Kina JR (2018) What Would Be the Most Important Approach to Treating Periodontal Disease? JSM Dent Surg 3(1): 1029.

To treat any disease it is always necessary to know what causes the disease. The etiology includes the sum of evidences related to the causes of a disease. To treat or to prevent any disease always will be necessary eliminating all etiologic factors, or/and improving host local defense or/and general resistance against the entire etiologic factors, or/and establishing control in all etiologic factors at levels below the degree of resistance of the host to promote homeostasis in diseased areas through a long stated period. To establish a treatment plan that would be used in treating a disease, it is essential to understand the vital role of the etiological agents that initiated the disease. Periodontal disease results from the association of the bacteria with many other etiologic factors. Although, bacteria are a critical etiologic factor that are needed to develop a periodontal disease, bacteria alone are insufficient to induce a periodontal disease; the host’s susceptibility as local and/or general predisposing risk factors, are important determinants of the disease status [1]. The diagnostic of the etiological agents of the periodontal disease is critical, due to the necessity of the association among a susceptible host and the various etiological agents, such as bacteria, and several local and/or general predisposing risk factors to induce the disease. However, the majority of all forms of periodontal diseases are considered as microorganisms-induced dependent, which promotes a defensive inflammatory host’s response against the bacteria and noxious materials from the biofilm. The inflammatory process inactivates the bacteria, but produces the liberation of bacterial and neutrophils products such as enzymes, which induce periodontal tissue destruction by lytic activities. Therefore, the characteristics of the periodontal disease are: presence of gingival inflammation, ulceration of the junctional epithelium, loss of connective tissue and alveolar bone, causing apical migration of the junctional epithelium. Then periodontal disease is a defensive mechanism which avoid penetration of bacteria into the periodontal tissues, to prevent infections and septicemia. However as a side effect this mechanism of protection induces the formation of periodontal pockets, the major pathognomonic sign characteristic of a periodontal disease: an increase in the depth of gingival sulcus, thereby, creating a favorable anaerobic environment to be infected, as a result of the recurrent contamination by the several species or the combination of the species as exogenous anaerobic and facultative bacteria (periodontopathogenic bacteria). These putative periodontal pathogens and their products may induce substantial pathological alterations, essentially in root surface exposed to the contaminated periodontal pocket. On the other side, due bacterial approximation to the ulcerated pocket epithelium, infected periodontal pocket also could be an infectious focus linked to the various systemic disorders, probably led by anachoresis, a process associated with dissemination of the microorganisms or/and toxics products into blood stream, assisting or causing infection in the various vital organs [2]. In addition, the destruction produced during the periodontal disease progression, may present similar characteristics, but the association among the bacteria and the various predisposing risk factors, may be distinct and inherent to each person, depending on the host’s susceptibility, which does not always present an identical susceptibility to the various local and/or general predisposing risk factors. Most of the periodontal disease induces local destruction, essentially due to the involvement between the opportunist bacteria and the various and inherent local predisposing risk factors. The local predisposing risk factor may provoke a mechanical vulnerability in the periodontal tissues around a tooth, and/or may assist in bacterial retention, development and organization, in order to originate periodontal tissue destruction. Generalized periodontal disease may arise, when the systemic predisposing risk factor interferes with the host’s defense mechanism against the opportunist bacteria, once the host factor operates in all periodontal tissues. The predisposing risk factor may statistically increase the occurrence of a disease, but it does not cause the disease. Predisposing risk factors may be defined as systemic factors, local factors, behavioral factors in nature, and factors related to the development of the acquired alterations that involve the periodontal tissues. All types of periodontal disease are multifactorial diseases, which progress through successive destructive acute phases, always interposed, by reparative chronic phases. The indication of the periodontal disease reparative phase is possible to find in untreated periodontal pocket, as cementum and the gingival-attached connective tissue zone, separating the apical end of the ulcerated periodontal pocket epithelium from the underlying destructed alveolar bone which always presents a repaired cortical bone at a range of levels protecting the cancellous bone. In untreated periodontal disease, the gingival-attached connective tissue zone should be destructed, but they arise most often in untreated periodontal pockets. After each successive destructive acute phase, variations in the quantity and quality of the etiological agents and the predisposing risk factors would arise. However, periodontal disease always ceases the brief acute destructive phase beginning in the sequence a long chronic reparative phase. This fact demonstrates that, etiological agents and predisposing risk factors during the periodontal disease progression, acquired better quality and quantity, but could not be able to maintain the periodontal disease destructive phase activity all the time. Probably, the periodontal disease initiates and progress when at a given time, a specific temporary fragility, inherent for each individual, assists involved etiological agents in initiating the destructive acute phase to establish the progression of the periodontal disease. One of the transitory predisposing risk factor may be emotional stress, which is intrinsic for each individual, inducing a temporary physical, mental, and functional fragility. The emotional stress, which can emerge from any situation or thought, appears or disappears at any moment, attacks in various aggressive levels, interferes in the host’s immune defense, and severely in the stomatognathic system, may possibly be the main predisposing risk factor that can activate or cease the periodontal destruction. Every individual with a preserved natural occlusion, presents a premature contact with the centric relation, and is almost impossible to remove all the interfering contacts promoting a stable and permanent artificial condition known as centric occlusion. Some mechanoreceptors from the periodontal ligaments maintain the proprioceptive impulses, by providing feedbacks to avoid occlusal interference. The stomatognathic system suffers adaptation compensating deleterious premature contact with a habitual occlusion, where a masticatory pattern is developed with the force applied, being dissipated normally in the periodontium. Despite a premature contact, during functional mastication, the antagonist teeth do not establish effective contact. However, during daytime and/or sleeping time, the individual under stress may develop centric and/or eccentric bruxism, with the antagonist teeth establishing an effective contact, and generating eccentric and intense forces in the periodontium which associated with bacteria may initiate or restart periodontal disease acute destructive phase [3]. The destructive acute phase is very fast and the reparative chronic phase may be long. Since the destructive acute phase of periodontal disease is very fast normally the treatment of the periodontal disease is applied in its reparative chronic phase which in this moment being reparative could not be in the best moment to be treated. In addition, the approach to treatment of the periodontal disease is based on scaling and root planning and on the biofilm control, without emphasizing the predisposing risk factors without which it seems impossible to initiate periodontal disease. All etiologic factors must be focused to keep periodontal disease stable for a long period. Then the following questions should be analyzed:

1. What would be the most important approach to treating periodontal disease?
2. What is the best moment to treat periodontal disease? In its acute destructive phase or in its chronic reparative phase?
3. Are there reliable tests to diagnose the phases of periodontal disease progression?
4.  The periodontal disease is still a challenge in terms of diagnosing their etiological factors: how these etiological factors act on each susceptible host at different and nonspecific moments? and also how to perform procedures to reconstruct the diseased periodontal tissues to the stage of pre-disease?

1. Kina JR, Kina J, Kina EF, Kina M, Soubhia AM. Presence of bacteria in dentinal tubules. J Appl Oral Sci. 2008; 16: 205-208.

2. Kina JR, Suzuki TY, Kina J, Kina M, Kina EF. Reparative phase events on periodontal disease progression: interpretation and considerations. Int J Microbiol Res. 2013; 5: 439-444.

3. Kina JR, Suzuki TY, Kina J, Kina M, Kina EF. Non-inflammatory destructive periodontal disease. Open Dent J. 2016; 10: 50-57