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Hindawi Publishing Corporation

International Journal of Dentistry
Volume 2014, Article ID 182513, 9 pages

Review Article
Risk Factors of Periodontal Disease: Review of the Literature
Yousef A. AlJehani
Dental Health Department, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia
Correspondence should be addressed to Yousef A. AlJehani;
Received 3 April 2014; Accepted 7 April 2014; Published 20 May 2014
Academic Editor: Jagan Kumar Baskaradoss
Copyright © 2014 Yousef A. AlJehani. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Objectives. This paper aims to review the evidence on the potential roles of modifiable and nonmodifiable risk factors associated
with periodontal disease. Data. Original articles that reported on the risk factors for periodontal disease were included. Sources.
MEDLINE (1980 to Jan 2014), PubMed (using medical subject headings), and Google Scholar were searched using the following
terms in different combinations: “periodontal disease,” “periodontitis,” “risk factors,” and “causal.” This was supplemented by handsearching in peer-reviewed journals and cross-referenced with the articles accessed. Conclusions. It is important to understand the
etiological factors and the pathogenesis of periodontal disease to recognize and appreciate the associated risk factors. As periodontal
disease is multifactorial, effective disease management requires a clear understanding of all the associated risk factors.

1. Introduction

2. Risk Factors of Periodontal Disease

Periodontitis is one of the most ubiquitous diseases and
is characterized by the destruction of connective tissue
and dental bone support following an inflammatory host
response secondary to infection by periodontal bacteria [1,
2]. Severe periodontitis, which may result in tooth loss, is
found in 5–20% of most adult populations worldwide [3–5].
Children and adolescents can have any of the several forms of
periodontitis such as aggressive periodontitis, chronic periodontitis, and periodontitis as a manifestation of systemic
diseases [6–8].
It is now generally agreed that almost all forms of periodontal disease occur as a result of mixed microbial infections within which specific groups of pathogenic bacteria
coexist [9–11]. Evidence is reviewed on the potential roles
of modifiable and nonmodifiable risk factors associated with
periodontal disease. An understanding of risk factors is
essential for clinical practice.

2.1. Modifiable Risk Factors

1.1. Search Strategy. MEDLINE (1980 to Jan 2014), PubMed
(using medical subject headings), and Google Scholar were
searched using the following terms in different combinations: “periodontal disease,” “periodontitis,” “risk factors,”
and “causal.” This was supplemented by hand-searching in
peer-reviewed journals and cross-referenced with the articles

2.1.1. Microorganisms and Periodontal Disease. The oral bacterial microbiome includes over 700 different phylotypes,
with approximately 400 species found in subgingival plaque
[12, 13]. The subgingival microflora in periodontitis can harbor hundreds of bacterial species but only a small number has
been associated with the progression of disease and considered etiologically important. Subgingival plaque from deepened periodontal pockets is dominated by gram-negative
anaerobic rods and spirochetes [14, 15]. Strong evidence has
implicated Porphyromonas gingivalis [16] and Aggregatibacter actinomycetemcomitans [17, 18] to the pathogenesis of
adult periodontitis. In addition, Bacteroides forsythus [19],
Prevotella intermedia [18], Peptostreptococcus micros [20], and
Fusobacterium nucleatum [21] have been strongly linked with
the progression of adult periodontitis.

2.1.2. Tobacco Smoking. There is accumulating evidence for a
higher level of periodontal disease among smokers [22, 23].
Tobacco smoking exerts a substantial destructive effect on
the periodontal tissues and increases the rate of periodontal
disease progression [24]. Risk factors including tobacco
smoking modify the host response to the challenge of bacteria

7. some tranquilizers and sedatives. which are sources of vitamin C. Wu et al. Younger people may have different dietary patterns than older study participants. Drugs such as anticonvulsants. One of the important oral signs of diabetes is gingivitis and periodontitis. increased glucocorticoid secretion that can depress immune function. Osteoporosis. 2. International Journal of Dentistry cerebrovascular disease [53]. 2. reducing blood flow. 70]. 67] and financial strains [68]. and clinical signs of inflammation [28]. and antimetabolites.2 in microbial dental plaque [25. Epidemiological and microbiological studies have lent credence to the concept that periodontal disease may be a separate risk factor for cardiovascular disease. In particular. Conversely.5. Obesity. Periodontal disease is capable of predisposing to vascular disease due to the rich source of subgingival microbial species and host’s response. edema. patients who have undergone heart valve surgery have a significant risk of life-threatening infective endocarditis. and preterm delivery of low birth weight infants [54]. Patients with undiagnosed or poorly controlled diabetes mellitus type 1 or type 2 are at higher risk for periodontal disease. The biological plausibility of the association between periodontal diseases and cardiovascular diseases is well studied and it includes some of the following possible mechanisms: high concentrations of cholesterol and the action of oral bacteria in the process of atherosclerosis or the participation of acute-phase proteins that may increase in chronic periodontitis [47. Research in dietary trends in adolescent’s ages from 11 to 18 reveals a significant decrease in raw fruit and nonpotato vegetables. Periodontitis also progresses more rapidly in poorly controlled diabetics [35]. Periodontitis is associated with the increase in the level of C-reactive protein and fibrinogen. Nicotine acetylcholine receptor has been found to play an important role in the development of nicotine related periodontitis [29]. These include antihypertensives. Cardiovascular Disease. Stress is associated with poor oral hygiene. periodontitis can probably elicit a systemic inflammatory response and it deserves more attention [49]. is associated with cardiovascular diseases [51]. most well-controlled diabetic patients can maintain periodontal health and will respond favorably to periodontal therapy [37]. and cyclosporine may induce gingival overgrowth [59]. we must be aware that these diseases share many risk factors and there are evident similarities to the basic pathogenic mechanisms [50]. Men who reported being angry on a daily basis had a 43% higher risk of developing periodontitis compared with men who reported being angry seldom [66]. such as the C-reactive protein (CRP) and interleukin-6 (IL6).1. increased insulin resistance. Furthermore.1. Despite discrepancy regarding this issue in the scientific literature. and potentially increased risk of periodontitis [66]. Several biological mechanisms have been proposed to explain the relationship between periodontal diseases and cardiovascular diseases. Smokers with periodontal disease seem to show less signs of clinical inflammation and gingival bleeding compared to nonsmokers [27].2. 2. Studies have found some periodontal disease indicators such as tooth loss and gingival bleeding to be associated with work stress [66. Nonmodifiable Risk Factors 2. alter the pH and composition of plaque. 2.1. 2. Diabetes Mellitus.1.1. calcium channel blocking agents. People who consume less than the recommended dietary allowance (RDA) for calcium and vitamin C have slightly higher rates of periodontal disease [74]. adolescents have decreased their calcium intake and increased their intake of soft drinks and noncitrus juices. particularly for ischemic stroke. Several explanations for the association between obesity and periodontal disease [71–73] in younger adults have been provided. making it more able to adhere to tooth surfaces [58]. This is important to oral health because low dietary intake of calcium and vitamin C has been associated with periodontal disease [74]. Some medications significantly decrease salivary flow. and particularly the mandible [81]. narcotic analgesics. Drugs can be a contributing factor in periodontal diseases. particularly those in liquid or chewable form that contain added sugar. There are many studies that demonstrate an association between diabetes and an increased susceptibility to oral infections including periodontal disease [30–34]. and early age of onset of the disease is seen as a risk factor for more severe diseases [36]. Obesity has been reported to be an important risk factor for periodontal disease [69. In addition. Therefore. Many of the studies conducted to date suggest there is a relationship between skeletal osteoporosis and bone loss [75–80] to the extent that postmenopausal osteoporosis may result in dental osteopenia involving the jaws.4. 2.1. Patients with inadequate stress behavior strategies (defensive coping) are at greater risk for severe periodontal disease [60–65]. 57]. antihistamines. Drug-Induced Disorders.3. there is evidence that suggests that the increase in the levels of systemic markers of inflammation. Many studies addressed the effect of periodontal treatment on glycemic control of diabetes patients [39–46]. it seems that the effect of glycemic control is related to the mode of periodontal therapy [38]. Some studies have found no relationship between periodontitis and ischemic heart disease [56. 48].2. Other drugs. Furthermore. [55] have shown that periodontal disease is another putative and independent risk factor for cerebrovascular disease. 26]. That could be explained by the fact that nicotine exerts local vasoconstriction.6. irrespective of coronary diseases. Osteoporosis was significantly associated with severe alveolar crestal bone loss and the prevalence of periodontitis cases in postmenopausal . Bacteremia from periodontitis and dental disease is known to be the primary cause of infective endocarditis [52]. Stress.

These cytokines activate the fibroblasts that reside in the periodontal tissues to the matrix metalloproteinases (MMPs). 2. Female Hormonal Alterations. 90]. [92] found significantly more periodontal attachment loss among mothers of PLBW infants compared with mothers of normal-term infants.4. and periodontal disease [83. in turn. 2. which has been defined in general terms as a decrease in normal mineralized bone. Papapanou et al.2. which is a disease caused by the cessation of estrogen production and characterized by spinal fractures that occur between the ages of 50 and 70 years. A recent review on the modifiable risk factors concluded that smoking and excess caloric intake contribute to increases in systemic markers of inflammation and can modify gene regulation through a variety of biologic mechanisms [97]. which can activate plasmin. sex may be a demographic factor. This outcome is thought to be the effect of biologic mediators of inflammatory processes such as prostaglandins E2 and TNF. oral bone loss. a plasminogen activator. Chronic periodontitis involves complex interactions between microbial factors and susceptible hosts [91. 119]. which is usually observed among males [118. With oral contraceptives. Such changes may occur during puberty. Risk Characteristics 3.28 mm compared to 0. The bacterial components such as lipopolysaccharides and cytokines activate the macrophages to produce cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF) [39.2. Host Response. 3.2. 2. Pregnancy. can activate some other types of latent MMPs. Chemotherapy or therapy associated with bone marrow transplantation may also adversely affect the gingival health [89. reported increased plasma levels of MMP-8 and MMP-9 in chronic periodontitis patients and emphasized the importance of periodontal treatment to avoid elevated MMP-8 and -9 levels which are associated with many systemic diseases. Sex.International Journal of Dentistry women [82]. among those with advanced disease. Age. which affects an older population and results in proximal femur fractures [86]. Numerous studies reported higher periodontal destruction among males compared to the female population [87. These studies have shown that advanced periodontal destruction and bone loss are seldom seen in individuals under the age of 40 [109. this increase in gingival inflammation is mainly related to the duration of use as it has been suggested that prolonged use of oral contraceptives may detrimentally affect the periodontium. Marcaccini et al. Hemorrhagic gingival overgrowth with or without necrosis is a common early manifestation of acute leukemia [88]. Taguchi et al. MMP-8 and -9 are released from the polymorphonuclear leukocytes (PMN) and are responsible for a substantial part of the destruction caused by the host response. 93]. However. or menopause.2. Women on hormonal replacement therapy (HRT) and oral contraceptives experience increased gingival inflammation [81. The common bacterial product lipopolysaccharide also may have a triggering role in adverse change of the course of pregnancy.2. Patients with chronic leukemia may experience similar but less severe periodontal changes. 114]. and osteoporosis. The possible relationship between periodontal disease and socioeconomic status was . where the periodontal tissues have been exposed to bacterial plaque. which is a primary component of the periodontal matrix. 114].07 on the 25-year-old individuals [112]. However.1. several other studies have suggested an adverse influence of periodontal disease on the course of pregnancy [100–103]. Offenbacher et al. A review of the relationship between osteopenia. Periodontitis and osteopenia may have common etiological agents that may either directly influence or modulate both disease processes [87]. the prolonged and excessive bacterial promotions of the MMPs induce the enhanced degradation of collagen. It has been suggested that periodontal disease may increase the risk of having preterm low birth weight (PLBW) infants [104. 3. 92]. 115–118]. [85] have stressed that it is important to distinguish among osteopenia. Similarly. the menstrual cycle. Plasmin. MMP-13 also facilitates bone resorption by degrading the collagenous matrix of the bone after the bone is demineralized by osteoclasts [95]. Thus. Studies among the elderly have shown that advanced periodontal disease affects only a small fraction of this age group [108. further breakdown does occur with increasing age.2. The reasons for these sex differences are not clear.3. which may interfere with the effects of other factors and it must be controlled for investigating the disease. 105]. The increased severity of periodontal disease and bone loss with age is probably related to the length of time. 3. particularly cardiovascular disorders [96]. A similar finding has been observed even in the elderly population. while tissue inhibitors of metalloproteinases (TIMPs) can inactivate the active MMPs [94]. the relationship observed between sex and the disease is not apparent and is not considered as strong and consistent.5. and is considered to reflect individual’s cumulative oral history [113]. Hematological Disorders. 2. Among susceptible individuals. pregnancy. The review indicated a direct association between skeletal and mandibular osteopenia and loss of alveolar crestal height and tooth loss in postmenopausal women. More studies carried out in some of the developed countries show changing patterns of periodontal disease progression. The most pronounced periodontal changes occur during pregnancy. demonstrated that the mean annual rate of bone loss among the initially 70-year-old subjects was 0. Several studies show that the prevalence and severity of periodontal disease increase with age [87. 84] concluded that osteopenia does play a role in the expression of periodontal disease. postmenopausal osteoporosis. Changes may also 3 be associated with the use of oral contraceptives.3. 99]. Hormonal fluctuations in the female patient may alter the status of periodontal health [98]. 106–112]. Socioeconomic Status (SES). but they are thought to be related to the ignorance of oral hygiene. as a significant proportion of pregnant women suffer from pregnancy gingivitis.

such as lifestyle. and alveolar bone to gram-negative anaerobic bacteria. most familial reports for periodontitis are for early-onset forms now called aggressive periodontitis [132–139]. One likely candidate is the Creactive protein (CRP). Many works in the literature report familial aggregation of periodontal diseases. Thus. but direct evidence for a differential genetic contribution to periodontitis comes from several sources. and serum amyloid [152]. It must be borne in mind that familial patterns may reflect exposure to common environmental factors within these families. 110. This aggregation within families strongly suggests a genetic predisposition. demonstrate that the composite IL-1 genotype is significantly associated with the severity of adult periodontitis. 3. and lack of standardized methods of clinical examination. Genetic Considerations. in the aggressive forms of periodontal disease.4 found in several studies [108. Risk for periodontitis is not shared equally by the population. Reports of the familial nature of chronic forms of periodontitis are less frequent. 1966). behavior. the local host inflammatory mediators are activated [94. race is not a modifiable factor. it is important to consider the shared environmental and behavioral risk factors in any family. the phenotype or disease characteristics do not present significantly until the third decade of life. Some of these factors. and environmental features. and lack of standardized methods of clinical examination. 149] and finally result in serum antibody response to the bacteria [150. the classical risk factors of CVD cannot account for all the variation in the incidence of CVD cases [141].4. These would include education. there are two major forms of periodontitis-chronic and aggressive periodontitis [6]. although this protein is part of the body’s normal response to infection and inflammation. may be under genetic control and may influence the standards of oral hygiene. it was found that the concentrations of hs-CRP and IL-6 were significantly higher in the sera of patients with periodontitis and periodontal treatment decreased the levels of serum hs-CRP and IL-6 [153]. thereby placing “apparently healthy” people at increased risk of cardiovascular disease. Some of the recent studies have reported elevated CRP levels among those with periodontitis [142–145]. such as passive smoking and sanitation. Gingival condition is clearly related to lower SES. possible transmission of bacteria. and education. especially among those having more active sites [146]. McDevitt et al. Although periodontal disease nosology has changed many times over the timeframe of these reports. Elevation of CRP levels among those with periodontitis indicates that periodontitis may also have systemic cytokine mediated effects that may in turn participate in atherogenesis. The participants of the MI Life Study [143] also reported positive association between elevated levels of CRP (>3 mg/L) and severity of periodontitis. Also. 151]. Bacterial infections may often provide a strong stimulus for a systemic acute phase response that may result in increased production of acute-phase proteins like CRP. whereas. In a recent study. But half of all heart attacks occur among people who do not have high cholesterol. and some discrepancies in disease expressions may be explained by the differences in other risk factors between populations. This may in turn help to explain conditions where dental infections may stimulate systemic inflammatory response.5. second. classification systems. since similar problems arise in the study of other delayedonset hereditary traits [133].. but due to different terminology. This variability in presentation of significant signs of disease makes diagnosis difficult. although German studies of the familial nature of chronic forms of periodontitis from the early 20th . 3. As a response to bacterial endotoxins. Periodontal disease has a reciprocal relationship with educational level. third. the lower the periodontal diseases (Department of Health Education and Welfare. Studies show genetic risk factors associated with periodontitis [123–129]. The complex interactions between genes and the environment must also be considered in the evaluation of familial risk for the periodontal diseases. This differential risk for periodontitis is consistent with heritable elements of susceptibility. C-Reactive Protein. International Journal of Dentistry In chronic periodontitis. SES is a modifiable factor and it can be examined in multivariate models for the disease. The higher the educational level. macroglobulin. Reports of the familial nature of chronic forms of periodontitis are less frequent. Education and Race. socioeconomic grouping. but due to different terminology. but the relationship between SES and periodontitis is less direct. incidence of chronic diseases such as diabetes. and fourth decades. Cholesterol has long been known to play a crucial role in predicting risk for heart attack in seemingly healthy people. in whom the disease quickly progresses from chronic gingivitis to destructive periodontitis [131]. 120–122]. although German studies of the familial nature of chronic forms of periodontitis from the early 20th century have been reviewed by [140]. it is difficult to compare reports directly. 147] that in turn initiate localized inflammatory response [148. classification systems. It can be certain that gingival health is better among individuals with higher education and with more secure income. It is clear that periodontitis severely affects a high-risk group representing around 10–15% of the population. not only in declaring if a patient suffers from the disease but also in detecting patients who do not suffer from the disease and differentiating between adult and aggressive forms of periodontitis. oral hygiene. The problems associated with the clinical differentiation of periodontal disease are not uncommon in medical genetics. Once again. Many works of the literature report familial aggregation of periodontal diseases. Several studies involving different racial populations have found some difference in the expression of periodontal disease [108].6. they reported significantly higher levels of CRP among those with adult periodontitis. Currently. Periodontitis is an inflammatory reaction of the supporting tissues of the teeth like the periodontal ligament. the presentation can occur in the first. cementum. As a result there is a growing interest to identify additional markers of coronary risk. In a study by Ebersole et al. 3. They also confirmed that both IL-1 genotyping and smoking history provide objective risk factors for periodontal disease in a private practice environment [130]. it is difficult to compare reports directly.

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