**Abstract**

Gender-based heterogeneity in periodontal disease has been witnessed in the recent past with huge mounting evidence. The composite effect of sex-based genetic structure and the sex steroid hormones runs in line with the corresponding genderrelated differences in risk for chronic periodontitis. Since estrogens, the predominant sex hormones in women, show immune protective and anti-inflammatory effects in hormonally active premenopausal women, they show better periodontal status compared to age-matched men. Conversely, after menopause with a weakening estrogen signal, women may show an equal or even more serious periodontal status compared to men. Periodontal status of postmenopausal women may be improved by menopausal hormone therapy. Alveolar bone loss, an irreversible sign of past periodontal disease activity can be easily observed on radiographs in an objective manner. Orthopantomographs provide a fairly accurate assessment of the status of alveolar bone in the whole mouth. A cross-sectional retrospective panoramic radiographic analysis has been carried out in a north Indian dental institute to decipher the gender-based distribution of periodontal bone loss. The current chapter shall provide an update on gender-based differences in oral health, underlying mechanisms, differences in patterns and distribution of alveolar bone loss (case study), and potential gender-specific disease protection and management strategies.

**Keywords:** oral health, periodontal, gender, alveolar bone loss, radiography, panoramic

#### **1. Introduction**

Many human diseases, specifically chronic immune-mediated diseases, present differentially in males and females [1]. Differential gene expression and immune system in the human body guided by sex steroid hormones are responsible for the differential physiologic constitution of the two genders [2]. Chronic periodontal disease is an immune-inflammatory disorder affecting teeth and

supporting tissues, inducing the destruction of alveolar bone, and ultimately leading to loss of teeth if it remains untreated. As evidence of periodontal infection's influence on overall chronic inflammatory disease states of human body continues to mount from last two decades, a whole new concept of the status of the oral cavity and its impact on systemic health and disease has evolved. Immense research efforts have been directed toward better understanding of the prevention and control of human periodontal diseases that have been warranted in the recent past [3].

Enhanced understanding regarding the causation mechanisms of human periodontal disease in the recent past and the identification and recognition of the potential significant susceptibility factors, which are a part of the causal chain for initiation and progression of periodontal disease, have led to focused research into specific risk factors for periodontal disease. Greater age [4–8], male sex [9, 10], bacterial plaque [4, 8], and smoking [8, 11–13] have been linked with an increased susceptibility to periodontal disease [14].

Epidemiological investigations have explored the role of these risk factors for periodontal disease causation and treatment needs of populations. A risk factor may be anything like environmental exposure, a behavioral aspect, or a constitutional feature which may enhance the chances of occurrence of disease. The term "determinant" is generally used interchangeably with risk factors, but it is more appropriate to limit its usage for the risk factors that cannot be modified, for example, age and sex. Readers are referred to go through many elaborate and exhaustive reviews on these particular aspects to enhance their understanding regarding differential risk and risk factors of periodontal diseases [15]. The current chapter shall provide an update specifically on gender-based differences in oral and periodontal health, underlying mechanisms, differences in patterns and distribution of alveolar bone loss (based on the case study), and potential gender-specific disease protection and management strategies.

#### **2. Periodontal disease**

Periodontal diseases primarily comprise the two most common oral inflammatory disorders, that is, gingivitis and periodontitis, which are caused by microbes residing in the subgingival dental plaque. To name a few, primary pathogens like *Porphyromonas gingivalis*, *Aggregatibacter actinomycetemcomitans*, *Tannerella forsythia*, and *Treponema denticola* trigger an immune reaction from the host, including innate, inflammatory, and adaptive components causing major part of the tissue destruction indirectly. Direct damage from the microbial products constitutes a minor part of the total tissue loss [16, 17]. Gingivitis is an inflammation of the gingiva, limited to soft-tissue compartment of the gingival epithelium and connective tissue only and the tooth does not suffer an attachment loss [18]. Periodontitis, on the other hand, is an inflammation of the supporting tissues of the teeth with progressive attachment loss and bone destruction [19, 20].

Many investigations have been conducted in diverse areas worldwide. A variable, yet significant prevalence of the periodontal disease has been noted, which amounts to an enormous disease burden in the domain of public health. The National Institute of Dental and Craniofacial Research refer to periodontal diseases as the leading cause of tooth loss in adults [21]. In 2013, Marcenes et al. ranked periodontitis as the sixth most prevalent condition while estimating the global burden of oral conditions from 1990 to 2010 [22]. Moreover, severe periodontitis is considered as the primary cause of disability-adjusted life years (DALYs) s in the age-group of 35- to 59-year-old. Several studies have reported the prevalence of periodontitis in

*Gender-Associated Oral and Periodontal Health Based on Retrospective Panoramic… DOI: http://dx.doi.org/10.5772/intechopen.93695*

the United States [23, 24]. The overall prevalence of periodontitis was 66% for all seniors 65 years of age or older with males being predominantly affected [25].

Prevalence of the periodontal disease varies in different regions of the world and a higher prevalence and severity of periodontal disease in Asian countries has been reported [26]. The authors looked into the geographic and economic risk factors, oral health distribution and practices in these vast groups of countries to enhance understanding regarding the oral health care needs and formulating health policy decisions [27]. A study from Pakistan revealed that 63.5% of the subjects had Community periodontal index score ≤ 2 while 34.5% had ≥3. Age, gender, occupation, smoking, diabetes, arthritis, cardiovascular disease, kidney disease, stress, medications, and oral hygiene habits of using tooth powder or tooth brushing were significantly associated with periodontal status [28]. Multiple studies to understand the occurrence, prevalence, and all associated factors have been carried out in many states and across the country in India also [29–34]. A systematic review pointed out that due to lack of homogeneous studies, it is difficult to estimate an overall prevalence rate. A nationwide multicentric prevalence studies initiative is needed to obtain the true prevalence rate of periodontal disease in India so that interventions should be provided for the same to maintain the oral health and quality of life of the affected population [29–34].

#### **2.1 Clinical features of periodontitis**

Generally speaking, periodontal disease is a chronic silent disease, which barely has any symptoms at an early stage. Most patients suffering from chronic periodontal disease seek treatment very late by the time the disease has progressed significantly. Redness or bleeding of gums with or without tooth brushing or flossing or biting into hard food, repeat episodes of gingival inflammation, oral malodor or bad breath, and a persistent metallic taste in the mouth. In progressed disease, gingival recession, resulting in loss of gums exposing the roots of teeth, deep pockets between the teeth and the gums mobile teeth, in the later stages, drifting and flaring of incisors, increased spacing between the teeth, tendency to dig between the teeth, packing of food in between teeth, itchy gums, sensitivity to hot and cold foods. Periodontal disease is generally regarded as painless. Patients generally consider only bleeding without pain from gums with or without brushing as an insignificant sign; however, this may be indicative of ongoing disease activity and progression of chronic periodontitis. Poor oral hygiene, soft sticky deposits, that is, dental plaque and hard mineralized subgingival as well as supragingival calculus are frequent findings of periodontal disease [35].

#### **2.2 Periodontal pathogenesis**

Periodontitis is a chronic multifactorial disease causing inflammation of the supporting tissues of teeth mediated by the host, which is associated with an imbalance in the existing microbial flora in dental plaque and resulting in a continuous loss of tooth-supporting apparatus [36, 37]. The bacteria in the dental plaque are the essential initiators of the gingival inflammation; however, not all cases suffering from gingivitis progress into periodontitis. This transition is largely determined by the host immune response. Once gingival inflammation is set in, tissue microenvironment changes and causes an alteration in the microbial ecology and also in host response mechanisms against the residing bacteria. This leads to the stimulation of several key molecular and cellular signaling pathways, which ultimately activate host-derived collagenases [matrix metalloproteinases (MMPs)] which are responsible for tissue destruction. Such lytic process cause loss of principal fibers of the

periodontal ligament, apical migration of the gingival attachment, and allows apical extension of biofilm and subjacent inflammation along the root surface and further spreads the disease process [36]. It leads to loss of clinical attachment, pocket formation, sometimes gingival recession, and radiographically accompanied bone loss [37, 38]. Gingivitis is a completely reversible disease process and the essential first step to progression to periodontitis, suggests periodontitis can be prevented at its early stage, yet it remains one of the most common causes of tooth loss. Therefore, prevention and early detection of periodontal disease are essential to reduce the damages it implies to the oral and systemic health of the individual.

#### **2.3 Alveolar bone loss in periodontal disease**

Alveolar bone loss is a characteristic sign of advanced periodontitis and ongoing bone loss is characteristic of the progression of periodontitis. The prevention of periodontal disease progression and bone loss is a key clinical challenge in periodontal therapy. Bone destruction is an eventual outcome of the host immune and inflammatory response and the dental plaque microbial challenge interplay. However, the underlying mechanism of disruption of the homeostatic balance of bone formation and resorption in favor of bone loss in these clinical situations remains to be understood.

#### *2.3.1 Immunopathogenesis of periodontal bone loss*

In chronic periodontal disease, many bioactive microbial molecules from dental plaque incite an immunological response from the resident and immune cells present in gingiva and periodontal tissues [39]. This leads to an influx of multiple cytokines that mediate the biochemical pathways of inflammation, for example, PGE2, IL-1, TNF-alpha and RANK-L, etc., which are responsible for osteoclastogenesis, the primary bone-resorbing process. Thus, the pathologic inflammatory process disrupts the fine balance between protective and destructive processes and leads to initiation of osteoclastic activity [40–45]. "Osteoimmunology" is the science which is dealing with the understanding of the intricacies of this immune-mediated bone destruction [46, 47]. The cellular inflammatory infiltrates of periodontal immunity cells such as T cells, B cells, macrophages, and neutrophils are increased within the gingival connective tissue and a concurrent increase in the inflammatory mediators' production is also evident [48, 49]. RANKL-mediated osteoclastogenesis is the prime mechanism underlying the inflammatory bone resorption in periodontal tissues [43, 50]. Activated T and B lymphocytes in inflamed periodontal tissues are the prime producers of RANKL- [43, 44, 51, 52]. An increase in osteoclast numbers on the alveolar bone crest has been observed in animal studies where antigen-specific lymphocytes are present and which can be suppressed by OPG [51, 53, 54].

Heterogenous populations of gingival fibroblasts are involved in dual actions in the inflammatory process. They are documented to have a protective role to suppress osteoclast formation as they produce OPG in response to LPS and IL-1; however, they may also augment chronic inflammatory processes through IL-6 and IFN production. The known periopathogens *Aggregatibacter actinomycetemcomitans* (*Aa*) and *Porphyromonas gingivalis* (*Pg*) induce the production of RANKL from the resident cells of periodontium viz. osteoblasts and gingival fibroblasts. Recently, it has been shown that an increased RANKL/OPG ratio is associated with periods of tissue destruction and ongoing disease activity. This ratio is further upregulated in patients in the presence of other known risk factors, for example, smokers and diabetics [55]. It has also been reported that the molecular mechanisms of T cellmediated regulation of osteoclast formation occurs through cross talk signaling between RANKL and IFN-gamma [56].

*Gender-Associated Oral and Periodontal Health Based on Retrospective Panoramic… DOI: http://dx.doi.org/10.5772/intechopen.93695*
