**1. Introduction**

In systemic diseases that can generate periodontal effects, it is worth mentioning osteoporosis as a separate entity in diseases of endocrine origin. Osteoporosis, as a skeletal disease, is characterized by reduced bone mass and micro-architectural changes in the bone that lead to bone fragility and an increased risk of fracture.

Bone tissues are dynamic, with healthy bone undergoing lifelong shaping and reshaping. Modelling is a process by which bone grows linearly in size in response to the stress applied to it. This involves bone neo-formation independent of a previous bone resorption, the skeleton being able to acquire new cortical shapes and thicknesses. On the other hand, remodelling is initiated by resorption and is followed by the formation of new bone tissue at the same resorption site. Bone remodelling repairs skeletal micro-destruction to preserve resistance and provides serum skeletal calcium for mineral homeostasis. Signals from mechanical stress are received by osteocytes and are transmitted to osteoclasts or osteoblasts or their precursors.

Bone resorption reflects the amount of osteoclast recruitment and death, as well as the rate of matrix degradation [1].

Hypothetical patterns linking the two conditions exist: it is assumed that reduced bone density in connection with osteoporosis may accelerate the resorption of alveolar bone caused by periodontitis, facilitating the invasion of pathogenic bacteria. This bacterial invasion affects normal bone homeostasis, increases osteoclastic activity, and reduces bone density both systemically and locally through both the direct effect of releasing toxins and the release of inflammatory mediators [2].

Since periodontal disease is a multifactorial condition, osteoporosis, although it may not be the cause of its onset, may be a factor in further exacerbation. Thus there is a greater predisposition to lose alveolar bone in subjects with osteoporosis, especially against the background of a pre-existing periodontal disease [3].

Oestrogen deficiency leads to the production of several cytokines produced by immune cells (monocytes and macrophages) and osteoblasts. When challenges arise from plaque biofilm products, bone resorption factors such as lipopolysaccharides, and toxins, the host's immune system produces several inflammatory cytokines that activate osteoclasts and cause bone resorption. The accumulation of bacterial plaque made up of periodontal bacteria seems to be necessary for a woman who is deficient in oestrogen to show changes such as loss of attachment and destruction of the alveolar bone.

The inflammatory response of the host to this biofilm starts the inflammatory cascade and can lead to a constant activation of proteinases and enzymes with the role of tissue degradation, leading to destruction of connective tissues, resorption of alveolar bone and finally bone loss, which explains the increased risk of periodontal damage in menopausal women [4].

Oestrogen deficiency-induced osteoporosis, characterized by an imbalance between bone formation and bone resorption, is caused by elevated inflammatory cytokines such as tumour necrosis factor α (TNFα), interleukin 1 (IL-1), IL-6 and gamma interferon (IFN-γ) [5]. Studies have shown that inflammatory cytokines increase osteoclast activity and activate bone resorption. Therefore, anti-resorptive therapy is widely used in the management of osteoporosis. This type of treatment, however, only prevents additional bone loss while barely stimulating bone formation and reversing bone loss. A number of studies have shown that elevated levels of inflammatory cytokines cause deficits in osteogenesis in postmenopausal osteoporosis and in inflammatory diseases such as arthritis and periodontitis [6].

## **2. Periodontal clinical and radiological status in patients with periodontal disease and osteoporosis**

To date, most studies focused on the relationship between periodontal disease and osteoporosis have been performed in small groups, with limited control of bias factors, with significant variations in defining the parameters of periodontal disease and osteoporosis; there are also few longitudinal studies that establish a temporal relationship.

Decreased systemic bone density in patients with osteoporosis, including the jaw bones, may provide circumstances of increased susceptibility of these patients to periodontal damage.

Orthopantomography can be used as a complementary examination of the patient with osteoporosis and periodontal disease, to assess the width of the mandibular cortex, the cortical mandibular angle, the cortical index and the degree of resorption of the alveolar ridge. We conducted a study on a group of 41 subjects, whose aim was to evaluate radiological parameters on digital orthopantomography in patients with chronic periodontitis and osteoporosis, as well as to establish a correlation between them [7], bone mineral density and periodontal clinical parameters. For radiographic analysis we used digital orthopantomographs. The following determinations were made:


C1: normal bone cortex, with regular endo-osteal margin at both sides; C2: moderately eroded bone cortex, with endo-osteal margin with semilunar defects;

C3: severely eroded bone cortex, with visibly porous endo-osteal margin.

The mean value of the plaque index was 1.21 ± 0.32. This index has been closely correlated with a C2 bone cortex class. A positive correlation was demonstrated between this index and the average loss of attachment. The mean value of the gingival index was 0.79 ± 0.21. This index was correlated with class C2 of bone cortex and with average loss of attachment. The mean value of the bleeding index was 2.3 ± 0.38, an index also correlated with class C2 of the bone cortex and loss of attachment. The mean value of the periodontal probe performed on all study participants was 4.72 ± 1.02 mm. There was no correlation between probing depth and bone resorption index [7].

The mean value of attachment loss was 4.35 ± 1.01 mm. There was a close positive correlation between the average loss of periodontal attachment and the C2 class of bone cortex. There was a negative correlation between mean attachment loss and bone resorption index. There was a link between the average loss of periodontal attachment and the plaque index, calculus index and gingival index [7].

A total of 58.7% of patients had 15–30 teeth remaining on the arches; 27.9% of the total number of examined patients had up to 15 remaining teeth and 13.4% of them - over 30 remaining teeth on the dental arches. A total of 36.5% of patients had loss of dental-periodontal units due to coronary dental lesions, 30.7% due to periodontal disease and 32.8% due to the association of carious lesions with periodontal disease. Only 3.8% of all patients had intact dental arches. Third molars were not considered in the calculation.

Using a threshold level of 3 mm for cortical thickness, only 2 patients had MCT <3 mm. We noticed an association between the T score value and MCT; low values of the T score were correlated with low values of cortical thickness (p < 0.05) [7].

We noticed that a decrease of MCT by 1 mm increases the risk of osteopenia/ osteoporosis by 43%. The p value for MCT was statistically significant (p = 0.033). Moreover, when the morphology class is C2 or C3 (moderate and severe erosions), the age is increased and the MCT decreases to a statistically significant level (p < 0.05). A decrease of one millimetre of MCT increases the probability of moderately or severely eroded cortex by 96%. In terms of tooth loss, a one-unit increase in the number of missing teeth increases the probability of moderate or severe erosion by 6%.

Given that periodontal examination, along with performing oral radiographs are common procedures [8], the clinical significance for the observation of additional

risk factors for osteoporosis is extremely high, and questions regarding skeletal status may arise. General condition of the patient.

An important result in this study is given by the close correlation between local factors and the loss of periodontal attachment and bone tissue. Moreover, the loss of attachment was closely related to the bone resorption index.

The oral cavity and jaws are examined radiologically more frequently than any other part of the human body. Orthopantomographic radiography can be a useful means of screening in the diagnosis of osteoporosis, providing valuable information on the quality of the maxillary bone.

The radiograph does not allow the visualization of the periodontal infection, nor the migration of the junction epithelium in the initial periodontal lesion. However, the radiographic image reflects the status of the mineralized structures of the periodontium. Thus, radiography is indispensable for assessing bone loss and for establishing residual value.

Clinical measurements by periodontal examination do not always fully and accurately reflect tissue loss, nor is radiography sufficient to establish a positive diagnosis. Radiography provides the image of two-dimensional bone changes, as well as abnormalities of radiopaque structures (carious, endodontic, reconstructive lesions). Radiographic images frequently used in periodontology are given by retro-dental-alveolar radiography, orthopantomography, as well as bite-wing radiography.

The panoramic x-ray represents a complex projection of the maxillary bones and dental arches, with multiple super-positions and distortions that can be exacerbated by image capture errors. Moreover, orthopantomography (OPT) illustrates numerous anatomical structures, in addition to the maxillary bones, which can represent interpretive challenges. In order to obtain a successful interpretation of panoramic radiographs, an understanding of the normal anatomy of the head and neck region and its radiologic aspects is absolutely mandatory.

Analysis of the density of the trabecular pattern of the maxillary bone, seen radiologically, showed that dense trabeculation is a strong indicator of increased mineral density, while thin trabeculation corresponds to low mineral density [9]. It is well known that in patients with osteoporosis the bone loss is not uniform and that the trabecular bone is earlier and more deeply affected than the cortical bone [10].

The mandible has a composition similar to the femoral neck [11], where fractures are mainly caused by a cortical loss rather than a trabecular bone. Given that the jaw consists mainly of trabecular bone, it is possible that the bone density measured at this level is more closely related to osteoporotic disease. However, the lack of fixed reference points in the upper jaw (such as the chin hole in the jaw) makes the assessment of standard points at this level a challenge.

Osteoporosis can be diagnosed by observing tooth loss, thinning of the lower mandibular cortex, and by changes in the morphology of the endo-osteal margin of the cortex and trabecular bone [12].

Mandibular bone mass correlates with systemic skeletal bone mass in numerous studies. Horner and Devlin reported a relationship between mandibular cortical thickness and mandibular bone density [12]. Cortical thickness at the gonial angle was determined by panoramic radiographs on a group of 180 patients; for patients aged 15 to 69 years, this was relatively constant; in subjects over 60 years of age, a decrease was observed, more significant for women than for men [13].

Devlin and Horner [12] reported that a cortical thickness of 3 mm is most appropriate as a threshold value for bone densitometry. White et al. [14] consider that this threshold value is more recommended to be 4 mm. Klemetti et al. [15] reported that the 4 mm threshold is optimal but not sufficient in itself for an

*The Role of Osteoporosis as a Systemic Risk Factor for Periodontal Disease DOI: http://dx.doi.org/10.5772/intechopen.96800*

optimal classification of subjects. In the present study we discovered values below 3 mm only on 3 radiographs; thus, we support the opinion of White et al. according to which, if panoramic radiographs are used, the threshold for cortical thickness is more appropriate at 4 mm [14].

As for quantitative computed tomography (QCT), it was first used to study the relationship between oral status and osteoporosis in 1989. Regardless of the technique used, the position of the sections and perspective should be documented by subsequent examinations to avoid the error of precision. The reported accuracy for QCT ranges from 1 to 3% for highly controlled settings and 4–5% for clinical settings [16]. Also, the cost of computed tomography is quite high, so it is not recommended only for a screening system in osteoporotic disease.

It has been demonstrated that mandibular cortex thickness can be a useful parameter to clinically assess metabolic bone loss and that a gonial thickness of less than 1 mm is an indicator of metabolic bone loss [12]. Dissemination of information on the prevention of osteoporosis produces a significant public effect for the implementation of appropriate ways to minimize the process of reducing bone mass.
