## 1 Introduction  
Periodontal disease is an inflammatory disorder that affects the supporting tissues of the teeth, gingiva, periodontal ligaments, cementum and alveolar bone. It is caused by the accumulation of oral bacteria, which organizes into a complex biofilm at the level of the gingival sulcus [1]. The clinical manifestations and evolution of the disease differ between individuals, being determined by the microbial composition of the subgingival biofilm and the host immune response. Moreover, the development of periodontal disease is influenced by a series of local and systemic predisposing factors [2]. The clinical manifestations of periodontal disease can vary from the inflammation of the gingiva to periodontal pockets, clinical attachment loss, bleeding on probing, deep resorption of the alveolar bone, progressive destruction of the periodontal ligament and finally, loss of teeth [2]. Local predisposing factors could act as biofilm retentors [3, 4] including dental calculus, caries, self-inflicted injuries, malocclusions, improperly designed or adapted prosthetic and orthodontic appliances. Most local risk factors are modifiable and correctable so as to offer a favorable status for good plaque control and resolution of inflammation, thus enhancing the risk profiles for periodontal and other common chronic illnesses [5]. Design, fabrication, delivery, and materials of tooth-supported fixed dental prostheses (FDP) are often associated with plaque retention and loss of periodontal attachment. Gingival inflammation and, potentially, gingival recession might be linked to the placement of restoration margins within the junctional epithelium. Additionally, the techniques used for creating fixed prostheses and dental restorations may severely damage the supporting tissues in the periodontium. Nevertheless, the same analysis concluded that if patients adhere to self-performed plaque management and routine maintenance, restoration margins located inside the gingival sulcus do not result in gingivitis [6]. Metal-ceramic (MC) crowns have long been used for dental prosthetic restorations [7], considered superior to composite crowns in terms of prognosis and complications [8] and with no significant differences in these parameters compared to all-ceramic ones [9]. There are studies that compare the implications of MC on the periodontal hygiene and inflammatory status, in regard to the technology used for frameworks, with other types of crowns [10; 11]. After prosthetic rehabilitation, one study showed that in comparison with patients wearing fixed partial dentures, single metal-ceramic crowns had no significant impact on plaque index and gingival inflammation after 14 days, respectively six months [11]. The adaptability of dental restorations is one of the most crucial variables that influence how long they survive. Significant marginal discrepancies expose the luting agent to saliva, which accelerates the process of dissolution. This enables bacterial infiltration to take place, which causes either tooth decay with endodontic problems, or periodontal complications with inflammation and bleeding gums. Eventually, all of these factors result in the failure of dental crowns, in terms of function or aesthetics [7; 8; 10]. In periodontal disease, local host inflammatory mediators are triggered in response to bacterial aggression. These mediators subsequently initiate a localized inflammatory response, which eventually leads to a serum antibody response to the bacteria. The synthesis of acute-phase proteins such as C reactive protein (CRP), macroglobulin, and serum amyloid may be enhanced as a result of bacterial infections, as these infections often serve as a potent trigger for a systemic acute phase response [4]. CRP, an important component of the body's normal defense against infection or inflammation, is an acute-phase protein that belongs to the pentraxins family and is considered to be an inflammatory marker.