# Periodontal Disease Diagnosis in the Context of Oral Rehabilitation Approaches
## 1 Introduction  
Oral rehabilitation, a particularly complex integrative concept of contemporary dental practice, is based on new therapeutic approaches, in which the etiopathogenic factor isof particular significance in establishing a precise diagnosis as the starting point for an individualized treatment plan [1]. The degree of periodontal damage decisively influences the predictability of rehabilitation therapy in a multifactorial context [2]. Considered in the past as \"essential\" diseases, inflammatory diseases of the marginal and deep periodontitis nowadays recognize a specific microbial etiology, with bacterial plaque as the primary factor, to which a collection of favoring and systemic factors are added [3]. Periodontal diseases generally correspond to a disturbance in the balance between the host's defense and the micro-organisms colonizing the periodontal environment [4]. The exact mechanisms by which destruction of the periodontium occurs remain to be fully elucidated. A multitude of etiological factors leads to the inclusion of periodontitis in the group of complex multifunctional etiology [5]. Periodontal disease is a mixed infection, caused by the microbiota of the bacterial plaque and its toxic products, and in this respect, it should be noted that there is not a single bacterium or a single product responsible for tissue destruction, but several, acting either synergistically or at different stages of the evolution of periodontal disease [6]. Some bacterial species are not directly responsible for the onset of the infectious process, but they maintain it and generate optimal conditions for promoting the virulent potential of others [7; 8]. The host organism's response to the action of the microbial factor is commensurate with its complexity and results in inflammation and infection, which are designed to protect the cells [9; 10]. The extent of the host's immune response, however, also affects the body's own structures, leading in part to their destruction and the progression of periodontal lesions [11]. The particularities of inflammation at this level are also related to the anatomy and physiology of the periodontium [12; 13]. Recognition of bacterial plaque site differences in various clinical patterns (disease vs. health) led to a renewed search for specific pathogens in periodontal disease and a conceptual transition from the nonspecific to the specific plaque hypothesis. [14; 15] The source of periodontal risk factors was discussed in detail in recent years. Risk factors may influence a subject in general or may affect localized periodontal tissues [16]. Individual variability in periodontal tissue destruction and documented longitudinally in untreated populations required certain procedures for diagnosis in order to identify early subjects at increased risk for severe periodontal disease [17; 18]. Monitoring untreated disease by investigating periodontal pocket depth, clinical attachment level, or bleeding on probing has limited value for indicating present activity or predicting future attachment loss [19]. On the other hand, the real impact of short bursts of activity on cumulative periodontal tissue loss also remains to be determined [20; 21]. Continued mild attachment loss may have considerable consequences eventually, although it is un-detectable in studies limited to a duration of a few months [22]. To give accuracy of periodontal probing, detection of a continuous disease process, leading to a 6 mm attachment loss over 60 years, may require a minimum study period of 20 years [23]. From the range of usual methods of quantifying periodontal damage in dental practice, subjective observational indices have an important significance, such as [PERSON]'s and Silness' indices, which are based on certain criteria: bleeding on light probing, pocket depth on probing, loss of clinical attachment level, and radiographic evidence of alveolar bone loss [24].