Dear  yes this is true and it is very clear in aggressive form of periodontitis in which there is altered host immune response. Neutrophils in such patients excrete more collagenase enzymes which destroy more host healthy tissues (friendly fire), so the net result willbe more destruction due to the summation of bacterial destruction plus the destruction by host neutrophils. This is why we have to give antibiotic for bacteria and host modulation therapy for host neutrophis called periostat (20mg capsule/ twice daily of doxycycline hyclate)

thank you Dr. Hossam, yes a part of that, patients with aggressive periodontitis have defect in neutrophils function like defect in chemotaxis and phagocytosis 

You bet it is both protective and destructive. Protective in the sense that the immune system works with different therapies to rid the pockets and biofilms of pathogenic bacteria. It becomes destructive when the immune system become "overactive" to certain pathogens and then treatment is the  reduction of the pathogens that illicit the destructive response. It is not one or the other either, both process are a factor in the spread of periodontal disease.

Host response has a protective role and is required for combating the putative periodontopathic pathogens but an exaggerated response proves to be detrimental. Dampening the overactive response is the key to successful periodontal therapy

Yes Dr Paul and Dr. Nithya,,,, when it is over active  or when there is an exaggerated response,,,,, but the question is when and where or how do you know it is over active to drop it down by giving anti immune therapy, host response is always needed when there is a challenge there you cant stop it or drop it down as it a natural defense mechanism or a natural response to stop a disease and overwhelm the situation.

I think at the end of the day the only thing we can do is to reduce the amount of the pathogens so we can reduce the reaction and stop the destruction.

The exaggerated response can also be controlled by reducing the inflammatory burden in the body. the anti inflammatory factors should keep this under check and switch to the resolution phase

yes Nithya studies suggested that patient under long time NSAIDs -  anti inflammatory drugs experience less amount of bone loss, which is an indication of part of tissue destruction and bone loss are due to host mechanism it self, when host response is modulated by anti-inflammatory drugs tissue destruction goes minimum

The pro/anti inflammatory balance could be tipped more towards anti by lifestyle factors and nutrition. Ridding the body of any kind of inflammatory burden is the basis of periodontal medicine

Chronic periodontitis itself is a protective phenomenon. The Host Derived Mediators of Inflammation (HDMI) are produced in response to hypoxia and agents from the inflammatory cells-- ,mainly neutrophils.  Working together with reactive oxygen species, they lead to the activation of latent matrix metalloproteinases (MMPs). The MMPs, HDMI etc are primarily protective of the host. However, in this process, the inflammatory products and MMPs end up digesting periodontal tissues of the host they are trying to protect.

Unfortunately, as the process continues, the dangers of hematogenous spread of LPS and other products of Inflammation increase. The Host most therefore FRANTICALLY attempt to keep the inflammation localized even at the expense of periodontal tissues. This perpetuates destructive chronic periodontitis which in turn increases inflammatory mediators and the vicious cycle continues!

Therefore, chronic periodontitis is a result of HDMIs, primarily protective but secondarily destructive. 

 well done Dr. Muhator,  yes it looks like a war, where ever the is war there is destruction, so this natural protective process has a destructive consequences on the host tissue it self at  the end of the day

The complexity of periodontitis is readily realized by the widely accepted fact that the immune response is a double-edged sword. For instance the cytokines IFN-γ and TNF-α are thought to participate in the periodontal tissue breakdown cascade, but are also considered important in the control of the periodontal infection. A competition at one scale among parts of a complex system can very well be maintained by cooperation of these parts at a finer scale below. A very important property of complex systems is self-organization (SO) in a space of scale invariance, provided by strange attractors like periodontal ligament. SO is a complex system’s evolutionary process without any external factor imposed. As SO is engaged, all involved parameters are tied up without being possible to isolate one of them in the description of the system. On the other hand, an emergent global behavior as a result of SO offers the ground for predictability out of the system’s chaotic (aperiodic, sensitive to initial conditions and therefore unpredictable) behaviour. So aggressive or chronic is a matter of probabilities of locking SO in a certain level of host defense (in a collective sense). We say the whole matters more than the parts, as it is well known in complexity theory.

Dear Dr. Faraedon, I must complement you on the wonderful thought provoking question. If we see from a broad perspective then mainly we have two forms i.e chronic and aggressive; though we do have periodontitis as a manifestation of systemic diseases etc but we don't touch that for now. As we are aware that Periodontal diseases in general are chronic infectious inflammatory diseases and are characterized by destruction of tooth-supporting structures. Now just the mere presence of periodontopathogens are not sufficient to cause this disease. Now as a general rule we know that host inflammatory mediators have been associated with tissue destruction, while anti-inflammatory mediators counteract and attenuate disease progression. With the discovery of several T-cell subsets bearing distinct immunoregulatory properties, this pro- vs. anti-inflammatory scenario has became all the more complex with a series of studies hypothesizing protective or destructive roles for Th1, Th2, Th17, and Treg subpopulations of polarized lymphocytes. Interestingly, the "protective vs. destructive" archetype is usually considered in a framework related to tissue destruction and disease progression. However, it is important to remember that periodontal diseases are infectious inflammatory conditions, and recent studies have demonstrated that cytokines (TNF-α and IFN-γ) considered harmful in the context of tissue destruction play important roles in the control of periodontal infection. The million dollar question is how do we know its the protective phase or the destructive phase.. To be frank I myself have no firm answer on it. Hajishengallis in his latest PSD model of periodontal disease etiology again tells speaks about keystone pathogens but doesn't mention how do we come to know if they have turned. Presently, research is on and maybe in a decades time I should be able to answer your question in a much better fashion. Till then the debate goes on..

Very briefly !!! As far as my knowledge is concerned, initially host response acts as a protective mechanism which fights against microbes by releasing inflammatory mediators and cells. But as the time progresses and when more plaque accumulates the inflammatory cells such as macrophages which were released earlier to fight microbes starts destructive process. keeping in mind that this is not the detailed answer but a brief one. Thats how this could be explained and i got this from ecological plaque hypothesis.

 More answers on this matter will certainly help in better understanding..

Thank you