The paper is a survey paper and he does summarize the work of others.
I'm not schooled enough in the art to identify Loesche's unique
contirbution.

I found the list of pathogens studied suprisingly small. At one point
he cites more thatn 400 species in the plaque. When he summarizes
earlier studies in table 2 and 5 he concentrates on 10. In his
conclusion he callls out only 3 (P. gingivalis, B. forsythus, and T.
denticola)

Bacterial species that were monitored listed in tables 2 and 5

Micro-aerophilic
Aa,       A. actinomycetemcomitans;
Cr,        C. rectus;
Ec,       E. corrodens;

Anerobic
Pg,         P. gingivalis;
Bf,          B. forsythus;
Td,        T. denticola;
Pi/Pn,   P. intermedia/nigrenscens;
Fn,        F. nucleatum;
Eub. Sp. = Eubacterium species;
Spir,     spirochetes;
Tv,       T. vincentii.

BTW... I hope my summaries have not mis represented Loesche's view.
I'll let him speak for himself in the conclusion to his survey paper

"The evidence presented in this review indicates that most, if not
all, forms of periodontal disease are specific, albeit chronic,
infections. Regardless of whether the host is genetically predisposed
to periodontal disease, as in Papillon-LeFevre syndrome or Down
syndrome, or if the host is compromised by leukocyte defects as in LJP
or diabetes, or is a smoker, or has poor oral hygiene, or has simply
aged, the clinical symptoms are almost always significantly associated
with the overgrowth of a finite number of anaerobic species, such as
P. gingivalis, B. forsythus, and T. denticola in the subgingival
plaque. This overgrowth can be periodically suppressed by mechanical
debridement over a lifetime, the current treatment paradigm, or the
flora can be altered by the judicious short-term usage of
antimicrobial agents targeted against the specific anaerobes. This
latter approach, while supported by several double-blind clinical
studies (147), goes contrary to centuries of dental teaching which
states that periodontal disease results from the overgrowth of plaque
on the tooth surfaces, i.e., a "dirty mouth." The challenge lies not
in proving that periodontal disease is an infection but in
implementing treatment procedures based on the fact that it is an
infection. The antimicrobial treatment of periodontal infections will
benefit from studies suggesting that periodontal disease may be a risk
factor for cardiovascular disease and stroke. If an antimicrobial
approach is as effective as a surgical approach in the restoration and
maintenance of a periodontally healthy dentition (147, 153), this
would give a cardiac or stroke patient and his or her physician a
choice in the implementation of treatment seeking to improve the
patient's periodontal condition so as to reduce and/or delay future
cardiovascular events.

I'm not sure.. I have not read the refeerences he cites. It may be
that the electron microscope observation is that  the the anerobic
pathogens preferentially occupy the tubules, and that when you scrape
the general population away when you debride, you leave the pathogens.
However.. that does not conform to my undestanding of the
symbiotic/ecological  relation among the species. By that I mean the
anaerobes don't show up  until the aerobes have created the proper
ecological niche.

That's my general understanding too

Spirochetes  are found in Acute necrotizing ulcerative gingivitis.(the
trench mouth of ww1)as well as AP.  Apparently the understanding of
the "cause " shifted from the anerobic spirochetes to the
microaerophilic  A. actinomycetemcomitans and now back to the
anerobes. Because their caracteristic structure is evident in a phase
contrast microscope, Loesche suggests spirochetes  be used as an
indicator of AP. He says

"The older literature identified anaerobic organisms such as
spirochetes and black-pigmented Bacteroides species (now classified as
Porphyromonas and Prevotella species), as putative periodontal
pathogens "

"With the identification of A. actinomycetemcomitans as a putative
periodontal pathogen, emphasis shifted from anaerobes to this
microaerophilic species. "

"The findings shown in Tables 2 through 4, involving large numbers of
samples and using diverse methods, indicate that anaerobes, rather
than A. actinomycetemcomitans or other microaerophilic species, are
more likely to be present or to dominate in plaques associated with
EOP and AP. This would suggest that treatment strategies and tactics
should be designed to selectively target certain anaerobic members of
the plaque flora."

By failure he means preiodontitis

" 30% <of the gerneral poulation> have periodontitis as defined by the
presence of three or more teeth with pockets of >= 4 mm ."

--George