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Review paper: dental treatment for patients with Papillon-Lefevre syndrome (PLS).


Aim: The aim of this article is to present a review of the most current literature regarding the aetiology of the periodontal disease that occurs in patients with Papillon-Lefevre syndrome (PLS). It is also to encourage clinicians to adopt a treatment regime intending to save permanent teeth and alveolar bone in young patients with PLS. Review: The phenotypic expression of Papillon-Lefevre syndrome is heterogeneous as regards the severity of the dermatological as well as the periodontal symptoms. The genetic defect is lack-of-function mutations of the gene encoding for cathepsin C, a lysosomal cysteine proteinase. The defect is associated with a severe reduction in the levels and activities of neutrophil-derived serine proteases (cathepsin G, elastase, Proteinase 3) and in the activation of granzyme B in natural killer cells. About 20% of patients with PLS experience infections besides the periodontal infection, although the patients are not known to be unusually susceptible to viral infections. The reason why many patients with PLS do develop periodontal inflammation is most likely due to the fact that the amount of aerobic and anaerobic pathogens in the periodontal pocket overpower a somewhat weakened innate immune response. Based on this literature review a standardised dental treatment protocol for patients with Papillon-Lefevre syndrome is suggested. Conclusion: It is evident that by regularly reducing the periopathogenic flora in the oral cavity and by instigating a potent antibiotic therapy at an early stage of any potential infection, patients with PLS are not predestined to be edentulous in the permanent dentition.

Key words: Papillon-Lefevre syndrome, dental treatment, cathepsin C


Papillon-Lefevre syndrome (PLS) is a rare autosomal recessive disorder presented with diffuse transgradient palmoplantar hyperkeratosis, and an aggressive periodontal inflammation leading to premature loss of primary and permanent teeth. PLS belongs to a group of genetically, as well as clinically, heterogenous group of skin disorders called palmoplantar keratodermas or keratoses (PPKs). All of the PPKs are characterized by hyperkeratotic lesions primarily affecting the palms of the hands (Figure 1 a) and the soles of the feet (Figure 1 b). PLS differs from other PPK disorders by the presence of early-onset and aggressive periodontitis. Haneke [1979] used the following criteria to classify a case as PLS:

* presence of palmoplantar hyperkeratosis,

* loss of primary and permanent teeth, and

* autosomal recessive inheritance.


The diagnosis of PLS is made through clinical examination of the skin and the oral tissues. A pedigree reveals the mode of inheritance and by using mutation analysis it is possible to identify the mutation through blood or tissue samples. PLS is inherited with an autosomal recessive trait and if both parents are carriers of the defective gene there is a 25% risk that their child will be born with the disorder. Between 2 and 4 people per 1,000 are heterozygous for the PLS gene and therefore, carriers of the disorder. This results in a population prevalence of 1 case per 1-4 million people [Hart and Shapira, 1994]. However, this rate is higher in isolated societies, and particularly those in which consanguineous marriages are common. It is calculated that one third of all cases of PLS are the result of consanguinity [Hart and Shapira, 1994].

An increased susceptibility to infection, besides periodontal inflammation, has been reported in approximately 20% of patients with PLS. Painful fissures and recurrent pyogenic infections of the skin seem to be the most common medical complications [Hart and Shapira, 1994; Marandian et al., 1979; Oguzkurt et al., 1996]. However, a number of patients with abscesses or pseudotumors of the liver have been described [Czauderna et al., 1999; Almuneef et al., 2003]. There have also been reports of PLS patients with other stigmata such as growth retardation [Ressa, 1970], non-symptomatic intracranial calcifications and mental retardation [Hart and Shapira, 1994].

The PLS disorder has, since the first report of this condition, been associated with an aggressive and devastating periodontal disease with consequential premature and extensive loss of teeth and alveolar bone in very young individuals. The oral symptoms have a severe impact on oral health in most patients with PLS, resulting in functional as well as cosmetic handicaps. A bad oral condition in addition to the dermatological lesions might instigate psychological and social problems in young children. Any attempt to achieve and preserve healthy oral conditions will improve quality of life for children with PLS.

The aim of this article is to present the most recent knowledge regarding the aetiology behind the periodontal disease in PLS and encourage clinicians to adopt a treatment regime intended to save permanent teeth and alveolar bone. There are several reports regarding occasional features seen in patients with PLS. As this review article is focused on dental treatment for patients with PLS and the list of references is extensive, we have decided to leave out case reports with occasional medical findings without relevance to the dental condition.

Periodontal inflammation in patients with PLS

The aggressive periodontal disease, with premature and extensive tooth loss, is a cardinal sign of PLS. In the very young patient with PLS, the oral mucosal and gingival tissues seem normal. After eruption of the primary teeth, the gingival tissues become inflamed, swollen and start to bleed easily. These changes are followed by a rapid destruction of the periodontal tissues causing hypermobility of the teeth and periodontal abscesses [Hart and Shapira, 1994]. In the primary dentition, treatment options are restricted due to very young patient's inability to cooperate with meticulous oral hygiene measurements and to conservative periodontal treatment, which will include scaling and professional tooth cleaning (prophylaxis). As a result the majority of the primary teeth acquire a severe periodontal inflammation and in most PLS patients the primary teeth are shed spontaneously and prematurely at an early age.

However, a number of young children with this disorder require primary tooth extractions in order to resolve their painful periodontal condition. Following the loss of the primary teeth the inflammation subsides and the gingival tissues resume normal conditions.

After the eruption of the permanent teeth, the inflammatory course often repeats itself leading to devastating periodontal destruction (Figures 2 and 3). The extent and the severity of the periodontal disease is more variable in the permanent dentition than in the primary dentition and conservative periodontal treatment has in many cases been proven successful (Wiebe et al., 2001; Lundgren and Renvert, 2004). Nevertheless, many patients with PLS will become edentulous by their early teens [Hart and Shapira, 1994]. In view of the aggressive periodontitis [Hart and Shapira, 1994], and reports of increased susceptibility to infections in patients with PLS [Almuneef et al., 2003], it is not unreasonable to assume that patients with this condition may possibly have an underlying dysfunctions of the immune or inflammatory defence mechanisms.


Despite being a rare disorder, the periodontal inflammation in patients with PLS has instigated numerous investigations regarding cell mediated immune response. This interest has mainly been focused on the polymorphonuclear neutrophil leukocytes (PMN) as they play a crucial role in the cell-mediated immune response against bacterial plaque at the gingival margin [Page et al., 1997]. The mechanism by which PMNs neutralize pathogenic microorganisms involves many different steps: adhesion to the capillary endothelium in the inflamed region, transendothelial migration, chemotaxis, phagocytosis, and bacterial killing by oxidative and non-oxidative mechanisms [Dennison and Van Dyke, 1997; Del Fabbro et al., 2000]. A defect in one of these steps leads to an altered neutrophil function and, thus, increased susceptibility to tissue infection. Depressed chemotaxis of PMNs [Liu et al., 2000; Firatli et al., 1996], significant depressed and lytic PMN activity [Ghaffer et al., 1999], defective leukocyte adhesion, impaired production or increased release of superoxide radicals, and impaired monocyte phagocytosis [Hart and Shapira, 1994] have been reported in patients with PLS. Different investigative techniques could, in part, explain the incoherent findings with regards to PMN function. Furthermore, the dysfunction could possibly be related to a toxic effect caused by extracellular toxins and lipopolysacharide antigen from periopathogens. The dysfunction of PMNs would then be secondary to the infection as suggested by Agarwal et al. [1996]. In line with this idea Tinanoff et al. [1995] found normalized PMN function after successful conservative periodontal treatment of a PLS patient, and Preus [1988] discovered a normalized monocyte function once the periodontitis and the presence of Actinobacillus actinomycetemcomitans (A.a) was eradicated.

Lyberg [1982] reported normal lymphocyte transformation in two patients with PLS and recent investigations of lymphocyte population in peripheral blood did not reveal any significant alterations in the T and B lymphocyte distribution, although natural killer cells were significantly increased [Hart and Shapira, 1994; Firatli et al., 1996]. A few studies have explored the level of immunoglobulins in patients with PLS. These include reports of a normal concentration of salivary IgA [Lundgren et al., 1996] and increased serum IgG titres against periopathogenic bacteria [Hart and Shapira, 1994; Wara-aswapati et al., 2001].

The relationship between periodontal disease and bacterial infection is well established and certain groups of predominantly gram-negative bacteria have been consistently found in periodontal lesions [Genco et al., 1988]. However, to date no direct relationship has been proven to exist between any specific bacteria and type of periodontitis [Hart, 1996; Kinane and Attstr6m, 2002]. Various types of periodontal diseases affect children and Actinobacillus actinomycetemcomitans (A.a) is the pathogen most frequently associated, including patients with PLS [Hart and Shapira, 1994; Kleinfelder et al., 1996; Velazco et al., 1999; De Vree et al., 2000]. The use of antibody data provides strong evidence of previous or current infection with a periodontal pathogen and Wara-aswapati et al. [2001] found an increased serum IgG1, IgG2, and IgG3 titres against A.a. in young patients with PLS. However, other investigators have failed to link PLS periodontitis to A.a. [Lundgren et al., 1998; Robertsson et al., 2001] and it has been suggested that other periopathogens [Clerehugh et al., 1996; Velazco et al., 1999] as well as viruses from the herpes group [Velazco et al., 1999; Ting et al., 2000] may be involved in the causation and/or progression of localized aggressive periodontitis and PLS periodontitis.


As a result of the increased knowledge of the human genome, and after an intense search for the genetics behind the PLS disorder, two research groups were able to identify the mutation linked to PLS as a lack-of-function mutations of the gene encoding cathepsin C [Hart et al., 1999; Toomes et al., 1999]. Cathepsin C is a lysosomal cysteine proteinase found in many cell types, although being particularly abundant in cells of the immune system [McCuire et al., 1992]. It functions as a central coordinator in degradation of proteins and as an activator of various serine proteases with vital functions in immune and inflammatory cells [Rao et al., 1997].

Today more than 41 different mutations of the cathepsin C gene have been identified in patients with PLS, all of them homozygous [Hart et al., 1999; Selvaraju et al., 2003]. However, compound heterozygous mutations in patients with PLS as well as "symptomless mutations" in the cathepsin C gene in homozygous individuals have also been described [Allende et al., 2003; Hewitt et al., 2004; Noack et al., 2004]. Heterozygous carriers of the mutation are clinically unaffected [Nakano et al., 2001] although one heterozygous patient presented with plantar hyperkeratosis without periodontal disease [Cury et al., 2002].

Mutations of the cathepsin C gene have also been confirmed in patients with Haim-Munk syndrome. The latter condition has a phenotypic expression similar to PLS, plus in addition arachnodactyly, atrophic changes of the nails, and deformity of the phalanges of the hand [Hart and Shapira, 1994]. The associated occurrence of severe early-onset periodontitis and PPK is unique to PLS and Haim-Munk syndrome [Hart et al., 2000] and it is a diagnostic distinction between other conditions with palmoplantar keratoses. However, this has been challenged by the reports of families affected by PLS in which some family members manifest the typical skin and periodontal lesions, whereas other siblings manifest the palmoplantar keratosis without any involvement of periodontal tissues either in the primary or the permanent dentition [Hart and Shapira, 1994]. Bullon et al. [1993] reported a family with 6 children where 4 were affected by PLS by having palmoplantar lesions although just 2 of the 4 children had periodontal inflammation involving the permanent dentition only. Haneke [1979], and Pilger et al. [2003] report patients with palmoplantar keratoses with periodontal inflammation in the permanent, but not in the primary dentition. In contrast, Ullbro et al. [2003] did not find any patients without periodontal inflammation in the primary dentition in their study of 47 patients with PLS. Single gene disorders, like PLS, are characterized by a variety of expressions where the phenotype may be modified by environmental factors. Consequently there is normally a wide phenotypic variance in patients with PLS. Whether the reported late onset periodontal disease is the result of genetic variance and if those patients have a confirmed PLS mutation is not known.

Mutations of the cathepsin C gene have also been reported in patients with prepubertal periodontitis, which is characterized by a periodontal condition similar to PLS periodontitis, albeit without the dermatological symptoms. It has been suggested that prepubertal aggressive periodontitis could be an allelic variant of PLS [Hart et al., 2000; Noack et al., 2004] or a genetically heterogeneous disease that, in some families, manifests as partially penetrant PLS [Hewitt et al., 2004]. However, conditions with aggressive periodontal disease are not always the result of cathepsin C mutations and there is no evidence that patients will suffer from aggressive periodontitis simply because they have a low activity cathepsin C variant [Hewitt et al., 2004].

Although the genetics behind the PLS disorder has been identified, the exact biological mechanism causing the dermatological or periodontal lesions is still unknown. The cathepsin C gene is expressed in epithelial regions normally affected by PLS such as the palms, soles, knees and keratinised oral gingiva [Rao et al., 1997]. However, the exact mechanism by which cathepsin C gene mutations cause or are involved in PPK is unclear as its role in the epidermis has not yet been studied in detail. Nuckols and Slavkin [1999] suggest that cathepsin C may be essential for establishing or maintaining the structural organization of the epidermis of the extremities and the integrity or immunologic properties of the tissues surrounding the teeth. They also suggest that cathepsin C might participate indirectly in the processing of proteins such as keratins that maintain the structural integrity of epithelia in a way that is unique to the tissues affected in patients with PLS. Preus [1988] speculated that the hereditary defect causing periodontitis in PLS patients could be located at the epithelial surface barrier and that this deficiency would lead to reduced defence against virulent pathogens when present. Mechanical tension and microbial strain, above a genetically determined threshold, could possibly interfere with the ability to prevent infiltration of periopathogens into the periodontal tissues [Kleinfelder et al., 1996]. In a study of the periodontal structure of cathepsin C deficient mice, de Haar et al. [2006] found normal structure of the gingiva, periodontal ligament, alveolar process, and cementum layer. They conclude that cathepsin C deficiency does not lead to major changes in the structure of the periodontium.

The importance of cathepsin C in the defence of the organism has been studied on cell lines from cathepsin C-deficient mice, which fail to activate serine proteinases in immune and inflammatory cells [Wolters et al., 2001]. According to these findings cathepsin C is required for the activation of the serine proteases, granzymes A and B in cytotoxic lymphocytes and natural killer cells. This activation is requisite for the cytotoxic lymphocytes granule-mediated apoptosis of tumour cells and infected cells [Pham and Ley, 1999]. Based on the phenotype seen in cathepsin C-deficient mice, patients with PLS would have generalized immunodeficiency as a result of the loss of activation of these serine proteases [Pham et al., 2004]. However, studies of patients with PLS have failed to detect a generalized T cell immunodeficiency phenotype and these patients are not known to be unusually susceptible to viral infections [Pham et al., 2004]. In their investigations these same authors reported that patients with PLS retain significant granzyme activities in a cytotoxic lymphocyte compartment and have well-preserved cytotoxic lymphocyte function. Those patients with PLS expressed normal lymphokine-activated killer-mediated (LAK) cytotoxicity against K562 cells [Pham et al., 2004]. A similar result was shown by Meade et al. [2006] who concluded that loss-of-function mutations in cathepsin C do not affect lymphokine activated killer cell function. However, Meade et al. [2006] also found that resting natural killer (NK) cells in humans with PLS have a cytolytic defect and contain inactive granzyme B. This finding indicates that cathepsin C is required for the granzyme B activation in unstimulated human NK cells. A similar result has earlier been presented by Lundgren et al. [2005] who found that cytotoxicity of NK cells was consistently and severely depressed in all their PLS patients.

Human keratinocytes in culture normally secrete granzyme B with antimicrobial activity that is able to protect against invading pathogens. The activation of granzyme B may thus provide protection against dermal inflammation [Berthou et al., 1997]. The failing activation of granzyme B in individuals with PLS might weaken the epithelial response towards bacterial infection and contribute to the individuals' propensity to develop gingival inflammation.

The earlier reported findings of PMN dysfunction may in part be explained by the lack-of-function mutation of the cathepsin C gene. Cathepsin C is essential in order to activate the serine proteinases cathepsin G, elastase and proteinase 3 in PMNs [Adkison et al., 2002] and this activation is essential for the phagocytic destruction of bacteria [De Haar et al., 2004]. Cagli et al. [2005] found an almost complete loss of cathepsin G and elastase activity in two siblings with PLS. Although loss of the cathepsin C activity is associated with severe reduction in the activity and stability of the neutrophil-derived serine proteases, Pham et al. [2004] showed that neutrophils from patients with PLS did not uniformly have a defect in their ability to kill Staphylococcus aureus and Escherichia coli. The authors suggested that other systems are involved in bacterial killing and that serine proteases do not represent the major mechanism by which human neutrophils kill common bacteria.

The activation of serine proteases is also important for the local activation and deactivation of cytokines. In addition, there are other inflammatory mediators, and for extracellular matrix degradation [Murphy et al., 1992; Turk et al., 2001; Hewitt et al., 2004].

Treatment of PLS periodontitis

Considerable heterogeneity has been reported regarding the oral manifestations in patients with PLS [Hart and Shapira, 1994]. In the past, the effects of various oral treatment regimens have been reported although the significance of this heterogeneity on the outcome of the treatment has rarely been considered. In many of these studies this consideration has not been possible since the studies deal with very small numbers of patients.

Early considerations. These concerned treatment of PLS periodontitis and was mainly restricted to extraction of severely affected teeth [Rosenthal, 1951]. Later, traditional mechanical scaling and chemotherapy were tried but proved ineffective [Hart and Shapira, 1994]. In order to create an edentulous period, free of infection, prior to eruption of the permanent teeth Baer and McDonald, [1981] extracted all primary teeth at a young age followed by treatment with systemic tetracycline while the permanent teeth were erupting. The extraction of all primary teeth was felt to be indicated due to the severe inflammation that in most cases affects the primary dentition. This treatment approach has successfully been used by others [Tinanoff et al., 1986; Hart and Shapira, 1994; Ullbro et al., 2005).

Antimicrobials. As the gram-negative periopathogenic bacteria A.a is considered to be an important periopathogen in PLS periodontitis it would seem valid to employ antimicrobials that target this microorganism in the treatment of the periodontal disease. Earlier studies report successful, as well as unsuccessful, systemic use of different antibiotics such as erythromycin [Tinanoff et al., 1986] penicillin [Glenwright and Rock, 1990] amoxicillin and clavulanic acid [Bullon et al., 1993; Eronat et al., 1993] and tetracycline [Hart and Shapira, 1994].

Preus and Gjermo [1987] used long-term systemic tetracycline treatment with successful outcome in two patients with PLS. Use of tetracycline, such as low dose doxycycline, minocycline and tetracycline HCL, is an interesting treatment modality due to its potential benefits in reduction of collagenase production, a mechanism independent of the antimicrobial properties of these agents [Ryan and Golub, 2000]. Tetracycline is not recommended for treatment in children under the age of 12 years; instead amoxicillin and metronidazole, taken concurrently, has proven to be effective against A.a. [Pavicic, 1994] and is now commonly used in the treatment of PLS periodontitis [Kleinfelder et al., 1996; Rudiger et al., 1999; Eickholz et al., 2001]. A seven-day long course of treatment with this antibiotic combination has been shown to eradicate A.a. for up to two years post-treatment in patients with chronic periodontitis as well as in one patient with PLS [Pavicic et al., 1994; Eickholz et al., 2001]. However, Kleinfelder et al. [1996] reported post-treatment improvement of clinical and radiological conditions in one PLS patient treated with amoxicillin/metranidazole in spite of recurrent findings of A.a. This suggests that other microbes might be implicated as well.

Chlorhexidine and Retinoids. Further treatment modalities reported in PLS patients are rinsing or subgingival irrigation with chlorhexidine solutions [Rudiger et al., 1999, Wiebe et al., 2001), and frequent professional prophylaxis including scaling and rootplaning (Kressin et al. 1995). Some authors have found that synthetic retinoids improve the periodontal condition (Kressin et al. 1995, Lee et al. 2005), while others find them ineffective (Lundgren et al. 1996).

Frequent follow-ups. A number of patients express a less severe periodontal disease and these patients are able to preserve some or most of their teeth into their adult life [Hart and Shapira, 1994; Wiebe et al., 2001; Kressin et al., 1995; Ullbro et al., 2005]. In a prospective study of 35 young patients with PLS, Ullbro et al. [2005] evaluated a systematic treatment protocol (Table 1). This protocol included follow-up appointments on a 3-month basis with education in and supervision of dental hygiene, professional tooth cleaning, and intervention with conservative periodontal treatment whenever needed. In their study patients with primary teeth had, without exception, severe periodontal inflammation affecting all the teeth. In order to create a period free of infection prior the eruption of the permanent teeth, all primary teeth were extracted approximately 6 months prior the eruption of the first permanent tooth. This study showed that young patients with PLS who were treated according to this protocol from an early age lost fewer permanent teeth and showed less signs of periodontal disease in comparison to the patients that received the same treatment later in life, when signs of periodontal disease had already emerged [Ullbro et al., 2005].

Good oral hygiene. An ability to obtain and maintain good oral hygiene was crucial in order to reach a successful outcome of this treatment protocol. Whenever deemed necessary the conservative periodontal treatment had to be combined with antibiotics in order to cure any episodes of periodontal inflammation [Ullbro et al., 2005].

Other considerations. It could be speculated that the active extraction of all primary teeth prior to the eruption of the first permanent molars is a key event in preserving the permanent dentition [Wiebe et al., 2001]. It could be hypothesized that young patients may develop periodontal disease later on in life in line with reports of late onset of periodontitis in patients with PLS [Brown et al., 1993; Hart and Shapira, 1994]. However, in one study it has been shown that amongst PLS patients with periodontitis, the majority of those that developed periodontal disease exhibited signs of the disease before the age of nine years [Ullbro et al., 2005]. Furthermore, patients with PLS are less prone to develop periodontal disease after they reach the latter part of their teens [Ullbro et al., 1997].

Many of the patients with PLS periodontitis, and premature and extensive loss of permanent teeth, suffer from functional oral handicaps as well as cosmetic inconvenience. Prosthetic rehabilitation with the help of osseointegrated implants has been used successful in many patients [Ullbro et al., 2000; Woo et al., 2003,].

Due to the early loss of primary teeth, ectopic positioning of permanent premolars and canines (cuspids) are not uncommon. After successful periodontal therapy moderate tooth movements may be possible in order to solve these difficulties [Lux et al., 2005].


The phenotypic expression of Papillon-Lefevre syndrome is heterogeneous as regards to the severity of the dermatological as well as the periodontal symptoms. The genetic defect is mutations of the gene encoding for cathepsin C, causing lack-of-function of this lysosomal cysteine proteinase. This defect is associated with a severe reduction in the levels and activity of neutrophil-derived serine proteases (cathepsin G, elastase, Proteinase 3) and in the activation of granzyme B in natural killer cells. Most patients with this disorder do not develop serious infections, except in the oral cavity where the amount of aerobic and anaerobic pathogens overpower a possibly weakened innate immune response [Pham et al., 2004]. It is evident that by regularly reducing the periopathogen flora in the oral cavity and by instigating a potent antibiotic therapy at an early stage of any potential infection (Ullbro et al. 2005), it has been shown that patients with PLS are not predestined to be edentulous in the permanent dentition.


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C. Ullbro *, S. Twetman **

* Institute for Postgraduate Dental Education, Jonkoping, and Dept. Odontology, Umed University,

Umed, Sweden; ** DeptCariology and Endodontics, School o f Dentistry, Faculty o f Health Sciences,

University of Copenhagen, Denmark.

Postal address: Dr. C. Ullbro. Department of Paediatric Dentistry, The Institute for Postgraduate Dental Education,

P.O. Box 1030, SE-551 11 Jonkoping, Sweden.

Table 1 A standardised dental treatment protocol for patients with
Papillon-Lefevre syndrome (PLS).

Primary dentition

1. Oral hygiene information and tooth brushing instructions.
Professional prophylaxis every 3rd month. Parents are encouraged
to supervise, and are trained in hands-on, tooth brushing.

2. Extraction of teeth with advanced periodontal disease

3. Extraction of all primary teeth at least 6 months prior eruption
of the first permanent tooth.

4. Antibiotics should be given for 2 weeks post extractions.
Recommended antibiotics: amoxicillin or amoxicillin + clavulanic
acid with a dose of 20-50 mg/kg/day or 20-40 mg/kg/day respectively,
in divided doses every 8th hour.

Permanent dentition

1. Oral hygiene information, tooth brushing instructions and
professional prophylaxis every 3rd month. Parents are encouraged to
supervise and physically help with tooth brushing until the child
reaches the age of 12.

2. Mouth rinses with chlorhexidine gluconate 0.2% twice daily.

3. Teeth with moderate periodontal disease (bone loss <30% of root
length, probing pocket depths <5 mm):

* Dental scaling and prophylaxis once a month,

* Systemic antibiotic treatment for 2 weeks,

Recommended antibiotics: amoxicillin 20-50 mg/kg/day +
metronidazole (15-35 mg/kg/day) in divided doses, every 8 hours.

4. Teeth with advanced periodontal disease (bone loss >30% of root
length [greater than or equal to]5 mm pocket depths):

* Extraction.
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Author:Ullbro, C.; Twetman, S.
Publication:European Archives of Paediatric Dentistry
Article Type:Disease/Disorder overview
Date:Jan 1, 2007
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Next Article:Case report: Air abrasion cavity preparation for caries removal in paediatric dentistry.

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