Why Is Periodontal Disease More Prevalent and More Severe in People with Down Syndrome?

James Morgan, BA, BDentSc
Co. Kildare, Ireland
Spec Care Dentist 27(5):197-202, 2007
  Reprinted with the permission of Ronald L. Ettinger, BDS, MDS, DDSc, Editor
Special Care Dentistry Association


Periodontal disease has been found to be significantly more prevalent and more severe in people with Down syndrome. A series of studies have reported a prevalence of between 58% and 96% for persons younger than 35 years of age. This phenomenon cannot simply be attributed to poor oral hygiene. The etiology of periodontal disease in persons with Down syndrome is complex. In recent years, much focus has been placed on the altered immune response resulting from the underlying genetic disorder. This paper presents an overview of contemporary knowledge on periodontal disease in patients with Down syndrome.
KEY WORDS: Down syndrome, periodontal disease, preventive care


Down syndrome (DS) is an autosomal chromosomal disorder resulting from trisomy of all or part of chromosome 21.1 Approximately 95% of people with DS have an extra complete chromosome 21. The remaining 5% result from other chromosomal abnormalities including translocation in 3% of people and mosaicism in 2% of people.2,3 The incidence of DS is generally cited as being between 1 in 600 to 1 in 1,000 live births.2 In Ireland, this condition affects approximately 1 in 580 live births, which is the highest incidence in Europe.4

Periodontal disease is defined as "an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both."5

The pathogenesis of periodontal disease is complex. In response to microbial substances released from plaque bacteria in the gingival sulcus, epithelial and connective tissue cells are stimulated to produce inflammatory mediators, leading to infiltration of the connective tissue by numerous defense cells. In the early stages of the immune response, neutrophils predominate. As further microbial substances enter the systemic circulation, committed lymphocytes return to the site of infection, and antibodies specific to bacterial antigens are produced by plasma cells. This essentially protective response is enough to control the infection in people who are not susceptible to periodontitis.6

In susceptible individuals, however, the primary host defenses are unable to control the microbial challenge, leading to the epithelium becoming increasingly permeable and ulcerated. There is increased migration of neutrophils into the tissues, which secrete a variety of inflammatory mediators and proteolytic enzymes. Once the concentration of these inflammatory mediators and enzymes becomes pathologically high, histological destruction of the collagen fibers, periodontal ligament, and alveolar bone occurs.6 Preshaw et al.6 noted that the majority of periodontal destruction is the result of "collateral damage arising from the activation of the host defenses against the presence of bacteria".

In 2005, the World Health Organization provided an overview of periodontal disease worldwide and reported that 10% to 15% of adults suffered from periodontal disease.7 Brown et al.8 reported that the prevalence of periodontal disease among the general population in the United States ranged from 29% for persons aged 19 to 45 years, to 50% for persons aged 45 years and older. An increased prevalence and severity of periodontal disease has been reported in people with DS compared with age-matched subjects of similar levels of intellectual impairment and compared with the general population.9-15 Prevalence varies between 58% and 96% for those under 35 years of age.11,14

The increased prevalence and severity of periodontal disease in persons with Down syndrome may be attributed to a range of local factors associated with the oral cavity, as well as systemic factors associated with the genetic disorder itself.

Prevalence and severity of periodontal disease

Johnson and Young14 examined 70 children with DS (mean age 10.8 ± 3.0 years) and compared them with 40 age-matched subjects who did not have DS but had similar learning disabilities. The presence of periodontal disease was observed in 96% of persons in the group with DS and it was much more severe than in the control group. Bone loss followed a horizontal pattern and was most obvious in the lower anterior segment. Agholme et al.,12 Cichon et al.,16 and Saxén et al.17 also observed this pattern of bone loss.

Saxén et al.17 used orthopantomograms to provide a more objective method for evaluating periodontal disease. Bone loss was measured from the cemento-enamel junction to the alveolar bone margin. A tooth with bone loss of 5mm or more was regarded as affected. It was reported that 69% of subjects with DS aged 9 to 39 years had more than 5mm bone loss compared with 20% of the control group, despite similar levels of plaque and calculus. In a follow-up study carried out five years later, the prevalence of bone loss of 5mm or more had increased to 75% in the subjects with DS.18

In a longitudinal study carried out by Agholme et al.,12 periapical and bitewing radiographs were used to aid in the diagnosis of periodontal disease. It was reported that 35% of subjects with DS (mean age 16.6 years) had experienced alveolar bone loss. Seven years later the prevalence of alveolar bone loss had increased to 74%.

Cutress19 reported that persons with DS who were living in institutions had poorer levels of plaque control, increased calculus deposits, and an increased prevalence of periodontal disease when compared to subjects living at home with DS. Swallow20 came to the same conclusions.

Etiology of periodontal disease in Down syndrome

Local factors

Systemic factors

Barriers to dental services

Kaye et al.48 reported that while most adults with DS regularly attended their dentist, little treatment was actually provided. Allison et al.49 observed that parents of children with Down syndrome frequently encounter problems with access to oral care for their children. Children with DS were significantly less likely to receive dental treatment than their non-DS siblings. Although some authors16,18 have reported that preventive programs have little effect on the progression of periodontal disease in patients with Down syndrome, more recent studies9,24 have shown the effectiveness of frequent preventive care. Yoshihara et al.9 demonstrated the usefulness of periodic preventive care in suppressing the severity and progression of periodontal disease in subjects with DS. In their study, patients were divided into two groups: those who had received frequent preventive care, and those who had not been treated professionally in more than a year. Significant reductions were noted in mean pocket depth (2.5mm and 3.1mm, respectively), mean frequency of periodontal pockets (46% and 91% respectively), and frequency of the prevalence of pathological alveolar bone loss (62% and 100% respectively), when the "managed group" was compared to the "interrupted group." Sasaki et al.24 showed the efficacy of monthly preventive care, which consisted of mechanical plaque control and oral hygiene instruction over a period of two and a half years. Significant reduction in gingival inflammation and probing pocket depths were noted at that time (mean pocket depth at baseline was 2.9mm and after 2.5 years was 1.3mm). The use of chlorhexidine mouthwash to compensate for ineffective plaque removal has also been advocated.50


People with Down syndrome experience more prevalent and severe periodontal disease.9-15 It has been reported16,37 that the progression of the disease in persons with DS was similar to aggressive periodontal disease. A multi-factorial etiology accounting for this prevalence and severity has been proposed. People with DS have poorer levels of oral hygiene,2,10,21,22 and increased calculus.14,17,21,23,24 However, most authors agree that the amount of plaque and calculus present was not commensurate with the severity of periodontal disease observed.16,17,19,21,47,51

Open-mouth breathing reduces the cleansing action of the saliva and encourages the accumulation of plaque; it also dehydrates the gingival tissues, which may impair the individual's resistance to infection.52 Shorter root lengths and an increased prevalence of fused roots may also influence periodontal disease.2,19,25 It has been suggested that the fused molar roots favor the progression of periodontal disease because occlusal forces have a greater effect on these than on teeth with divergent roots.25

Subgingival plaque in people with DS harbors increased amounts of suspected periodontal pathogens.10,26-28 Gram-negative bacteria contain lipopolysaccharide in their cell wall. Among other effects, lipopolysaccharide has the potential to activate the complement system, produce inflammation, and stimulate bone resorption.53 Herpes virus can also influence periodontal disease. Hanookai et al.28 suggested that periodontal herpes virus and bacterial co-infections might favor destructive periodontal disease. However, few studies have been carried out on this subject.

ANUG is more prevalent in Down syndrome.29,30 ANUG can result in the formation of characteristic gingival craters, which encourages plaque stagnation, and can favor the progression of any underlying periodontal disease.31

Neutrophils and T-lymphocyte function is impaired in people with DS.16,33,35,36 Neutrophils play an intimate role in the periodontal disease process because they have the ability to detect and migrate toward infection and phagocytose microorganisms.34 Van Dyke et al.54 suggested that because of this close involvement in periodontal disease, a decrease in neutrophil function might result in more severe periodontal breakdown. They also suggested that in diseases where neutrophil function was impaired (for example, neutropenia, Papillon-Lefèvre syndrome, and Down syndrome), an increase in periodontal disease was usually seen.54 The immune system can be further compromised by the T-cell dysfunction in Down syndrome. Whittingham et al.38 proposed that the T-cell dysfunction "might be explained by failing immuno-competence due to accelerated ageing". He further proposed that it might even be caused "by a heavy load of infections early in life because of an incapacity to maintain adequate standards of personal hygiene".

Preshaw et al.6 highlighted the important role played by both inflammatory mediators and proteolytic enzymes in the pathogenesis of periodontal disease. Both PGE2 and matrix metalloproteinases have been shown to be present in significantly higher levels in people with DS.41-43 PGE2 is a vasodilator, which is "involved in the increased vascular permeability occurring at sites of inflammation, and a mediator of bone demineralization".44 Matrix metalloproteinases can degrade type I-V collagens, laminin, gelatin, fibronectin, and elastin.44

Institutionalization has been shown19,20 to be associated with an increased prevalence and severity of periodontal disease. Swallow20 proposed that this may be a reflection of the quality of oral hygiene practiced, whereby aid given to non-institutionalized children by their parents may slow the disease's process. Cutress19 suggested that fecal-oral transmission of contagious microorganisms in institutionalized patients may account for the increased prevalence of periodontal disease.

Recent studies9,22,24 have reported the effectiveness of frequent preventive care in slowing the progression and reducing the severity of periodontal disease. Therefore, any barriers that hinder the access of people with DS to dental services could have detrimental effects on their oral health. Fiske and Shafik3 recommended the development and instigation of a realistic preventive program that would include regular scaling and root planing, and advice regarding anti-microbial agents. The results obtained by Yoshihara et al.9 suggest that to combat the severity and progression of periodontal disease in persons with DS, a more frequent treatment interval than the six months suggested by Hennequin et al.1 should be employed. In their study, the mean interval between dental visits in the managed group was 3.7 (± 1.3 months). Sakellari et al.21 also recommended a three-month treatment interval. It has been suggested that an oral hygiene regime that includes chlorhexidine — as a mouthwash, a gel, or as a professionally applied varnish — may be beneficial in reducing oral plaque, and may help compensate for inadequate tooth-brushing.50


The increased prevalence and severity of periodontal disease in persons with Down syndrome is due partly to an inability to adequately maintain oral hygiene. Other contributing factors include an earlier and more extensive colonization with known periodontal pathogens along with other local factors such as open-mouth breathing, tooth morphology, altered microbial plaque composition, and acute necrotizing ulcerative gingivitis. Increasing evidence, however, supports the theory that an impaired immunity due to a reduction in neutrophil chemotaxis, neutrophil phagocytosis, and T-lymphocyte function, as well as an increased production of inflammatory mediators and proteolytic enzymes, may contribute most to the prevalence and severity of periodontal disease in persons with Down syndrome.

Down syndrome is the most commonly diagnosed intellectual disability in Ireland.4 In recent years, trends toward de-institutionalizing people with Down syndrome and placing them in community settings have emerged.15 Therefore, it is increasingly likely that most dental practitioners will encounter a patient with Down syndrome. Every effort must be made to encourage the implementation of frequent preventive care in order to decrease the severity and progression of periodontal disease in their patients.


The author acknowledges Prof. June Nunn for her advice and encouragement in writing this article.


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