Anatomia Patologica

UNIVERSIDAD AUTONOMA DE NUEVO LEON

FACULTAD DE ODONTOLOGIA

ANATOMIA PATOLOGICA

2da EVIDENCIA
“CASO CLINICO”

Catedrático: Dra. Nora Amelia Villegas.

Alumnos: Joaquín Galván.
Hilda Elizondo.
Irema Gamboa Aburto.
Arleth García Fuentes.


GRUPO 06 Equipo:0413 DE FEBRERO DE 2012

SHOULD OUR FOCUS ON INFLAMMATION CHANGE THE WAY WE PRACTICE?
Dr. Michael K. McGuire*
Some scientists say, ‘‘Forget about bacteria; treat, or even better yet, prevent inflammation.’’ We understand that periodontal diseases originate as bacterial assaults, but some two-thirds of the destruction comesfrom the inflammatory response to the bacterial invasion. There is growing evidence that inflammation can be transferred from the oral cavity to other parts of the body (and vice versa), explaining the possible association between periodontitis and other chronic inflammatory conditions. As a clinician, I find this intellectually interesting, but when I ask myself whether or not this shift from aninfection model to an inflammation model changes the way I treat my patients, the answer is, ‘‘not really.’’ But should it? Have I been so busy in my daily practice that I missed something important? Although I may not understand inflammation on the molecular level, I do know when my patients have inflammation, and when I do what I have been trained to do as a diagnostician and a clinician toeliminate it, most of my patients end up with a good clinical outcome. My job as a clinician is to translate what is going on in research and incorporate it into my practice to provide the best possible patient care. What I offer you in this commentary are the results of my journey to discover how or if our new emphasis on inflammation should affect how I care for my patients. My conclusion at thistime is that I should err on the side of aggressive control of periodontal inflammation, since, until proven otherwise, the consequences of under treatment could be more than the loss of a few teeth. It is your job to decide how this information influences the treatment of your patients.
KEY WORDS
Clinical practice; inflammation; periodontal diseases; risk factors. In an effort to explore how thenew emphasis on inflammation may change the way we treat our patients, I studied the literature on inflammation and queried experts in the field to find answers to the questions in Table 1. I confirmed much of what I was already doing in my practice, but I also considered some changes I might make.
INFLAMMATION AND RISK ASSESSMENT
The real challenge in assessing risk is to identify individualswho are most susceptible to inflammation: those patients with a proinflammatory phenotype, whose response to inflammation seems exaggerated and whose disease seems intractable. How effective are our present tools for identifying these patients before severe attachment loss results? Currently, the answer is, ‘‘not very.’’ Periodontists have been trained in identifying the outward signs ofinflammation: changes in tissue color and bleeding on probing that signal vascular proliferation, tissue fragility, and edema. As we monitor attachment levels and probing depths, surrogates for connective tissue remodeling during the inflammatory process and wound healing, we must not forget that clinical presentation does not always correlate with infection and inflammation. Infection with certainbacteria, for example, Eikenella corrodens, does not always result in clinical inflammation; the inflammation exists at the biochemical level but is not clinically visible. Clearly, our patients’ clinical presentations, although important, do not allow us to identify hyperresponders to inflammation in advance.
Moreover, as we demonstrated in a series of articles on prognosis,1-4 clinical parameters,...