostic process, 1024-6 goals, 1024 mechanical and biologic viewpoints, 813-17 mucositis, 1014, 1015-16 multiple-unit anterior fixed implant restorations, 931-4 multiple-unit tooth-bound posterior implant restorations, 958-61 orthodontics and, 766-8, 971-5 anchoring, 1004-12 peri-implantitis, 1015, 1016-19 microbiology, 1020-21 treatment, 1019-20 posterior single-tooth replacement, 961-5 radiography and, 838-50 postoperative, 847-50 preoperative, 838-47, 855 rehabilitation and, 980-1003 cross-arch bridge restoration, 991-6 fixed restorations on implants and teeth, 984-7 restoration of mandible function, 980-83 restoration of maxilla function, 987-90 solving restorative problems during maintenance therapy, 997-1002 solving root fracture problems, 1002-3 scalloped implant design, 936 screw-retained implant restorations, 965-8 segmented fixed implant restorations, 936 sites with extended horizontal deficiencies, 925-8, 934, 954-5 sites with limited vertical bone volume, 964 sites with localized horizontal deficiencies, 925 sites with major vertical tissue loss, 928-31, 934 sites without significant tissue deficiencies, 921-5, 932-4 surgery, 852-63 abutment selection, 863 bone drilling, 858-9 cortical stabilization, 861-2 flap design, 857-S healing time, 862-3 implant direction, 860-61 implant position, 859-60 implant selection, 862 preoperative examination, 852-7 1038 • INDEX implants (contd) titanium, 821-8, 829, 879 transmucosal attachment, 829-37 normal peri-implant mucosa, 829-36 probing gingiva and peri-implant mucosa, 836-7 impressions, 968 inferior alveolar nerve, 48 inflammation assessment of, 51 periodontopathogens and inflammatory reaction, 163, 175 inflammatory cells, 11, 21 inflammatory paraental cysts, 314 infrabony pockets, 752-4 infraorbital nerve, 48 initial therapy, see cause-related therapy initial treatment plan, 416-17 innate defense system, 165-9, 172, 175 instruments scaling and root planing, 433-41 hand, 433-9 laser, 441 reciprocating, 440-41 rotating, 439-40 ultrasonic and sonic, 439 surgical, 540-43 interdental cleaning, 454-7, 465, 466 interproximal brushes, 455-7 intrabony defects, guided tissue regeneration (GTR), 674-83 intraseptal artery, 43 intrusion of single teeth, 759-62 irrigation devices, 457, 470, 481 irritation fibroma, 298 Kaposi's sarcoma, 310 keratinocytes, 11, 12, 14, 15 keratocysts, 314-15 Klebsellia oxytoca, 121 Klebsellia pneumoniae, 107, 121 knives, surgical, 541-2 Lactobacillus spp., 319 lactoferrin, 165, 169 lamina propria, 19-24 cells, 19-21 regenerative capacity, 658 fibers, 21-3 matrix, 23-4 Langerhans cells, 11, 12, 170, 175 Langerhans cell disease, 311-12 laser instruments, 441 lateral periodontal cysts, 313-14 Legionella pneumophilia, 107 leukemia, 203, 212, 250, 287-9, 538 leukocytes endothelial cells and, 169 polymorphonuclear (PMN), 21, 167-9, 175, 182, 191, 212 lichen planus, 275, 277-80, 854 lidocaine, 538-9 linear gingival erythema (LGE), 274-5 lining mucosa, liver insufficiency, 514 load carrying implants, 945-76 excessive load, 1014 local anesthesia, 538-40 localized aggressive periodontitis (LAP), 58, 60-61, 217-18, 234, 235, 502-3 long sphenopalatine nerve, 48 loss of teeth dental caries and, 61 periodontal abscesses and, 266 periodontal disease and, 61, 213 risk assessment and, 791 lungs chronic obstructive pulmonary disease (COPD), 380 see also respiratory infections lupus erythematosus (LE), 284 lymphatic system necrotizing periodontal disease and, 246, 248 periodontium, 47 lymphocyte signaling cytokines, 167 lymphocytes, 21 lymphogranulomatosis, 538 lymphoma, malignant, 310 macrophages, 20 maintenance implants, 1024-9 cumulative interceptive supportive therapy (CIST), 1026-9 diagnostic process, 1024-6 goals, 1024 see also supportive periodontal therapy (SPT) malnutrition chronic periodontitis, 212 gingivitis and, 202-3 necrotizing periodontal disease and, 254 mandible function restoration, 980-83 mast cells, 19-20 masticatory mucosa, see also gingiva matrix metalloproteinases (MMP), 166 maxilla function restoration, 987-90 medication chronic periodontitis and, 212, 213 drug induced mucocutaneous disorders, 284-6 gingivitis and, 203-5 implants and, 855 melanocytes, 11, 14 membrane barriers, grafting procedures and, 601-3 menopause, 179, 183, 186-7, 212 menstruation, 184, 202 mental nerve, 48 mepivacaine, 538-9 Merkel's cells, 11, 12 mesiodital enamel reduction, 771-2 metal salts, 474 metastatic tumors, 309 metronidazole, 499, 500, 501, 503, 504-5, 566-8, 571 microbiology; see bacteria mineralization of dental calculus, 100, 101 minocycline, 504 mobility of implants, 1026 mobility of teeth, 731-43, 793-4 assessment of, 409 clinical assessment, 733-4 initial and secondary, 731-3 treatment, 734-43 modified flap operation, 524 INDEX • 1039 motion tomography, 842 mouthrinses, 466, 470, 478 mucogingival junction/line, 6, mucogingival therapy, 576—644 crown lengthening procedures, 619-30 ectopic tooth eruption, 628—30 excessive gingival display, 619-22 exposure of sound tooth structure, 622—8 deformed edentulous ridge, 630—44 correction of ridge defects with soft tissue grafts, 631—44 prevention of soft tissue collapse following tooth extraction, 630—31 gingival augmentation, 577—92 healing after, 589—92 indications for, 586—7 procedures, 587—9 interdental papilla reconstruction, 616—19 root coverage procedures, 592—616 clinical outcome, 610—16 grafting procedures, 597—610 healing after, 613—16 mucositis, 1014, 1015—16 multiple sclerosis, 538 multiple-unit anterior fixed implant restorations, 931—4 multiple-unit tooth-bound posterior implant restorations, 958—61 Mycobacterium chelonae, 269 Mycobacterium tuberculosis, 106, 107 myocardial infarction, 537 necrotizing periodontal disease, 243—57 clinical characteristics, 244—9 acute and recurrent forms, 249 development of lesions, 244 fever and malaise, 248 interproximal craters, 244, 246 involvement of alveolar mucosa, 246 oral hygiene, 248—9 sequestrum formation, 246 swelling of lymph nodes, 246, 248 diagnosis, 249—50 histopathology, 250—51 microbiology, 251—3 nomenclature, 243 predisposing factors, 253—5 prevalence, 243—4 treatment, 255—7 acute phase, 255—7 maintenance phase, 257 necrotizing ulcerative gingivitis (NUG/ANUG), 108-9, 110, 111, 130, 189, 205—7, 243 Neisseria gonorrhea, 269 Neisseria meningitidis, 106 neoplasia, see tumors nerves gingiva, 48, 49 periodontium, 48—9 Neumann flap, 522—3 neutrophil collagenase, 166 neutrophilic granulocytes (polymorphonuclear leukocytes), 21, 167—9, 175, 182, 191, 212 nevus, 304 non-specific plaque hypothesis, 82, 110 nutritional deficiencies, see malnutrition occlusal therapy, 731—43 occlusion trauma from, 352—65 clinical symptoms, 731 definitions and terminology, 352 furcation involvement and, 712 jiggling-type trauma, 359-64 orthodontic trauma, 356—9 orthodontics and, 763—6 octopenol, 475 odontogenic keratocysts, 314—15 odontogenic tumors peripheral, 305—6 squamous, 307—8 oestrogen (estrogen), 183, 186, 187 opportunistic infections, 82 oral epithelium, 8—15 oral hygiene, 82, 150, 189, 201, 213—14, 788—9 adjunctive aids, 457—9 allergic reaction to materials, 286—7 antiseptics, 464—87 agents, 471-5 approaches, 468-9 chlorhexidine, 473, 475, 476—81, 506 clinical trial design, 485—7 evaluation of, 481—5 history, 466—7 rationale for, 467—8 vehicles for delivery, 469—71 brushing, 450—53, 465—6 electric toothbrushes, 453, 466 frequency and effectiveness, 452—3 interproximal brushes, 455—7 methods, 451—2 toothbrush wear and replacement, 453 contraindication to surgery of poor oral hygiene, 537 effects of incorrect use of devices, 459 effects on microbiota, 569—70 healing after cause-related therapy and, 441—2, 443 instruction and motivation, 459—61 interdental cleaning, 454—7, 465, 466 necrotizing periodontal disease and, 248—9, 254, 255, 257 orthodontics and, 749, 751 postsurgical care, 550, 553—5 root coverage procedure outcome and, 611 status, 412 supragingival plaque removal, 450—61 trauma from, 289—91, 459, 579, 580 oral mucosa, see also gingiva organ transplantation as contraindication for surgery, 537—8 ornidazole, 499 orofacial granulomatosis, 287 orthodontics, 744—78 in adults with periodontal tissue breakdown, 744—52 esthetic finishing of treatment results, 751 legal aspects, 752 orthodontic treatment considerations, 748—51 possibilities and limitations, 752 retention, 751—2 chlorhexidine use and, 480 esthetics and, 751, 766—8 extrusion of single teeth, 756—9 gingival recession and, 583—6, 768—72 1040 • INDEX orthodontics (contd) interdental recession, 771-2 labial recession, 768-71 implants and, 766-8, 971-5 anchoring, 1004-12 intrusion of single teeth, 759-62 minor surgery associated with, 772-8 molar uprighting with furcation involvement, 766 regenerative procedures and, 762-3 specific factors associated with, 752-68 tooth movement into compromised bone areas, 754-6 tooth movement into infrabony pockets, 752-4 tooth movement through cortical bone, 756 trauma from, 356-9 traumatic occlusion and, 763-6 osseointegrated implants, see implants osseous surgery, 534 ostectomy, 534 osteoblasts, 21, 39, 40, 866 osteoclasts, 41 osteocytes, 38-9, 40, 858, 866 osteopenia, 68 osteoplasty, 534 osteoporosis, 68, 186-7, 212, 853, 855 osteoradionecrosis, 854 osteosarcoma, 311 oxygenating agents, 474 oxytalan fibers, 22 ozena, 513 pain local anesthesia, 538-40 postoperative, 539, 550 palatal implants, 1011-12 pancreatic insufficiency, 514 papilla, 6-7 interdental gingival recession, 771-2 papilla preservation flap, 530-31 reconstruction, 616-19 papilloma, 304-5 papillomavirus, 121, 304 Parkinson's disease, 538 pemphigoid, 280-82 pemphigus vulgaris, 282-3 penicillins, 499, 500 Peptostreptococcus micros, 107, 120, 127, 129, 134, 262, 266, 319, 1020 perforated roots, 328-9 periapical cemental dysplasia, 302-3 peri-implant plaque, 98 periimplantitis, 1015, 1016-19 microbiology, 1020-21 treatment, 1019-20 periodontal disease, 82 abscesses, 240-66, 333 adult, 54-7 aggressive, sec aggressive periodontitis children/adolescents, 57-61 chronic, see chronic periodontitis combined endodontic and periodontal lesions, 346-7 composition of dental plaque and, 127-9 development and progression, 150-63, 175 initiation, 150-55 prerequisites for, 132-5 stages, 155-63 diagnosis, 410-12, 416 aggressive periodontitis, 233-7 necrotizing periodontal disease, 249-50 periodontal abscesses, 262-4 examination of patients, 50-52, 403-13, 798 alveolar bone, 409-10 diagnosis of periodontal lesions, 410-12 gingiva, 404-6 oral hygiene status, 412 periodontal ligament and root cementum, 406-9 genetics and, 387-97 aggressive periodontitis, 231-2, 237, 388 chronic periodontitis, 213, 388 cytokine gene polymorphisms, 392-6 evidence, 388-90 FCy gene polymorphisms, 396-7 gene modification, 392 major gene associated with, 392 twin model, 388-90 host-parasite interactions, 163-76 diabetes mellitus and, 182-3 influence on condition of pulp, 339-40 microbiology, sec bacteria necrotizing periodontal disease, 243-57 non-specific plaque hypothesis, 82, 110 orthodontics and, 744-52 prevention, 782-4 risk factors, 61-70, 387 chronic periodontitis, 211-13 diabetes mellitus, 67-8, 134-5, 180-83, 791 HIV infection, 68 hormonal changes, 179, 183-8 longitudinal studies, 68-70 multiple factors, 61, 63-4 other factors, 68 patients at risk without supportive therapy, 784-5 tobacco smoking, 64-7, 70, 135, 189-92, 792 screening, 415-16 aggressive periodontitis, 221-5 similarity to other infectious diseases, 106-7 symptoms, 403-4 systemic disease and, 70-73, 74, 366-83 aggressive periodontitis, 234 atherosclerosis, 70-72, 370, 375 cardiovascular disease, 7072, 370-76, 382-3 chronic periodontitis, 212-13 diabetes mellitus, 67-8, 73, 134-5, 180-83, 212, 378-80 gingivitis, 203 history of belief that oral infection caused systemic disease, 366-7 necrotizing periodontal disease, 253-4 periodontal abscesses, 266 preterm birth, 72-3, 376-8, 381-2 respiratory infections, 380-81 risk concept, 367-70 tooth loss and, 61, 213 trauma from occlusion and plaque-associated periodontal disease, 352-65 unique features, 107-8 Periodontal Disease Index, 51, 57 Periodontal Index, 51 periodontal ligament, 3, 27-31, 46, 49, 166 examination of patients, 406-9 regenerative capacity of cells, 659 periodontal plastic surgery, see mucogingival therapy INDEX • 1041 periodontium anatomy, 3—49 blood supply, 43—6 embryonic development, 3—5, 24, 34, 37 endodontic lesions in marginal periodontium, 323—6 impact of endodontic treatment on, 326—33 influence of pathologic conditions in the pulp on the periodontium, 319—24 lymphatic system, 47 nerves, 48-9 root cementum, 3, 31—4 see also alveolar bone; gingiva; periodontal ligament peripheral giant cell granuloma, 301—2 peripheral inflammatory root resorption (PIRR), 337—8 peripheral odontogenic tumors, 305—6 peroxyborate, 474 peroxycarbonate, 474 phenols, 473—4 phenytoin sodium (epinutin), 203, 204 picks, 455 planning treatment, 414—31 additional (corrective) therapy, 420—22 case presentation, 418—19 case reports, 422—31 diagnosis, 416 implants, 857 initial (cause-related) therapy, 414, 419 initial treatment plan, 416—17 re-evaluation, 419—22 screening for periodontal disease, 415—16 single tooth risk assessment, 417—18 supportive therapy, 415, 422 Plaque Index, 51 plaque, see atheromatic plaque; dental plaque plasma cells, 21 plastic surgery, see mucogingival therapy pneumonia, 380 polymers, 666 polymorphonuclear (PMN) leukocytes, 21, 167—9, 175, 182, 191, 212 polyvinylmethyl ether maleic acid, 473 Porphyrornonas endodontalis, 513 Porphyromonas gingivalis, 64, 66, 70, 71, 73, 82, 107, 113, 116— 17, 126, 129, 133, 134, 135, 136, 137, 138, 164, 166, 169, 172, 182, 319, 375, 389, 494, 497, 681 aggressive periodontitis and, 217, 227—8, 235 antibiotics and, 499, 502 breath malodor (halitosis) and, 513 coronary heart disease and, 375—6 effects of therapy on, 563, 564, 565, 568, 571 linear gingival erythema (LGE) and, 274 peri-implantitis and, 1020 periodontal abscesses, 262 pregnancy complications and, 377 posterior single-tooth replacement, 961—5 posterior superior dental nerve, 48 postnasal drip, 513 postoperative pain, 539, 550 postsurgical care, 550 povidone iodine, 475 pregnancy, 179, 183, 184—6, 201—2 periodontal disease and complications in, 72—3, 376—8, 381—2 preterm birth, periodontal disease and, 72—3, 376—8, 381—2 preventive measures implant maintenance, 1026—9 periodontal disease, 782—4 Prevotella spp., 319 P intermedia, 64, 107, 119, 127, 134, 135, 136, 137, 182, 184, 185, 375, 389 aggressive periodontitis and, 225, 227 antibiotics and, 502 breath malodor (halitosis) and, 513 effects of therapy on, 563, 565, 571 linear gingival erythema (LGE) and, 274 necrotizing periodontal disease and, 252 peri-implantitis and, 1020 periodontal abscesses, 262 P loeschii, 513 P melaninogenica, 135, 137, 262 P nigrescens, 107, 119, 127 prilocaine, 538—9 primary herpetic gingivostomatitis (PHG), 249—50, 270—72 progesterone, 183, 185, 187 proinflammatory cytokines, 167 prostaglandins, 167 proteinase inhibitors, 166 proteinases, 165—6 Pseudomonas aeruginosa, 121, 380 psychological diseases, 854 puberty, 179, 183, 184, 202 pulp, 318 furcation involvement and, 711 influence of pathologic conditions in the pulp on the periodontium, 319—24 influence of periodontal disease on condition of, 339—40 influence of periodontal treatment measures on, 340—44 necrosis, 319—23 pus, 795 pyogenic granuloma, 301 pregnancy, 185, 202 quaternary ammonium compounds, 473 cetylpyridinium chloride, 471, 473 race, necrotizing periodontal disease and, 255 radicular cysts, 315—16 radiography, 838—50 aggressive periodontitis, 223—4 alveolar bone, 52, 409—10 assessment of periodontal regeneration, 652 basic principles, 838 digital intraoral radiography, 850 evaluation of periodontal disease progression, 796 furcation involvement diagnosis, 711 implant maintenance, 1025—6 intraoral and panoramic, 838—40 periodontally compromised patient, 838 postoperative, 847—50 preoperative evaluations, 838—47, 855—6 root resorption, 334, 335 symptoms of periodontal disease, 403 radiotherapy, 309, 854 recall system, compliance with, 787—8 reciprocating instruments, 440—41 reduced dental epithelium, 16 refractory periodontitis, antibiotic therapy, 502 regenerative therapy, 650—95 access therapy, 531 1042 • INDEX regenerative therapy (contd) furcation defects, 683-9, 723-6 indications, 650-51 orthodontics and, 762-3 procedures, 651, 661-9 reliability of assessments of regeneration, 652 wound healing, 652-61 see also guided tissue regeneration (GTR) rehabilitation implants and, 980-1003 cross-arch bridge restoration, 991-6 fixed restorations on implants and teeth, 984-7 restoration of mandible function, 980-83 restoration of maxilla function, 987-90 solving restorative problems during maintenance therapy, 997-1002 solving root fracture problems, 1002-3 renal insufficiency, 275, 514 respiratory infections breath malodor (halitosis) and, 513 periodontal disease and, 380-81 rete pegs, 10 reticulin fibers, 22 rheumatic endocarditis, 537 ridge augmentation, 631-44, 767-8, 880-83, 885-9, 897-913 risk, 367-70 assessment process, 62-3 single tooth risk assessment, 417-18 continuous multilevel risk assessment, 787-97 periodontal disease risk factors, 61-70, 387 chronic periodontitis, 211-13 diabetes mellitus, 67-8, 134-5, 180-83, 791 HIV infection, 68 hormonal changes, 179, 183-8 longitudinal studies, 68-70 multiple factors, 61, 63-4 other factors, 68 patients at risk without supportive therapy, 784-5 tobacco smoking, 64-7, 70, 135, 189-92, 792 roll flap procedure, 633-4 roots coverage procedures, 592-616 clinical outcome, 610-16 grafting procedures, 597-610, 613-16 healing after, 613-16 dentin hypersensitivity, 341-4, 651 endodontic lesions, 318, 323-6 fractures, 201, 330-33, 1002-3 impact of endodontic treatment on periodontium, 326-33 perforations, 328-9 periodontal abscesses and root morphology alterations, 261 resorption, 201, 333-9, 659, 660-61 clinical manifestations, 334-5 external inflammatory resorption (EIRR), 337, 339 forms of, 335-9 mechanisms, 333-4 peripheral inflammatory resorption (PIRR), 337-8 replacement resorption, 336 surface, 336 treatment, 338 root cementum, 3, 31-4 examination of patients, 406-9 scaling and planing, 240-41, 432-41, 563, 712 separation and resection (RSR), 344, 714-23 surface conditioning/biomodification, 546 50, 667-8 surface instrumentation, 545-6 see also furcation involvement rotating instruments, 439-40 rotational flap procedures, 597 Salmonella typhi, 107 sanguinarine, 474, 475 scalers, 542 scaling and root planing, 240-41, 432-41, 563, 712 scalloped implant design, 934-6 screening periodontal disease, 415-16 aggressive periodontitis, 221-5 screw-retained implant restorations, 965-8 scurvy, 202-3 segmented fixed implant restorations, 936 Selenomonas spp., 121, 252 self-inflicted injuries, 291 semilunar coronally repositioned flap, 597-8, 600 sequestrum formation in necrotizing periodontal disease, 246 Shigella dysenteriae, 107 sickles, 433 single tooth risk assessment, 417-18 sleep patterns, 254 smoking, see tobacco smoking sodium chlorites, 475 sodium lauryl sulphate, 474 sonic instruments, 439 sounding, 410 specific plaque hypothesis, 82 spirochetes, 108, 110, 111, 118-19 sprays, 470, 479 squamous cell carcinoma, 308-9 squamous odontogenic tumor, 307-8 staining, chlorhexidine and, 477-8 Staphylococcus spp., 1021 S aureus, 380, 471 S epidermidis, 82 steroid medication, 855 stitches/suturing, 546-9 stomach, see gastro-intestinal diseases Streptococcus spp., 109, 121, 127, 269 S anginosus, 121 S constellatus, 121, 127 S intermedius, 107, 121 S mitis, 136 S prreumoniae, 107, 380 S sanguis, 71, 83, 129, 133, 136, 137, 375 S uberis, 133 stress, 68, 213, 254 subgingival plaque, 82, 90-98 removal, 434-8 sublingual nerve, 48 superior alveolar plexus, 48 support assessment of loss of, 51-2 see also mobility of teeth supportive periodontal therapy (SPT), 781-801 basic paradigms for prevention of periodontal disease, 782-4 continuous multilevel risk assessment, 787-97 in daily practice, 797-801 INDEX • 1043 supportive periodontal therapy (SPT) (contd) definitions, 781 gingivitis and, 786 implants solving restorative problems during maintenance therapy, 997—1002 objectives, 797 patients at risk of periodontitis without SPT, 784—5 periodontitis patients, 786—7 planning, 415, 422 supragingival plaque, 82, 85—90 removal, 433, 449—61 chemical control, 464, 465—87 effects of, 568—71 importance of, 449—50 self-performed, 450—61 surgical treatment, 519—58, 576—644 anesthesia, 538—40 chronic periodontitis, 214—15 comparison with non-surgical therapy, 552—8 contraindications for, 537—8 crown lengthening procedures, 619—30 ectopic tooth eruption, 628—30 excessive gingival display, 619—22 exposure of sound tooth structure, 622—8 deformed edentulous ridge, 630—44 correction of ridge defects with soft tissue grafts, 631—44 prevention of soft tissue collapse following tooth extraction, 630—31 distal wedge procedures, 531—4 dressings, 549—50 flap procedures, 522—31, 544—5 furcation involvement plasty, 712—13 root separation and resection, 714—17 tunnel preparation, 713—14 general guidelines, 535—46 gingival augmentation, 577—92 healing after, 589—92 indications for, 586—7 procedures, 587—9 gingival hyperplasia, 276 gingivectomy procedures, 520—22, 543—4, 550—51, 776—8 healing after, 550—52, 589—92, 613—16 implants, 852—63 abutment selection, 863 bone drilling, 858—9 cortical stabilization, 861—2 flap design, 857—8 healing time, 862—3 implant direction, 860–61 implant position, 859–60 implant selection, 862 preoperative examination, 852—7 indications for, 535—7 instruments, 540—43 interdental papilla reconstruction, 616—19 necrotizing periodontal disease, 257 objectives, 535 orthodontics and, 772—8 osseous surgery, 534 outcome, 550—58 post-surgery periodontal abscesses, 261 postoperative pain, 539, 550 postoperative radiography, 847—50 postsurgical care, 550 preoperative procedures chlorhexidine rinsing, 480—81 examination for implants, 852—7 radiographic evaluations, 838—47, 855—6 regenerative therapy, 650—95 access therapy, 531 indications, 650—51 orthodontics and, 762—3 procedures, 651, 661—9 reliability of assessments of regeneration, 652 wound healing, 652—61 see also guided tissue regeneration (GTR) ridge augmentation, 631—44, 767—8, 880—83, 885—9, 897 —913 root coverage procedures, 592—616 clinical outcome, 610—16 grafting procedures, 597—610, 613—16 healing after, 613—16 root surface conditioning/biomodification, 546—50, 667—8 root surface instrumentation, 545—6 selection of technique, 543—5 suturing, 546—9 suturing, 546—9 symptoms diabetes mellitus, 180 of periodontal disease, 403—4 trauma from occlusion, 731 systemic diseases gingival lesions, 277—89 lupus erythematosus (LE), 284 periodontal disease and, 70—73, 74, 366—83 aggressive periodontitis, 234 atherosclerosis, 70—72, 370, 375 cardiovascular disease, 70—72, 370—76, 382—3 chronic periodontitis, 212—13 diabetes mellitus, 67—8, 73, 134—5, 180—83, 212, 378—80 gingivitis, 203 history of belief that oral infection caused systemic disease, 366—7 necrotizing periodontal disease, 253—4 periodontal abscesses, 266 preterm birth, 72—3, 376—8, 381—2 respiratory infections, 380—81 risk assessment, 791—2 risk concept, 367—70 T-helper cells, 167, 170, 174 tape (floss), 454—5 tartar, see dental calculus telangiectatic granuloma, 301 tetracyclines, 499, 500, 501, 502, 503, 505—6, 537 thermal injuries, 291 tin salts, 474 titanium implants, 821—8, 829, 879 measurement of surface topography, 821—3 surface roughness, 823—8 tobacco smoking, 179, 188—92 cessation, 192 implants, and, 854 osteoporosis and, 187 periodontal disease and, 64—7, 70, 135, 189—92 aggressive periodontitis, 232 chronic periodontitis, 211—12 4 • INDEX tobacco smoking (contd) necrotizing periodontal disease, 254—5 risk assessment, 792 surgery and, 538 tongue scrapers, 457—8, 516 toothbrusing, see brushing toothpastes, 458—9, 466—7, 469—70, 479 toothpicks, 455 transmission periodontal disease, 129—31 necrotizing periodontal disease, 252 transmucosal attachment of implants, 829—37 normal peri-implant mucosa, 829—36 probing gingiva and peri-implant mucosa, 836—7 transplantation as contraindication for surgery, 537-8 trauma from brushing, 459, 579, 580 from occlusion, 352—65 clinical symptoms, 731 furcation involvement and, 712 jiggling-type trauma, 359—64 orthodontic trauma, 356—9 orthodontics and, 763—6 from oral hygiene, 289—91, 459, 579, 580 gingival lesions, 289—91 treatment acute necrotizing ulcerative gingivitis (ANUG), 207 aggressive periodontitis, 237—8 assessment of needs, 52 benign neoplasms of periodontal hard tissues, 307, 308 benign neoplasms of periodontal soft tissues, 303, 304, 305—6 breath malodor (halitosis), 516 cause-related therapy, 432—47 evaluation of effects, 446—7 healing after, 441—6 methods, 432—41 objectives, 432 planning, 414, 419 chronic periodontitis, 213—15 combined endodontic and periodontal lesions, 346—7 cysts, 313, 314, 315, 316 diabetic patients, 183 during pregnancy, 186 effect on microbiota in dentogingival region, 561—72 focal fibrous hyperplasia, 300 fungal gingival lesions, 274, 275 furcation involvement, 712—26 guided tissue regeneration (GTR), 683—9, 724—6 granulomas, 301, 302 influence of periodontal treatment measures on pulp, 340—44 malignant neoplasms of periodontal hard tissues, 311, 312 malignant neoplasms of periodontal soft tissues, 309, 310 mobility of teeth, 734—43 necrotizing periodontal disease, 255—7 acute phase, 255—7 maintenance phase, 257 occlusal therapy, 731—43 periapical cemental dysplasia, 303 peri-implantitis, 1019—20 periodontal abscesses, 264—5 planning, 414—31 additional (corrective) therapy, 420—22 case presentation, 418—19 case reports, 422—31 diagnosis, 416 implants, 857 initial (cause-related) therapy, 414, 419 initial treatment plan, 416—17 re-evaluation, 419—22 screening for periodontal disease, 415—16 single tooth risk assessment, 417—18 supportive therapy, 415, 422 plaque induced gingivitis, 201 post-therapy periodontal abscesses, 240—41 root resection, 344 root resorption, 338 supportive therapy (SPT), 415, 422, 781—801 systemic gingival lesions, 279—80, 282, 283, 284, 287, 289 tobacco smokers, 192 viral gingival lesions, 271—2 see also antibiotics; antiseptics; orthodontics; surgical treatment Trench mouth, see acute necrotizing ulcerative gingivitis ( ANUG) Treponema spp., 107, 119, 251, 252, 262 T dent/cola, 66, 118, 126, 129, 137, 513, 563, 564, 565 T pallidti in, 118, 119, 269 triclosan, 473—4 tumors, 298—312 benign neoplasms of periodontal hard tissues, 306—8 benign neoplasms of periodontal soft tissues, 303—6 malignant neoplasms of periodontal hard tissues, 310 12 malignant neoplasms of periodontal soft tissues, 308—10 oral lichen planus and, 278 reactive processes of periodontal hard tissues, 302—3 reactive processes of periodontal soft tissues, 298—302 ulceration, 480 ultrasonic and sonic instruments, 439 vaccines, 109 varnishes, 470, 479 vasoconstrictors, 539 Veillonella spp., 84 verruca vulgaris, 305 vertical root fracture, 330—33 vestibular/gingival extension procedures, 588, 589—92 Vihrio cholera, 107 Vincent's infection, see acute necrotizing ulcerative gingivitis (ANUG) viruses, 121 gingival lesions, 269—72 herpes viruses, 121, 269—72 papillomavirus, 121, 304 vitamin deficiency chronic periodontitis and, 212 gingivitis and, 202—3 Widman flap modified, 528, 529, 551—2 original, 522 wound healing, see healing X rays, see radiography zinc citrate, 473 zinc salts, 474 ... the mandible As a rule, analgesia of the teeth and the soft and hard tissues of the mandible should be obtained by a mandibular block and/ or a mental block In the anterior region of the mandible,... of Clinical Periodontology 9, 115-128 Loos, B., Claffey, N & Egelberg, J (1988) Clinical and microbiological effects of root debridement in periodontal furcation pockets Journal of Clinical Periodontology. .. healing Scandinavian Journal of Plastic and Reconstructive Surgery and Hand Surgery 23, 207-209 Stahl, S.S., Witkin, G.J., Cantor, M & Brown, R (1968) Gingival healing IT Clinical and histologic